A hypoperfusion of the BLOOD through an organ or tissue caused by a PATHOLOGIC CONSTRICTION or obstruction of its BLOOD VESSELS, or an absence of BLOOD CIRCULATION.
A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (CORONARY ARTERY DISEASE), to obstruction by a thrombus (CORONARY THROMBOSIS), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (MYOCARDIAL INFARCTION).
Localized reduction of blood flow to brain tissue due to arterial obstruction or systemic hypoperfusion. This frequently occurs in conjunction with brain hypoxia (HYPOXIA, BRAIN). Prolonged ischemia is associated with BRAIN INFARCTION.
Adverse functional, metabolic, or structural changes in ischemic tissues resulting from the restoration of blood flow to the tissue (REPERFUSION), including swelling; HEMORRHAGE; NECROSIS; and damage from FREE RADICALS. The most common instance is MYOCARDIAL REPERFUSION INJURY.
Damage to the MYOCARDIUM resulting from MYOCARDIAL REPERFUSION (restoration of blood flow to ischemic areas of the HEART.) Reperfusion takes place when there is spontaneous thrombolysis, THROMBOLYTIC THERAPY, collateral flow from other coronary vascular beds, or reversal of vasospasm.
Brief reversible episodes of focal, nonconvulsive ischemic dysfunction of the brain having a duration of less than 24 hours, and usually less than one hour, caused by transient thrombotic or embolic blood vessel occlusion or stenosis. Events may be classified by arterial distribution, temporal pattern, or etiology (e.g., embolic vs. thrombotic). (From Adams et al., Principles of Neurology, 6th ed, pp814-6)
Restoration of blood supply to tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. It is primarily a procedure for treating infarction or other ischemia, by enabling viable ischemic tissue to recover, thus limiting further necrosis. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing REPERFUSION INJURY.
A tissue or organ remaining at physiological temperature during decreased BLOOD perfusion or in the absence of blood supply. During ORGAN TRANSPLANTATION it begins when the organ reaches physiological temperature before the completion of SURGICAL ANASTOMOSIS and ends with reestablishment of the BLOOD CIRCULATION through the tissue.
The chilling of a tissue or organ during decreased BLOOD perfusion or in the absence of blood supply. Cold ischemia time during ORGAN TRANSPLANTATION begins when the organ is cooled with a cold perfusion solution after ORGAN PROCUREMENT surgery, and ends after the tissue reaches physiological temperature during implantation procedures.
A technique in which tissue is rendered resistant to the deleterious effects of prolonged ISCHEMIA and REPERFUSION by prior exposure to brief, repeated periods of vascular occlusion. (Am J Physiol 1995 May;268(5 Pt 2):H2063-7, Abstract)
A subfamily of the Muridae consisting of several genera including Gerbillus, Rhombomys, Tatera, Meriones, and Psammomys.
Reduced blood flow to the spinal cord which is supplied by the anterior spinal artery and the paired posterior spinal arteries. This condition may be associated with ARTERIOSCLEROSIS, trauma, emboli, diseases of the aorta, and other disorders. Prolonged ischemia may lead to INFARCTION of spinal cord tissue.
Elements of limited time intervals, contributing to particular results or situations.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
Exposure of myocardial tissue to brief, repeated periods of vascular occlusion in order to render the myocardium resistant to the deleterious effects of ISCHEMIA or REPERFUSION. The period of pre-exposure and the number of times the tissue is exposed to ischemia and reperfusion vary, the average being 3 to 5 minutes.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids.
NECROSIS occurring in the MIDDLE CEREBRAL ARTERY distribution system which brings blood to the entire lateral aspects of each CEREBRAL HEMISPHERE. Clinical signs include impaired cognition; APHASIA; AGRAPHIA; weak and numbness in the face and arms, contralaterally or bilaterally depending on the infarction.
Generally, restoration of blood supply to heart tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. Reperfusion can be induced to treat ischemia. Methods include chemical dissolution of an occluding thrombus, administration of vasodilator drugs, angioplasty, catheterization, and artery bypass graft surgery. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing MYOCARDIAL REPERFUSION INJURY.
The circulation of blood through the BLOOD VESSELS of the BRAIN.
The circulation of blood through the CORONARY VESSELS of the HEART.
The formation of an area of NECROSIS in the CEREBRUM caused by an insufficiency of arterial or venous blood flow. Infarcts of the cerebrum are generally classified by hemisphere (i.e., left vs. right), lobe (e.g., frontal lobe infarction), arterial distribution (e.g., INFARCTION, ANTERIOR CEREBRAL ARTERY), and etiology (e.g., embolic infarction).
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.
Either of two extremities of four-footed non-primate land animals. It usually consists of a FEMUR; TIBIA; and FIBULA; tarsals; METATARSALS; and TOES. (From Storer et al., General Zoology, 6th ed, p73)
The hollow, muscular organ that maintains the circulation of the blood.
NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).
Treatment process involving the injection of fluid into an organ or tissue.
An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels.
The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.
Agents that have a strengthening effect on the heart or that can increase cardiac output. They may be CARDIAC GLYCOSIDES; SYMPATHOMIMETICS; or other drugs. They are used after MYOCARDIAL INFARCT; CARDIAC SURGICAL PROCEDURES; in SHOCK; or in congestive heart failure (HEART FAILURE).
The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)
The act of constricting.
Obstruction of the flow in the SPLANCHNIC CIRCULATION by ATHEROSCLEROSIS; EMBOLISM; THROMBOSIS; STENOSIS; TRAUMA; and compression or intrinsic pressure from adjacent tumors. Rare causes are drugs, intestinal parasites, and vascular immunoinflammatory diseases such as PERIARTERITIS NODOSA and THROMBOANGIITIS OBLITERANS. (From Juergens et al., Peripheral Vascular Diseases, 5th ed, pp295-6)
Pathological processes which result in the partial or complete obstruction of ARTERIES. They are characterized by greatly reduced or absence of blood flow through these vessels. They are also known as arterial insufficiency.
Increased intracellular or extracellular fluid in brain tissue. Cytotoxic brain edema (swelling due to increased intracellular fluid) is indicative of a disturbance in cell metabolism, and is commonly associated with hypoxic or ischemic injuries (see HYPOXIA, BRAIN). An increase in extracellular fluid may be caused by increased brain capillary permeability (vasogenic edema), an osmotic gradient, local blockages in interstitial fluid pathways, or by obstruction of CSF flow (e.g., obstructive HYDROCEPHALUS). (From Childs Nerv Syst 1992 Sep; 8(6):301-6)
Recording of the moment-to-moment electromotive forces of the HEART as projected onto various sites on the body's surface, delineated as a scalar function of time. The recording is monitored by a tracing on slow moving chart paper or by observing it on a cardioscope, which is a CATHODE RAY TUBE DISPLAY.
Contractile activity of the MYOCARDIUM.
The inferior part of the lower extremity between the KNEE and the ANKLE.
The region of the lower limb in animals, extending from the gluteal region to the FOOT, and including the BUTTOCKS; HIP; and LEG.
The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.
Controlled physical activity which is performed in order to allow assessment of physiological functions, particularly cardiovascular and pulmonary, but also aerobic capacity. Maximal (most intense) exercise is usually required but submaximal exercise is also used.
The pathological process occurring in cells that are dying from irreparable injuries. It is caused by the progressive, uncontrolled action of degradative ENZYMES, leading to MITOCHONDRIAL SWELLING, nuclear flocculation, and cell lysis. It is distinct it from APOPTOSIS, which is a normal, regulated cellular process.
The flow of BLOOD through or around an organ or region of the body.
Prolonged dysfunction of the myocardium after a brief episode of severe ischemia, with gradual return of contractile activity.
A curved elevation of GRAY MATTER extending the entire length of the floor of the TEMPORAL HORN of the LATERAL VENTRICLE (see also TEMPORAL LOBE). The hippocampus proper, subiculum, and DENTATE GYRUS constitute the hippocampal formation. Sometimes authors include the ENTORHINAL CORTEX in the hippocampal formation.
Abnormally low BODY TEMPERATURE that is intentionally induced in warm-blooded animals by artificial means. In humans, mild or moderate hypothermia has been used to reduce tissue damages, particularly after cardiac or spinal cord injuries and during subsequent surgeries.
The application of repeated, brief periods of vascular occlusion at the onset of REPERFUSION to reduce REPERFUSION INJURY that follows a prolonged ischemic event. The techniques are similar to ISCHEMIC PRECONDITIONING but the time of application is after the ischemic event instead of before.
The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
The removal of a limb or other appendage or outgrowth of the body. (Dorland, 28th ed)
PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.
A method of non-invasive, continuous measurement of MICROCIRCULATION. The technique is based on the values of the DOPPLER EFFECT of low-power laser light scattered randomly by static structures and moving tissue particulates.
The thin layer of GRAY MATTER on the surface of the CEREBRAL HEMISPHERES that develops from the TELENCEPHALON and folds into gyri and sulchi. It reaches its highest development in humans and is responsible for intellectual faculties and higher mental functions.
The mitochondria of the myocardium.
An endogenous substance found mainly in skeletal muscle of vertebrates. It has been tried in the treatment of cardiac disorders and has been added to cardioplegic solutions. (Reynolds JEF(Ed): Martindale: The Extra Pharmacopoeia (electronic version). Micromedex, Inc, Englewood, CO, 1996)
A nucleoside that is composed of ADENINE and D-RIBOSE. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter.
The symptom of paroxysmal pain consequent to MYOCARDIAL ISCHEMIA usually of distinctive character, location and radiation. It is thought to be provoked by a transient stressful situation during which the oxygen requirements of the MYOCARDIUM exceed that supplied by the CORONARY CIRCULATION.
The anterior of the three primitive cerebral vesicles of the embryonic brain arising from the NEURAL TUBE. It subdivides to form DIENCEPHALON and TELENCEPHALON. (Stedmans Medical Dictionary, 27th ed)
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
The development of new BLOOD VESSELS during the restoration of BLOOD CIRCULATION during the healing process.
A transferase that catalyzes formation of PHOSPHOCREATINE from ATP + CREATINE. The reaction stores ATP energy as phosphocreatine. Three cytoplasmic ISOENZYMES have been identified in human tissues: the MM type from SKELETAL MUSCLE, the MB type from myocardial tissue and the BB type from nervous tissue as well as a mitochondrial isoenzyme. Macro-creatine kinase refers to creatine kinase complexed with other serum proteins.
An element with atomic symbol O, atomic number 8, and atomic weight [15.99903; 15.99977]. It is the most abundant element on earth and essential for respiration.
An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter.
Disease having a short and relatively severe course.
A process involving chance used in therapeutic trials or other research endeavor for allocating experimental subjects, human or animal, between treatment and control groups, or among treatment groups. It may also apply to experiments on inanimate objects.
Maintenance of blood flow to an organ despite obstruction of a principal vessel. Blood flow is maintained through small vessels.
A normal intermediate in the fermentation (oxidation, metabolism) of sugar. The concentrated form is used internally to prevent gastrointestinal fermentation. (From Stedman, 26th ed)
Any disturbances of the normal rhythmic beating of the heart or MYOCARDIAL CONTRACTION. Cardiac arrhythmias can be classified by the abnormalities in HEART RATE, disorders of electrical impulse generation, or impulse conduction.
The veins and arteries of the HEART.
Tissue NECROSIS in any area of the brain, including the CEREBRAL HEMISPHERES, the CEREBELLUM, and the BRAIN STEM. Brain infarction is the result of a cascade of events initiated by inadequate blood flow through the brain that is followed by HYPOXIA and HYPOGLYCEMIA in brain tissue. Damage may be temporary, permanent, selective or pan-necrosis.
A disorder characterized by a reduction of oxygen in the blood combined with reduced blood flow (ISCHEMIA) to the brain from a localized obstruction of a cerebral artery or from systemic hypoperfusion. Prolonged hypoxia-ischemia is associated with ISCHEMIC ATTACK, TRANSIENT; BRAIN INFARCTION; BRAIN EDEMA; COMA; and other conditions.
A hemeprotein from leukocytes. Deficiency of this enzyme leads to a hereditary disorder coupled with disseminated moniliasis. It catalyzes the conversion of a donor and peroxide to an oxidized donor and water. EC 1.11.1.7.
The circulation of the BLOOD through the MICROVASCULAR NETWORK.
The arterial blood vessels supplying the CEREBRUM.
The number of times the HEART VENTRICLES contract per unit of time, usually per minute.
The hemodynamic and electrophysiological action of the left HEART VENTRICLE. Its measurement is an important aspect of the clinical evaluation of patients with heart disease to determine the effects of the disease on cardiac performance.
An alternative to amputation in patients with neoplasms, ischemia, fractures, and other limb-threatening conditions. Generally, sophisticated surgical procedures such as vascular surgery and reconstruction are used to salvage diseased limbs.
Method in which prolonged electrocardiographic recordings are made on a portable tape recorder (Holter-type system) or solid-state device ("real-time" system), while the patient undergoes normal daily activities. It is useful in the diagnosis and management of intermittent cardiac arrhythmias and transient myocardial ischemia.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.
Salts or esters of LACTIC ACID containing the general formula CH3CHOHCOOR.
A large vessel supplying the whole length of the small intestine except the superior part of the duodenum. It also supplies the cecum and the ascending part of the colon and about half the transverse part of the colon. It arises from the anterior surface of the aorta below the celiac artery at the level of the first lumbar vertebra.
A tetrameric enzyme that, along with the coenzyme NAD+, catalyzes the interconversion of LACTATE and PYRUVATE. In vertebrates, genes for three different subunits (LDH-A, LDH-B and LDH-C) exist.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).
An in situ method for detecting areas of DNA which are nicked during APOPTOSIS. Terminal deoxynucleotidyl transferase is used to add labeled dUTP, in a template-independent manner, to the 3 prime OH ends of either single- or double-stranded DNA. The terminal deoxynucleotidyl transferase nick end labeling, or TUNEL, assay labels apoptosis on a single-cell level, making it more sensitive than agarose gel electrophoresis for analysis of DNA FRAGMENTATION.
Any of various animals that constitute the family Suidae and comprise stout-bodied, short-legged omnivorous mammals with thick skin, usually covered with coarse bristles, a rather long mobile snout, and small tail. Included are the genera Babyrousa, Phacochoerus (wart hogs), and Sus, the latter containing the domestic pig (see SUS SCROFA).
Operative procedures for the treatment of vascular disorders.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Relatively complete absence of oxygen in one or more tissues.
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
Devices for the compression of a blood vessel by application around an extremity to control the circulation and prevent the flow of blood to or from the distal area. (From Dorland, 28th ed)
A condition of decreased oxygen content at the cellular level.
The process by which chemical compounds provide protection to cells against harmful agents.
Application of a ligature to tie a vessel or strangulate a part.
A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.
Drugs used to cause dilation of the blood vessels.
A partial or complete return to the normal or proper physiologic activity of an organ or part following disease or trauma.
The main artery of the thigh, a continuation of the external iliac artery.
Organic compounds containing both the hydroxyl and carboxyl radicals.
The blood vessels which supply and drain the RETINA.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
A method of computed tomography that uses radionuclides which emit a single photon of a given energy. The camera is rotated 180 or 360 degrees around the patient to capture images at multiple positions along the arc. The computer is then used to reconstruct the transaxial, sagittal, and coronal images from the 3-dimensional distribution of radionuclides in the organ. The advantages of SPECT are that it can be used to observe biochemical and physiological processes as well as size and volume of the organ. The disadvantage is that, unlike positron-emission tomography where the positron-electron annihilation results in the emission of 2 photons at 180 degrees from each other, SPECT requires physical collimation to line up the photons, which results in the loss of many available photons and hence degrades the image.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
10-carbon saturated monocarboxylic acids.
A reduction in brain oxygen supply due to ANOXEMIA (a reduced amount of oxygen being carried in the blood by HEMOGLOBIN), or to a restriction of the blood supply to the brain, or both. Severe hypoxia is referred to as anoxia, and is a relatively common cause of injury to the central nervous system. Prolonged brain anoxia may lead to BRAIN DEATH or a PERSISTENT VEGETATIVE STATE. Histologically, this condition is characterized by neuronal loss which is most prominent in the HIPPOCAMPUS; GLOBUS PALLIDUS; CEREBELLUM; and inferior olives.
A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.
Non-human animals, selected because of specific characteristics, for use in experimental research, teaching, or testing.
The dialdehyde of malonic acid.
Inflammation of the COLON due to colonic ISCHEMIA resulting from alterations in systemic circulation or local vasculature.
A pathologic condition of acid accumulation or depletion of base in the body. The two main types are RESPIRATORY ACIDOSIS and metabolic acidosis, due to metabolic acid build up.
A group of pathological conditions characterized by sudden, non-convulsive loss of neurological function due to BRAIN ISCHEMIA or INTRACRANIAL HEMORRHAGES. Stroke is classified by the type of tissue NECROSIS, such as the anatomic location, vasculature involved, etiology, age of the affected individual, and hemorrhagic vs. non-hemorrhagic nature. (From Adams et al., Principles of Neurology, 6th ed, pp777-810)
The process by which organs are kept viable outside of the organism from which they were removed (i.e., kept from decay by means of a chemical agent, cooling, or a fluid substitute that mimics the natural state within the organism).
Pregnane derivatives containing three double bonds in the ring structures.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
The rate at which oxygen is used by a tissue; microliters of oxygen STPD used per milligram of tissue per hour; the rate at which oxygen enters the blood from alveolar gas, equal in the steady state to the consumption of oxygen by tissue metabolism throughout the body. (Stedman, 25th ed, p346)
A value equal to the total volume flow divided by the cross-sectional area of the vascular bed.
Synthetic or natural substances which are given to prevent a disease or disorder or are used in the process of treating a disease or injury due to a poisonous agent.
The lower right and left chambers of the heart. The right ventricle pumps venous BLOOD into the LUNGS and the left ventricle pumps oxygenated blood into the systemic arterial circulation.
Molecules or ions formed by the incomplete one-electron reduction of oxygen. These reactive oxygen intermediates include SINGLET OXYGEN; SUPEROXIDES; PEROXIDES; HYDROXYL RADICAL; and HYPOCHLOROUS ACID. They contribute to the microbicidal activity of PHAGOCYTES, regulation of signal transduction and gene expression, and the oxidative damage to NUCLEIC ACIDS; PROTEINS; and LIPIDS.
Solutions which, upon administration, will temporarily arrest cardiac activity. They are used in the performance of heart surgery.
Radiography of the vascular system of the heart muscle after injection of a contrast medium.
A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group.
The minute vessels that connect the arterioles and venules.
The largest of the cerebral arteries. It trifurcates into temporal, frontal, and parietal branches supplying blood to most of the parenchyma of these lobes in the CEREBRAL CORTEX. These are the areas involved in motor, sensory, and speech activities.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A procedure to stop the contraction of MYOCARDIUM during HEART SURGERY. It is usually achieved with the use of chemicals (CARDIOPLEGIC SOLUTIONS) or cold temperature (such as chilled perfusate).
The chemical reactions involved in the production and utilization of various forms of energy in cells.
Radiography of blood vessels after injection of a contrast medium.
The degree to which BLOOD VESSELS are not blocked or obstructed.
The domestic cat, Felis catus, of the carnivore family FELIDAE, comprising over 30 different breeds. The domestic cat is descended primarily from the wild cat of Africa and extreme southwestern Asia. Though probably present in towns in Palestine as long ago as 7000 years, actual domestication occurred in Egypt about 4000 years ago. (From Walker's Mammals of the World, 6th ed, p801)
The pressure within a CARDIAC VENTRICLE. Ventricular pressure waveforms can be measured in the beating heart by catheterization or estimated using imaging techniques (e.g., DOPPLER ECHOCARDIOGRAPHY). The information is useful in evaluating the function of the MYOCARDIUM; CARDIAC VALVES; and PERICARDIUM, particularly with simultaneous measurement of other (e.g., aortic or atrial) pressures.
Specialized non-fenestrated tightly-joined ENDOTHELIAL CELLS with TIGHT JUNCTIONS that form a transport barrier for certain substances between the cerebral capillaries and the BRAIN tissue.
An oxidoreductase that catalyzes the reaction between superoxide anions and hydrogen to yield molecular oxygen and hydrogen peroxide. The enzyme protects the cell against dangerous levels of superoxide. EC 1.15.1.1.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
Naturally occurring or synthetic substances that inhibit or retard the oxidation of a substance to which it is added. They counteract the harmful and damaging effects of oxidation in animal tissues.
A short pro-domain caspase that plays an effector role in APOPTOSIS. It is activated by INITIATOR CASPASES such as CASPASE 9. Isoforms of this protein exist due to multiple alternative splicing of its MESSENGER RNA.
A potentially lethal cardiac arrhythmia that is characterized by uncoordinated extremely rapid firing of electrical impulses (400-600/min) in HEART VENTRICLES. Such asynchronous ventricular quivering or fibrillation prevents any effective cardiac output and results in unconsciousness (SYNCOPE). It is one of the major electrocardiographic patterns seen with CARDIAC ARREST.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
Substances that influence the course of a chemical reaction by ready combination with free radicals. Among other effects, this combining activity protects pancreatic islets against damage by cytokines and prevents myocardial and pulmonary perfusion injuries.
The creation and display of functional images showing where the blood is flowing into the MYOCARDIUM by following over time the distribution of tracers injected into the blood stream.
The measure of the level of heat of a human or animal.
The continuation of the femoral artery coursing through the popliteal fossa; it divides into the anterior and posterior tibial arteries.
The normality of a solution with respect to HYDROGEN ions; H+. It is related to acidity measurements in most cases by pH = log 1/2[1/(H+)], where (H+) is the hydrogen ion concentration in gram equivalents per liter of solution. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)
Abrupt reduction in kidney function. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; ACUTE KIDNEY TUBULAR NECROSIS; and other less severe conditions.
Pathological processes involving any one of the BLOOD VESSELS in the vasculature outside the HEART.
Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.
A subtype of striated muscle, attached by TENDONS to the SKELETON. Skeletal muscles are innervated and their movement can be consciously controlled. They are also called voluntary muscles.
The section of the alimentary canal from the STOMACH to the ANAL CANAL. It includes the LARGE INTESTINE and SMALL INTESTINE.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
Surgical removal of an obstructing clot or foreign material which has been transported from a distant vessel by the bloodstream. Removal of a clot at its original site is called THROMBECTOMY.
An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.
The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.
Studies in which individuals or populations are followed to assess the outcome of exposures, procedures, or effects of a characteristic, e.g., occurrence of disease.
In screening and diagnostic tests, the probability that a person with a positive test is a true positive (i.e., has the disease), is referred to as the predictive value of a positive test; whereas, the predictive value of a negative test is the probability that the person with a negative test does not have the disease. Predictive value is related to the sensitivity and specificity of the test.
The electric response evoked in the CEREBRAL CORTEX by stimulation along AFFERENT PATHWAYS from PERIPHERAL NERVES to CEREBRUM.
A potent noncompetitive antagonist of the NMDA receptor (RECEPTORS, N-METHYL-D-ASPARTATE) used mainly as a research tool. The drug has been considered for the wide variety of neurodegenerative conditions or disorders in which NMDA receptors may play an important role. Its use has been primarily limited to animal and tissue experiments because of its psychotropic effects.
Death and putrefaction of tissue usually due to a loss of blood supply.
An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
A method of recording heart motion and internal structures by combining ultrasonic imaging with exercise testing (EXERCISE TEST) or pharmacologic stress.
A family of iminourea derivatives. The parent compound has been isolated from mushrooms, corn germ, rice hulls, mussels, earthworms, and turnip juice. Derivatives may have antiviral and antifungal properties.
Compounds based on N-phenylacetamide, that are similar in structure to 2-PHENYLACETAMIDES. They are precursors of many other compounds. They were formerly used as ANALGESICS and ANTIPYRETICS, but often caused lethal METHEMOGLOBINEMIA.
Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques.
Solutions used to store organs and minimize tissue damage, particularly while awaiting implantation.
Highly reactive molecules with an unsatisfied electron valence pair. Free radicals are produced in both normal and pathological processes. They are proven or suspected agents of tissue damage in a wide variety of circumstances including radiation, damage from environment chemicals, and aging. Natural and pharmacological prevention of free radical damage is being actively investigated.
Use of a balloon catheter for dilation of an occluded artery. It is used in treatment of arterial occlusive diseases, including renal artery stenosis and arterial occlusions in the leg. For the specific technique of BALLOON DILATION in coronary arteries, ANGIOPLASTY, BALLOON, CORONARY is available.
Studies used to test etiologic hypotheses in which inferences about an exposure to putative causal factors are derived from data relating to characteristics of persons under study or to events or experiences in their past. The essential feature is that some of the persons under study have the disease or outcome of interest and their characteristics are compared with those of unaffected persons.
Compounds that bind to and block the stimulation of PURINERGIC P1 RECEPTORS.
Either of two large arteries originating from the abdominal aorta; they supply blood to the pelvis, abdominal wall and legs.
A stable, non-explosive inhalation anesthetic, relatively free from significant side effects.
Complications that affect patients during surgery. They may or may not be associated with the disease for which the surgery is done, or within the same surgical procedure.
A spectrum of pathological conditions of impaired blood flow in the brain. They can involve vessels (ARTERIES or VEINS) in the CEREBRUM, the CEREBELLUM, and the BRAIN STEM. Major categories include INTRACRANIAL ARTERIOVENOUS MALFORMATIONS; BRAIN ISCHEMIA; CEREBRAL HEMORRHAGE; and others.
Agents that affect the rate or intensity of cardiac contraction, blood vessel diameter, or blood volume.
A XANTHINE OXIDASE inhibitor that decreases URIC ACID production. It also acts as an antimetabolite on some simpler organisms.
An antidiabetic sulfonylurea derivative with actions similar to those of chlorpropamide.
Levels within a diagnostic group which are established by various measurement criteria applied to the seriousness of a patient's disorder.
A symptom complex characterized by pain and weakness in SKELETAL MUSCLE group associated with exercise, such as leg pain and weakness brought on by walking. Such muscle limpness disappears after a brief rest and is often relates to arterial STENOSIS; muscle ISCHEMIA; and accumulation of LACTATE.
Pathologic processes that affect patients after a surgical procedure. They may or may not be related to the disease for which the surgery was done, and they may or may not be direct results of the surgery.
Interstitial space between cells, occupied by INTERSTITIAL FLUID as well as amorphous and fibrous substances. For organisms with a CELL WALL, the extracellular space includes everything outside of the CELL MEMBRANE including the PERIPLASM and the cell wall.
A class of large neuroglial (macroglial) cells in the central nervous system - the largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the BLOOD-BRAIN BARRIER. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with MICROGLIA) respond to injury.
A technique for measuring extracellular concentrations of substances in tissues, usually in vivo, by means of a small probe equipped with a semipermeable membrane. Substances may also be introduced into the extracellular space through the membrane.
A non-essential amino acid naturally occurring in the L-form. Glutamic acid is the most common excitatory neurotransmitter in the CENTRAL NERVOUS SYSTEM.
Unstable isotopes of thallium that decay or disintegrate emitting radiation. Tl atoms with atomic weights 198-202, 204, and 206-210 are thallium radioisotopes.
Formation of an infarct, which is NECROSIS in tissue due to local ISCHEMIA resulting from obstruction of BLOOD CIRCULATION, most commonly by a THROMBUS or EMBOLUS.
The property of blood capillary ENDOTHELIUM that allows for the selective exchange of substances between the blood and surrounding tissues and through membranous barriers such as the BLOOD-AIR BARRIER; BLOOD-AQUEOUS BARRIER; BLOOD-BRAIN BARRIER; BLOOD-NERVE BARRIER; BLOOD-RETINAL BARRIER; and BLOOD-TESTIS BARRIER. Small lipid-soluble molecules such as carbon dioxide and oxygen move freely by diffusion. Water and water-soluble molecules cannot pass through the endothelial walls and are dependent on microscopic pores. These pores show narrow areas (TIGHT JUNCTIONS) which may limit large molecule movement.
The circulation of blood through the BLOOD VESSELS supplying the abdominal VISCERA.
The diffusion or accumulation of neutrophils in tissues or cells in response to a wide variety of substances released at the sites of inflammatory reactions.
Tomography using x-ray transmission and a computer algorithm to reconstruct the image.
Recording of electric currents developed in the brain by means of electrodes applied to the scalp, to the surface of the brain, or placed within the substance of the brain.
The farthest or outermost projections of the body, such as the HAND and FOOT.
Cell membrane glycoproteins that are selectively permeable to potassium ions. At least eight major groups of K channels exist and they are made up of dozens of different subunits.
Genetically developed small pigs for use in biomedical research. There are several strains - Yucatan miniature, Sinclair miniature, and Minnesota miniature.
A phosphodiesterase inhibitor that blocks uptake and metabolism of adenosine by erythrocytes and vascular endothelial cells. Dipyridamole also potentiates the antiaggregating action of prostacyclin. (From AMA Drug Evaluations Annual, 1994, p752)
An analgesic and antipyretic that has been given by mouth and as ear drops. Antipyrine is often used in testing the effects of other drugs or diseases on drug-metabolizing enzymes in the liver. (From Martindale, The Extra Pharmacopoeia, 30th ed, p29)
The condition of an anatomical structure's being constricted beyond normal dimensions.

Expression of thrombospondin-1 in ischemia-induced retinal neovascularization. (1/5696)

Thrombospondin-1 is an extracellular matrix protein that inhibits endothelial cell proliferation, migration, and angiogenesis. This study was performed to investigate the role of thrombospondin-1 in ischemic retinal neovascularization. In a murine model of retinal neovascularization, thrombospondin-1 mRNA was increased from postnatal day 13 (P13), with a threefold peak response observed on P15, corresponding to the time of development of retinal neovascularization. Prominent expression of thrombospondin-1 was observed in neovascular cells, specifically, cells adjacent to the area of nonperfusion. It has been suggested that vascular endothelial growth factor (VEGF) plays a major role in ischemia-induced retinal neovascularization of this model, so we studied the effects of VEGF on thrombospondin-1 expression. In bovine retinal microcapillary endothelial cells, VEGF induced a biphasic response of thrombospondin-1 expression; VEGF decreased thrombospondin-1 mRNA 0.41-fold after 4 hours, whereas it increased, with a threefold peak response, after 24 hours. VEGF-induced endothelial cell proliferation was completely inhibited by exogenous thrombospondin-1 and increased by 37.5% with anti-thrombospondin-1 antibody. The present findings suggest that, in the ischemic retina, retinal neovascular cells increase thrombospondin-1 expression, and VEGF may stimulate endogenous thrombospondin-1 induction, which inhibits endothelial cell growth. VEGF-mediated thrombospondin-1 induction in ischemia-induced angiogenesis may be a negative feedback mechanism.  (+info)

Rescue of diabetes-related impairment of angiogenesis by intramuscular gene therapy with adeno-VEGF. (2/5696)

Diabetes is a major risk factor for coronary and peripheral artery diseases. Although diabetic patients often present with advanced forms of these diseases, it is not known whether the compensatory mechanisms to vascular ischemia are affected in this condition. Accordingly, we sought to determine whether diabetes could: 1) impair the development of new collateral vessel formation in response to tissue ischemia and 2) inhibit cytokine-induced therapeutic neovascularization. Hindlimb ischemia was created by femoral artery ligation in nonobese diabetic mice (NOD mice, n = 20) and in control C57 mice (n = 20). Hindlimb perfusion was evaluated by serial laser Doppler studies after the surgery. In NOD mice, measurement of the Doppler flow ratio between the ischemic and the normal limb indicated that restoration of perfusion in the ischemic hindlimb was significantly impaired. At day 14 after surgery, Doppler flow ratio in the NOD mice was 0.49+/-0.04 versus 0.73+/-0.06 for the C57 mice (P< or =0.005). This impairment in blood flow recovery persisted throughout the duration of the study with Doppler flow ratio values at day 35 of 0.50+/-0.05 versus 0.90+/-0.07 in the NOD and C57 mice, respectively (P< or =0.001). CD31 immunostaining confirmed the laser Doppler data by showing a significant reduction in capillary density in the NOD mice at 35 days after surgery (302+/-4 capillaries/mm2 versus 782+/-78 in C57 mice (P< or =0.005). The reduction in neovascularization in the NOD mice was the result of a lower level of vascular endothelial growth factor (VEGF) in the ischemic tissues, as assessed by Northern blot, Western blot and immunohistochemistry. The central role of VEGF was confirmed by showing that normal levels of neovascularization (compared with C57) could be achieved in NOD mice that had been supplemented for this growth factor via intramuscular injection of an adenoviral vector encoding for VEGF. We conclude that 1) diabetes impairs endogenous neovascularization of ischemic tissues; 2) the impairment in new blood vessel formation results from reduced expression of VEGF; and 3) cytokine supplementation achieved by intramuscular adeno-VEGF gene transfer restores neovascularization in a mouse model of diabetes.  (+info)

Modulation of the thermoregulatory sweating response to mild hyperthermia during activation of the muscle metaboreflex in humans. (3/5696)

1. To investigate the effect of the muscle metaboreflex on the thermoregulatory sweating response in humans, eight healthy male subjects performed sustained isometric handgrip exercise in an environmental chamber (35 C and 50 % relative humidity) at 30 or 45 % maximal voluntary contraction (MVC), at the end of which the blood circulation to the forearm was occluded for 120 s. The environmental conditions were such as to produce sweating by increase in skin temperature without a marked change in oesophageal temperature. 2. During circulatory occlusion after handgrip exercise at 30 % MVC for 120 s or at 45 % MVC for 60 s, the sweating rate (SR) on the chest and forearm (hairy regions), and the mean arterial blood pressure were significantly above baseline values (P < 0.05). There were no changes from baseline values in the oesophageal temperature, mean skin temperature, or SR on the palm (hairless regions). 3. During the occlusion after handgrip exercise at 30 % MVC for 60 s and during the occlusion alone, none of the measured parameters differed from baseline values. 4. It is concluded that, under mildly hyperthermic conditions, the thermoregulatory sweating response on the hairy regions is modulated by afferent signals from muscle metaboreceptors.  (+info)

Hypothermic neuroprotection of peripheral nerve of rats from ischaemia-reperfusion injury. (4/5696)

Although there is much information on experimental ischaemic neuropathy, there are only scant data on neuroprotection. We evaluated the effectiveness of hypothermia in protecting peripheral nerve from ischaemia-reperfusion injury using the model of experimental nerve ischaemia. Forty-eight male Sprague-Dawley rats were divided into six groups. We used a ligation-reperfusion model of nerve ischaemia where each of the supplying arteries to the sciatic-tibial nerves of the right hind limb was ligated and the ligatures were released after a predetermined period of ischaemia. The right hind limbs of one group (24 rats) were made ischaemic for 5 h and those of the other group (24 rats) for 3 h. Each group was further divided into three and the limbs were maintained at 37 degrees C (36 degrees C for 5 h of ischaemia) in one, 32 degrees C in the second and 28 degrees C in the third of these groups for the final 2 h of the ischaemic period and an additional 2 h of the reperfusion period. A behavioural score was recorded and nerve electrophysiology of motor and sensory nerves was undertaken 1 week after surgical procedures. At that time, entire sciatic-tibial nerves were harvested and fixed in situ. Four portions of each nerve were examined: proximal sciatic nerve, distal sciatic nerve, mid-tibial nerve and distal tibial nerve. To determine the degree of fibre degeneration, each section was studied by light microscopy, and we estimated an oedema index and a fibre degeneration index. The groups treated at 36-37 degrees C underwent marked fibre degeneration, associated with a reduction in action potential and impairment in behavioural score. The groups treated at 28 degrees C (for both 3 and 5 h) showed significantly less (P < 0.01; ANOVA, Bonferoni post hoc test) reperfusion injury for all indices (behavioural score, electrophysiology and neuropathology), and the groups treated at 32 degrees C had scores intermediate between the groups treated at 36-37 degrees C and 28 degrees C. Our results showed that cooling the limbs dramatically protects the peripheral nerve from ischaemia-reperfusion injury.  (+info)

Age-related outcome for peripheral thrombolysis. (5/5696)

OBJECTIVES: To investigate the age-related outcome of peripheral thrombolysis and determine for which patient group this treatment is worthwhile. DESIGN AND METHODS: A combined retrospective and prospective analysis of consecutive patients undergoing thrombolysis for acute lower-limb ischaemia was made with respect to age-related outcome and other risk factors. RESULTS: One hundred and two patients underwent thrombolysis for acute limb ischaemia. In the under 60 age group there was a 40% amputation rate. Seventy-three per cent of this group smoked. In the over 80 age group, the amputation rate was 15% and only 8% were smokers. CONCLUSION: Advancing age is not an adverse risk factor for thrombolysis which appears to be safe and effective in this patient group. There is a high incidence of smoking in the younger age group (< 60 years), in whom failed thrombolysis frequently leads to amputation.  (+info)

Accumulation of N-acyl-ethanolamine phospholipids in rat brains during post-decapitative ischemia: a 31p NMR study. (6/5696)

Phosphorus-31 nuclear magnetic resonance (31P NMR) spectroscopy has been used to study accumulation of N-acyl-ethanolamine phospholipids in rat brains during post-decapitative ischemia. Lipids were extracted from rat brain homogenates and the extracts were thoroughly washed with aq. potassium ethylenediaminetetraacetic acid (EDTA). The lower organic phases were isolated and evaporated to dryness under a stream of nitrogen and the lipids were redissolved in CDCl3-CH3OH-H2O 100.0:29.9:5.2 (v/v/v) for NMR analysis. Increasing the period of post-decapitative ischemia resulted in an accumulation of two signals in the NMR spectra at 0.18 and 0.22 ppm (relative to the chemical shift of 1,2-diacyl-sn-glycero-3-phosphocholine (PCDIACYL) at -0.84 ppm). These signals were identified as originating from 1,2-diacyl-sn-glycero-3-phospho-(N-acyl)-ethanolamine (NAPEDIACYL) and 1-(1'-alkenyl)-2-acyl-sn -glycero-3-phospho-(N-acyl)-ethanolamine (NAPEPLAS), respectively, by spiking with authentic materials. Additionally, the identification was verified by thin-layer chromatography, which also showed the accumulation of N-acyl-ethanolamine phospholipids. The use of K-EDTA instead of the commonly used Cs-EDTA in the preparation of the NMR samples allowed the separation of the chemical shifts of N-acyl-ethanolamine phospholipids from those of the ethanolamine phospholipids. Moreover, the chemical shift of cardiolipin was moved from 0.15 ppm observed with Cs-EDTA to about 0.31 ppm with K-EDTA. The present study demonstrates that it is possible to detect and quantify post-decapitative accumulation of NAPE subclasses (NAPEDIACYL and NAPEPLAS) in rat brains by the use of 31P NMR spectroscopy.  (+info)

Heart rate during exercise with leg vascular occlusion in spinal cord-injured humans. (7/5696)

Feed-forward and feedback mechanisms are both important for control of the heart rate response to muscular exercise, but their origin and relative importance remain inadequately understood. To evaluate whether humoral mechanisms are of importance, the heart rate response to electrically induced cycling was studied in participants with spinal cord injury (SCI) and compared with that elicited during volitional cycling in able-bodied persons (C). During voluntary exercise at an oxygen uptake of approximately 1 l/min, heart rate increased from 66 +/- 4 to 86 +/- 4 (SE) beats/min in seven C, and during electrically induced exercise at a similar oxygen uptake in SCI it increased from 73 +/- 3 to 110 +/- 8 beats/min. In contrast, blood pressure increased only in C (from 88 +/- 3 to 99 +/- 4 mmHg), confirming that, during exercise, blood pressure control is dominated by peripheral neural feedback mechanisms. With vascular occlusion of the legs, the exercise-induced increase in heart rate was reduced or even eliminated in the electrically stimulated SCI. For C, heart rate tended to be lower than during exercise with free circulation to the legs. Release of the cuff elevated heart rate only in SCI. These data suggest that humoral feedback is of importance for the heart rate response to exercise and especially so when influence from the central nervous system and peripheral neural feedback from the working muscles are impaired or eliminated during electrically induced exercise in individuals with SCI.  (+info)

CT angiography and Doppler sonography for emergency assessment in acute basilar artery ischemia. (8/5696)

BACKGROUND AND PURPOSE: Both Doppler sonography (DS) and spiral CT angiography (CTA) are noninvasive vascular assessment tools with a high potential for application in acute cerebral ischemia. The usefulness of CTA for vascular diagnosis in acute basilar artery (BA) ischemia has not yet been studied. METHODS: We prospectively studied 19 patients (mean+/-SD age, 58+/-11 years) with clinically suspected acute BA occlusion by DS and CTA. Prior extracranial and transcranial DS was performed in all but 1 patient, with DS 4 hours after CTA. In 6 of 19 patients, we performed digital subtraction angiography. RESULTS: CTA was diagnostic in all but 1 patient. CTA revealed complete BA occlusion in 9 patients and incomplete BA occlusion with some residual flow in 2 patients. A patent BA was shown in 7 patients. Because of severe BA calcification, CTA results were inconclusive in 1 patient. DS was diagnostic in only 7 of 19 patients, indicating certain BA occlusion in 3 patients and BA patency in 4 patients. In an additional 9 patients, the results of DS were inconclusive. DS was false-negative in 2 patients with distal BA occlusion shown by CTA and digital subtraction angiography. In 1 patient with DS performed after CTA, recanalization was demonstrated. In addition to the diagnosis or exclusion of BA occlusion, CTA provided information on the exact site and length of BA occlusion and collateral pathways. In our series, CTA results prompted indication for intra-arterial thrombolysis in 5 patients. CONCLUSIONS: CTA was superior to DS in the assessment of BA patency in patients with the syndrome of acute BA ischemia in terms of feasibility and conclusiveness, particularly in cases with distal BA occlusion. Our study confirmed the usefulness of combined extracranial and transcranial DS in the diagnosis and exclusion of proximal BA occlusion.  (+info)

There are several types of ischemia, including:

1. Myocardial ischemia: Reduced blood flow to the heart muscle, which can lead to chest pain or a heart attack.
2. Cerebral ischemia: Reduced blood flow to the brain, which can lead to stroke or cognitive impairment.
3. Peripheral arterial ischemia: Reduced blood flow to the legs and arms.
4. Renal ischemia: Reduced blood flow to the kidneys.
5. Hepatic ischemia: Reduced blood flow to the liver.

Ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as CT or MRI scans. Treatment for ischemia depends on the underlying cause and may include medications, lifestyle changes, or surgical interventions.

Myocardial ischemia can be caused by a variety of factors, including coronary artery disease, high blood pressure, diabetes, and smoking. It can also be triggered by physical exertion or stress.

There are several types of myocardial ischemia, including:

1. Stable angina: This is the most common type of myocardial ischemia, and it is characterized by a predictable pattern of chest pain that occurs during physical activity or emotional stress.
2. Unstable angina: This is a more severe type of myocardial ischemia that can occur without any identifiable trigger, and can be accompanied by other symptoms such as shortness of breath or vomiting.
3. Acute coronary syndrome (ACS): This is a condition that includes both stable angina and unstable angina, and it is characterized by a sudden reduction in blood flow to the heart muscle.
4. Heart attack (myocardial infarction): This is a type of myocardial ischemia that occurs when the blood flow to the heart muscle is completely blocked, resulting in damage or death of the cardiac tissue.

Myocardial ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as echocardiography or cardiac magnetic resonance imaging (MRI). Treatment options for myocardial ischemia include medications such as nitrates, beta blockers, and calcium channel blockers, as well as lifestyle changes such as quitting smoking, losing weight, and exercising regularly. In severe cases, surgical procedures such as coronary artery bypass grafting or angioplasty may be necessary.

The term ischemia refers to the reduction of blood flow, and it is often used interchangeably with the term stroke. However, not all strokes are caused by ischemia, as some can be caused by other factors such as bleeding in the brain. Ischemic stroke accounts for about 87% of all strokes.

There are different types of brain ischemia, including:

1. Cerebral ischemia: This refers to the reduction of blood flow to the cerebrum, which is the largest part of the brain and responsible for higher cognitive functions such as thought, emotion, and voluntary movement.
2. Cerebellar ischemia: This refers to the reduction of blood flow to the cerebellum, which is responsible for coordinating and regulating movement, balance, and posture.
3. Brainstem ischemia: This refers to the reduction of blood flow to the brainstem, which is responsible for controlling many of the body's automatic functions such as breathing, heart rate, and blood pressure.
4. Territorial ischemia: This refers to the reduction of blood flow to a specific area of the brain, often caused by a blockage in a blood vessel.
5. Global ischemia: This refers to the reduction of blood flow to the entire brain, which can be caused by a cardiac arrest or other systemic conditions.

The symptoms of brain ischemia can vary depending on the location and severity of the condition, but may include:

1. Weakness or paralysis of the face, arm, or leg on one side of the body
2. Difficulty speaking or understanding speech
3. Sudden vision loss or double vision
4. Dizziness or loss of balance
5. Confusion or difficulty with memory
6. Seizures
7. Slurred speech or inability to speak
8. Numbness or tingling sensations in the face, arm, or leg
9. Vision changes, such as blurred vision or loss of peripheral vision
10. Difficulty with coordination and balance.

It is important to seek medical attention immediately if you experience any of these symptoms, as brain ischemia can cause permanent damage or death if left untreated.

Reperfusion injury can cause inflammation, cell death, and impaired function in the affected tissue or organ. The severity of reperfusion injury can vary depending on the duration and severity of the initial ischemic event, as well as the promptness and effectiveness of treatment to restore blood flow.

Reperfusion injury can be a complicating factor in various medical conditions, including:

1. Myocardial infarction (heart attack): Reperfusion injury can occur when blood flow is restored to the heart muscle after a heart attack, leading to inflammation and cell death.
2. Stroke: Reperfusion injury can occur when blood flow is restored to the brain after an ischemic stroke, leading to inflammation and damage to brain tissue.
3. Organ transplantation: Reperfusion injury can occur when a transplanted organ is subjected to ischemia during harvesting or preservation, and then reperfused with blood.
4. Peripheral arterial disease: Reperfusion injury can occur when blood flow is restored to a previously occluded peripheral artery, leading to inflammation and damage to the affected tissue.

Treatment of reperfusion injury often involves medications to reduce inflammation and oxidative stress, as well as supportive care to manage symptoms and prevent further complications. In some cases, experimental therapies such as stem cell transplantation or gene therapy may be used to promote tissue repair and regeneration.

MRI can occur in various cardiovascular conditions, such as myocardial infarction (heart attack), cardiac arrest, and cardiac surgery. The severity of MRI can range from mild to severe, depending on the extent and duration of the ischemic event.

The pathophysiology of MRI involves a complex interplay of various cellular and molecular mechanisms. During ischemia, the heart muscle cells undergo changes in energy metabolism, electrolyte balance, and cell membrane function. When blood flow is restored, these changes can lead to an influx of calcium ions into the cells, activation of enzymes, and production of reactive oxygen species (ROS), which can damage the cells and their membranes.

The clinical presentation of MRI can vary depending on the severity of the injury. Some patients may experience chest pain, shortness of breath, and fatigue. Others may have more severe symptoms, such as cardiogenic shock or ventricular arrhythmias. The diagnosis of MRI is based on a combination of clinical findings, electrocardiography (ECG), echocardiography, and cardiac biomarkers.

The treatment of MRI is focused on addressing the underlying cause of the injury and managing its symptoms. For example, in patients with myocardial infarction, thrombolysis or percutaneous coronary intervention may be used to restore blood flow to the affected area. In patients with cardiac arrest, cardiopulmonary resuscitation (CPR) and other life-saving interventions may be necessary.

Prevention of MRI is crucial in reducing its incidence and severity. This involves aggressive risk factor management, such as controlling hypertension, diabetes, and dyslipidemia, as well as smoking cessation and stress reduction. Additionally, patients with a history of MI should adhere to their medication regimen, which may include beta blockers, ACE inhibitors or ARBs, statins, and aspirin.

In conclusion, myocardial injury with ST-segment elevation (MRI) is a life-threatening condition that requires prompt recognition and treatment. While the clinical presentation can vary depending on the severity of the injury, early diagnosis and management are crucial in reducing morbidity and mortality. Prevention through aggressive risk factor management and adherence to medication regimens is also essential in preventing MRI.

Example sentence: "The patient experienced a transient ischemic attack, which was caused by a temporary blockage in one of the blood vessels in their brain."

Synonyms: TIA, mini-stroke.

Symptoms of Spinal Cord Ischemia may include weakness, paralysis, loss of sensation, and loss of reflexes in the affected area. Diagnosis is typically made through a combination of physical examination, imaging studies such as MRI or CT scans, and laboratory tests.

Treatment for Spinal Cord Ischemia depends on the underlying cause and may include medications to dissolve blood clots, surgery to repair arterial damage, or supportive care to manage symptoms and prevent further damage. In severe cases, Spinal Cord Ischemia can lead to permanent neurological damage or death.

Spinal Cord Ischemia is a serious medical condition that requires prompt diagnosis and treatment to prevent long-term neurological damage or death.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

Infarction Middle Cerebral Artery (MCA) is a type of ischemic stroke that occurs when there is an obstruction in the middle cerebral artery. This artery supplies blood to the temporal lobe of the brain, which controls many important functions such as memory, language, and spatial reasoning. When this artery becomes blocked or ruptured, it can cause a lack of blood supply to the affected areas resulting in tissue death (infarction).

The symptoms of an MCA infarction can vary depending on the location and severity of the blockage. Some common symptoms include weakness or paralysis on one side of the body, difficulty with speech and language, memory loss, confusion, vision problems, and difficulty with coordination and balance. Patients may also experience sudden severe headache, nausea, vomiting, and fever.

The diagnosis of MCA infarction is based on a combination of clinical examination, imaging studies such as CT or MRI scans, and laboratory tests. Imaging studies can help to identify the location and severity of the blockage, while laboratory tests may be used to rule out other conditions that may cause similar symptoms.

Treatment for MCA infarction depends on the underlying cause of the blockage or rupture. In some cases, medications such as thrombolytics may be given to dissolve blood clots and restore blood flow to the affected areas. Surgery may also be required to remove any blockages or repair damaged blood vessels. Other interventions such as endovascular procedures or brain bypass surgery may also be used to restore blood flow.

In summary, middle cerebral artery infarction is a type of stroke that occurs when the blood supply to the brain is blocked or interrupted, leading to damage to the brain tissue. It can cause a range of symptoms including weakness or paralysis on one side of the body, difficulty with speech and language, memory loss, confusion, vision problems, and difficulty with coordination and balance. The diagnosis is based on a combination of clinical examination, imaging studies, and laboratory tests. Treatment options include medications, surgery, endovascular procedures, or brain bypass surgery.

Cerebral infarction can result in a range of symptoms, including sudden weakness or numbness in the face, arm, or leg on one side of the body, difficulty speaking or understanding speech, sudden vision loss, dizziness, and confusion. Depending on the location and severity of the infarction, it can lead to long-term disability or even death.

There are several types of cerebral infarction, including:

1. Ischemic stroke: This is the most common type of cerebral infarction, accounting for around 87% of all cases. It occurs when a blood clot blocks the flow of blood to the brain, leading to cell death and tissue damage.
2. Hemorrhagic stroke: This type of cerebral infarction occurs when a blood vessel in the brain ruptures, leading to bleeding and cell death.
3. Lacunar infarction: This type of cerebral infarction affects the deep structures of the brain, particularly the basal ganglia, and is often caused by small blockages or stenosis (narrowing) in the blood vessels.
4. Territorial infarction: This type of cerebral infarction occurs when there is a complete blockage of a blood vessel that supplies a specific area of the brain, leading to cell death and tissue damage in that area.

Diagnosis of cerebral infarction typically involves a combination of physical examination, medical history, and imaging tests such as CT or MRI scans. Treatment options vary depending on the cause and location of the infarction, but may include medication to dissolve blood clots, surgery to remove blockages, or supportive care to manage symptoms and prevent complications.

There are different types of myocardial infarctions, including:

1. ST-segment elevation myocardial infarction (STEMI): This is the most severe type of heart attack, where a large area of the heart muscle is damaged. It is characterized by a specific pattern on an electrocardiogram (ECG) called the ST segment.
2. Non-ST-segment elevation myocardial infarction (NSTEMI): This type of heart attack is less severe than STEMI, and the damage to the heart muscle may not be as extensive. It is characterized by a smaller area of damage or a different pattern on an ECG.
3. Incomplete myocardial infarction: This type of heart attack is when there is some damage to the heart muscle but not a complete blockage of blood flow.
4. Collateral circulation myocardial infarction: This type of heart attack occurs when there are existing collateral vessels that bypass the blocked coronary artery, which reduces the amount of damage to the heart muscle.

Symptoms of a myocardial infarction can include chest pain or discomfort, shortness of breath, lightheadedness, and fatigue. These symptoms may be accompanied by anxiety, fear, and a sense of impending doom. In some cases, there may be no noticeable symptoms at all.

Diagnosis of myocardial infarction is typically made based on a combination of physical examination findings, medical history, and diagnostic tests such as an electrocardiogram (ECG), cardiac enzyme tests, and imaging studies like echocardiography or cardiac magnetic resonance imaging.

Treatment of myocardial infarction usually involves medications to relieve pain, reduce the amount of work the heart has to do, and prevent further damage to the heart muscle. These may include aspirin, beta blockers, ACE inhibitors or angiotensin receptor blockers, and statins. In some cases, a procedure such as angioplasty or coronary artery bypass surgery may be necessary to restore blood flow to the affected area.

Prevention of myocardial infarction involves managing risk factors such as high blood pressure, high cholesterol, smoking, diabetes, and obesity. This can include lifestyle changes such as a healthy diet, regular exercise, and stress reduction, as well as medications to control these conditions. Early detection and treatment of heart disease can help prevent myocardial infarction from occurring in the first place.

Coronary disease is often caused by a combination of genetic and lifestyle factors, such as high blood pressure, high cholesterol levels, smoking, obesity, and a lack of physical activity. It can also be triggered by other medical conditions, such as diabetes and kidney disease.

The symptoms of coronary disease can vary depending on the severity of the condition, but may include:

* Chest pain or discomfort (angina)
* Shortness of breath
* Fatigue
* Swelling of the legs and feet
* Pain in the arms and back

Coronary disease is typically diagnosed through a combination of physical examination, medical history, and diagnostic tests such as electrocardiograms (ECGs), stress tests, and cardiac imaging. Treatment for coronary disease may include lifestyle changes, medications to control symptoms, and surgical procedures such as angioplasty or bypass surgery to improve blood flow to the heart.

Preventative measures for coronary disease include:

* Maintaining a healthy diet and exercise routine
* Quitting smoking and limiting alcohol consumption
* Managing high blood pressure, high cholesterol levels, and other underlying medical conditions
* Reducing stress through relaxation techniques or therapy.

Mesenteric vascular occlusion can be caused by various factors, such as atherosclerosis (hardening of the arteries), blood clots, or inflammation. This condition can lead to a reduction in blood flow to the intestines, which can cause symptoms such as abdominal pain, diarrhea, and vomiting. In severe cases, it can also lead to tissue death and potentially life-threatening complications.

There are several types of mesenteric vascular occlusion, including:

1. Acute mesenteric ischemia (AMI): This is a sudden and severe blockage of the blood vessels that supply the intestines, which can cause tissue death and potentially life-threatening complications.
2. Chronic mesenteric ischemia (CMI): This is a gradual and less severe blockage of the blood vessels that supply the intestines, which can cause symptoms such as abdominal pain and diarrhea.
3. Mesenteric venous thrombosis: This is the formation of a blood clot in the veins that drain blood from the intestines.

Diagnosis of mesenteric vascular occlusion typically involves imaging tests such as CT or MRI scans, and blood tests to check for signs of inflammation or tissue damage. Treatment options vary depending on the severity and cause of the condition, and may include medications to dissolve blood clots, surgery to repair or bypass blocked blood vessels, or in severe cases, removal of the affected intestine.

Types of Arterial Occlusive Diseases:

1. Atherosclerosis: Atherosclerosis is a condition where plaque builds up inside the arteries, leading to narrowing or blockages that can restrict blood flow to certain areas of the body.
2. Peripheral Artery Disease (PAD): PAD is a condition where the blood vessels in the legs and arms become narrowed or blocked, leading to pain or cramping in the affected limbs.
3. Coronary Artery Disease (CAD): CAD is a condition where the coronary arteries, which supply blood to the heart, become narrowed or blocked, leading to chest pain or a heart attack.
4. Carotid Artery Disease: Carotid artery disease is a condition where the carotid arteries, which supply blood to the brain, become narrowed or blocked, leading to stroke or mini-stroke.
5. Renal Artery Stenosis: Renal artery stenosis is a condition where the blood vessels that supply the kidneys become narrowed or blocked, leading to high blood pressure and decreased kidney function.

Symptoms of Arterial Occlusive Diseases:

1. Pain or cramping in the affected limbs
2. Weakness or fatigue
3. Difficulty walking or standing
4. Chest pain or discomfort
5. Shortness of breath
6. Dizziness or lightheadedness
7. Stroke or mini-stroke

Treatment for Arterial Occlusive Diseases:

1. Medications: Medications such as blood thinners, cholesterol-lowering drugs, and blood pressure medications may be prescribed to treat arterial occlusive diseases.
2. Lifestyle Changes: Lifestyle changes such as quitting smoking, exercising regularly, and eating a healthy diet can help manage symptoms and slow the progression of the disease.
3. Endovascular Procedures: Endovascular procedures such as angioplasty and stenting may be performed to open up narrowed or blocked blood vessels.
4. Surgery: In some cases, surgery may be necessary to treat arterial occlusive diseases, such as bypass surgery or carotid endarterectomy.

Prevention of Arterial Occlusive Diseases:

1. Maintain a healthy diet and lifestyle
2. Quit smoking and avoid exposure to secondhand smoke
3. Exercise regularly
4. Manage high blood pressure, high cholesterol, and diabetes
5. Avoid excessive alcohol consumption
6. Get regular check-ups with your healthcare provider

Early detection and treatment of arterial occlusive diseases can help manage symptoms, slow the progression of the disease, and prevent complications such as heart attack or stroke.

The word "edema" comes from the Greek word "oidema", meaning swelling.

Necrosis is a type of cell death that occurs when cells are exposed to excessive stress, injury, or inflammation, leading to damage to the cell membrane and the release of cellular contents into the surrounding tissue. This can lead to the formation of gangrene, which is the death of body tissue due to lack of blood supply.

There are several types of necrosis, including:

1. Coagulative necrosis: This type of necrosis occurs when there is a lack of blood supply to the tissues, leading to the formation of a firm, white plaque on the surface of the affected area.
2. Liquefactive necrosis: This type of necrosis occurs when there is an infection or inflammation that causes the death of cells and the formation of pus.
3. Caseous necrosis: This type of necrosis occurs when there is a chronic infection, such as tuberculosis, and the affected tissue becomes soft and cheese-like.
4. Fat necrosis: This type of necrosis occurs when there is trauma to fatty tissue, leading to the formation of firm, yellowish nodules.
5. Necrotizing fasciitis: This is a severe and life-threatening form of necrosis that affects the skin and underlying tissues, often as a result of bacterial infection.

The diagnosis of necrosis is typically made through a combination of physical examination, imaging studies such as X-rays or CT scans, and laboratory tests such as biopsy. Treatment depends on the underlying cause of the necrosis and may include antibiotics, surgical debridement, or amputation in severe cases.

During myocardial stunning, the heart muscle cells experience a temporary reduction in contractility and an increase in the amount of lactic acid produced. This can lead to symptoms such as chest pain, shortness of breath, and fatigue. In severe cases, myocardial stunning can progress to myocardial infarction (heart attack) or cardiac arrest.

Myocardial stunning is often seen in athletes who engage in intense exercise, such as marathon runners or professional football players. It can also occur in people with pre-existing heart conditions, such as coronary artery disease or hypertension.

Treatment of myocardial stunning typically involves addressing the underlying cause, such as reducing stress on the heart or improving blood flow to the myocardium. In severe cases, medications such as nitrates or beta blockers may be used to reduce the workload on the heart and improve contractility. In some cases, hospitalization may be necessary to monitor the condition and provide appropriate treatment.

Prevention of myocardial stunning involves taking steps to reduce the risk factors for heart disease, such as maintaining a healthy diet, exercising regularly, and managing stress. It is also important to seek medical attention if symptoms of myocardial stunning are present, as prompt treatment can help prevent more severe complications.

Angina pectoris is a medical condition that is characterized by recurring chest pain or discomfort due to reduced blood flow and oxygen supply to the heart muscle, specifically the myocardium. It is also known as stable angina or effort angina. The symptoms of angina pectoris typically occur during physical activity or emotional stress and are relieved by rest.

The term "angina" comes from the Latin word for "strangulation," which refers to the feeling of tightness or constriction in the chest that is associated with the condition. Angina pectoris can be caused by atherosclerosis, or the buildup of plaque in the coronary arteries, which supply blood to the heart muscle. This buildup can lead to the formation of atherosclerotic plaques that can narrow the coronary arteries and reduce blood flow to the heart muscle, causing chest pain.

There are several types of angina pectoris, including:

1. Stable angina: This is the most common type of angina and is characterized by predictable and reproducible symptoms that occur during specific situations or activities, such as exercise or emotional stress.
2. Unstable angina: This type of angina is characterized by unpredictable and changing symptoms that can occur at rest or with minimal exertion. It is often a sign of a more severe underlying condition, such as a heart attack.
3. Variant angina: This type of angina occurs during physical activity, but the symptoms are not relieved by rest.
4. Prinzmetal's angina: This is a rare type of angina that occurs at rest and is characterized by a feeling of tightness or constriction in the chest.

The diagnosis of angina pectoris is typically made based on a combination of physical examination, medical history, and diagnostic tests such as electrocardiogram (ECG), stress test, and imaging studies. Treatment for angina pectoris usually involves lifestyle modifications, such as regular exercise, a healthy diet, and stress management, as well as medications to relieve symptoms and reduce the risk of complications. In some cases, surgery or other procedures may be necessary to treat the underlying condition causing the angina.

Examples of acute diseases include:

1. Common cold and flu
2. Pneumonia and bronchitis
3. Appendicitis and other abdominal emergencies
4. Heart attacks and strokes
5. Asthma attacks and allergic reactions
6. Skin infections and cellulitis
7. Urinary tract infections
8. Sinusitis and meningitis
9. Gastroenteritis and food poisoning
10. Sprains, strains, and fractures.

Acute diseases can be treated effectively with antibiotics, medications, or other therapies. However, if left untreated, they can lead to chronic conditions or complications that may require long-term care. Therefore, it is important to seek medical attention promptly if symptoms persist or worsen over time.

There are many different types of cardiac arrhythmias, including:

1. Tachycardias: These are fast heart rhythms that can be too fast for the body's needs. Examples include atrial fibrillation and ventricular tachycardia.
2. Bradycardias: These are slow heart rhythms that can cause symptoms like fatigue, dizziness, and fainting. Examples include sinus bradycardia and heart block.
3. Premature beats: These are extra beats that occur before the next regular beat should come in. They can be benign but can also indicate an underlying arrhythmia.
4. Supraventricular arrhythmias: These are arrhythmias that originate above the ventricles, such as atrial fibrillation and paroxysmal atrial tachycardia.
5. Ventricular arrhythmias: These are arrhythmias that originate in the ventricles, such as ventricular tachycardia and ventricular fibrillation.

Cardiac arrhythmias can be diagnosed through a variety of tests including electrocardiograms (ECGs), stress tests, and holter monitors. Treatment options for cardiac arrhythmias vary depending on the type and severity of the condition and may include medications, cardioversion, catheter ablation, or implantable devices like pacemakers or defibrillators.

Types: There are several types of brain infarction, including:

1. Cerebral infarction: This type of infarction occurs when there is a blockage or obstruction in the blood vessels that supply the cerebrum, which is the largest part of the brain.
2. Cerebellar infarction: This type of infarction occurs when there is a blockage or obstruction in the blood vessels that supply the cerebellum, which is located at the base of the brain.
3. Brain stem infarction: This type of infarction occurs when there is a blockage or obstruction in the blood vessels that supply the brain stem, which is the part of the brain that controls vital functions such as breathing, heart rate, and blood pressure.

Symptoms: The symptoms of brain infarction can vary depending on the location and size of the affected area, but common symptoms include:

1. Sudden weakness or numbness in the face, arm, or leg
2. Sudden confusion or trouble speaking or understanding speech
3. Sudden difficulty seeing or blindness
4. Sudden difficulty walking or loss of balance
5. Sudden severe headache
6. Difficulty with coordination and movement
7. Slurred speech
8. Vision changes
9. Seizures

Diagnosis: Brain infarction is typically diagnosed using a combination of physical examination, medical history, and imaging tests such as CT or MRI scans. Other diagnostic tests may include blood tests to check for signs of infection or blood clotting abnormalities, and an electroencephalogram (EEG) to measure the electrical activity of the brain.

Treatment: The treatment of brain infarction depends on the underlying cause, but common treatments include:

1. Medications: To control symptoms such as high blood pressure, seizures, and swelling in the brain.
2. Endovascular therapy: A minimally invasive procedure to open or remove blockages in the blood vessels.
3. Surgery: To relieve pressure on the brain or repair damaged blood vessels.
4. Rehabilitation: To help regain lost function and improve quality of life.

Prognosis: The prognosis for brain infarction depends on the location and size of the affected area, as well as the promptness and effectiveness of treatment. In general, the earlier treatment is received, the better the outcome. However, some individuals may experience long-term or permanent disability, or even death.

The effects of hypoxia-ischemia on the brain can vary depending on the severity and duration of the insult, but may include:

* Cellular damage and death
* Inflammation and oxidative stress
* Neurotransmitter imbalances
* Blood-brain barrier disruption
* White matter degeneration

The long-term consequences of hypoxia-ischemia, brain may include cognitive impairments such as memory loss, attention deficits, and language difficulties. Behavioral changes, such as depression, anxiety, and mood swings, may also occur. In severe cases, the condition can lead to permanent vegetative state or death.

The diagnosis of hypoxia-ischemia, brain is based on a combination of clinical evaluation, laboratory tests, and imaging studies such as CT or MRI scans. Treatment options may include supportive care, medications, and rehabilitation therapies to address cognitive and behavioral impairments. In some cases, surgical interventions may be necessary to relieve pressure or restore blood flow to the affected areas.

Overall, hypoxia-ischemia, brain is a serious medical condition that requires prompt recognition and appropriate treatment to minimize long-term cognitive and functional impairments.

There are different types of anoxia, including:

1. Cerebral anoxia: This occurs when the brain does not receive enough oxygen, leading to cognitive impairment, confusion, and loss of consciousness.
2. Pulmonary anoxia: This occurs when the lungs do not receive enough oxygen, leading to shortness of breath, coughing, and chest pain.
3. Cardiac anoxia: This occurs when the heart does not receive enough oxygen, leading to cardiac arrest and potentially death.
4. Global anoxia: This is a complete lack of oxygen to the entire body, leading to widespread tissue damage and death.

Treatment for anoxia depends on the underlying cause and the severity of the condition. In some cases, hospitalization may be necessary to provide oxygen therapy, pain management, and other supportive care. In severe cases, anoxia can lead to long-term disability or death.

Prevention of anoxia is important, and this includes managing underlying medical conditions such as heart disease, diabetes, and respiratory problems. It also involves avoiding activities that can lead to oxygen deprivation, such as scuba diving or high-altitude climbing, without proper training and equipment.

In summary, anoxia is a serious medical condition that occurs when there is a lack of oxygen in the body or specific tissues or organs. It can cause cell death and tissue damage, leading to serious health complications and even death if left untreated. Early diagnosis and treatment are crucial to prevent long-term disability or death.

Brain hypoxia is a serious medical condition that requires prompt treatment to prevent long-term damage and improve outcomes for patients. Treatment options may include oxygen therapy, medications to improve blood flow to the brain, and surgery to remove any blockages or obstructions in blood vessels.

Examples of retinal diseases include:

1. Age-related macular degeneration (AMD): a leading cause of vision loss in people over the age of 50, AMD affects the macula, the part of the retina responsible for central vision.
2. Diabetic retinopathy (DR): a complication of diabetes that damages blood vessels in the retina and can cause blindness.
3. Retinal detachment: a condition where the retina becomes separated from the underlying tissue, causing vision loss.
4. Macular edema: swelling of the macula that can cause vision loss.
5. Retinal vein occlusion (RVO): a blockage of the small veins in the retina that can cause vision loss.
6. Retinitis pigmentosa (RP): a group of inherited disorders that affect the retina and can cause progressive vision loss.
7. Leber congenital amaurosis (LCA): an inherited disorder that causes blindness or severe visual impairment at birth or in early childhood.
8. Stargardt disease: a rare inherited disorder that affects the retina and can cause progressive vision loss, usually starting in childhood.
9. Juvenile macular degeneration: a rare inherited disorder that causes vision loss in young adults.
10. Retinal dystrophy: a group of inherited disorders that affect the retina and can cause progressive vision loss.

Retinal diseases can be diagnosed with a comprehensive eye exam, which includes a visual acuity test, dilated eye exam, and imaging tests such as optical coherence tomography (OCT) or fluorescein angiography. Treatment options vary depending on the specific disease and can include medication, laser surgery, or vitrectomy.

It's important to note that many retinal diseases can be inherited, so if you have a family history of eye problems, it's important to discuss your risk factors with your eye doctor. Early detection and treatment can help preserve vision and improve quality of life for those affected by these diseases.

The term "ischemic" refers to the reduction of blood flow, which can be caused by a blockage in the blood vessels or a narrowing of the vessels. Ischemic colitis is often caused by atherosclerosis, which is the buildup of plaque in the arteries.

Treatment for ischemic colitis typically involves addressing the underlying cause of the reduced blood flow and managing the symptoms. In some cases, this may involve medications to dissolve blood clots or widen the blood vessels. In severe cases, surgery may be necessary to repair or bypass the damaged blood vessels.

It is important to note that ischemic colitis can be a serious condition and may require prompt medical attention to prevent complications such as infection, perforation of the colon, or death.

There are several types of acidosis, including:

1. Respiratory acidosis: This occurs when the lung's ability to remove carbon dioxide from the blood is impaired, leading to an increase in blood acidity.
2. Metabolic acidosis: This type of acidosis occurs when there is an excessive production of acid in the body due to factors such as diabetes, starvation, or kidney disease.
3. Mixed acidosis: This type of acidosis is a combination of respiratory and metabolic acidosis.
4. Severe acute respiratory acidosis (SARA): This is a life-threatening condition that occurs suddenly, usually due to a severe lung injury or aspiration of a corrosive substance.

The symptoms of acidosis can vary depending on the type and severity of the condition. Common symptoms include:

1. Fatigue
2. Weakness
3. Confusion
4. Headaches
5. Nausea and vomiting
6. Abdominal pain
7. Difficulty breathing
8. Rapid heart rate
9. Muscle twitching

If left untreated, acidosis can lead to complications such as:

1. Kidney damage
2. Seizures
3. Coma
4. Heart arrhythmias
5. Respiratory failure

Treatment of acidosis depends on the underlying cause and the severity of the condition. Some common treatments include:

1. Oxygen therapy
2. Medications to help regulate breathing and heart rate
3. Fluid and electrolyte replacement
4. Dietary changes
5. Surgery, in severe cases.

In conclusion, acidosis is a serious medical condition that can have severe consequences if left untreated. It is important to seek medical attention immediately if you suspect that you or someone else may have acidosis. With prompt and appropriate treatment, it is possible to effectively manage the condition and prevent complications.

1. Ischemic stroke: This is the most common type of stroke, accounting for about 87% of all strokes. It occurs when a blood vessel in the brain becomes blocked, reducing blood flow to the brain.
2. Hemorrhagic stroke: This type of stroke occurs when a blood vessel in the brain ruptures, causing bleeding in the brain. High blood pressure, aneurysms, and blood vessel malformations can all cause hemorrhagic strokes.
3. Transient ischemic attack (TIA): Also known as a "mini-stroke," a TIA is a temporary interruption of blood flow to the brain that lasts for a short period of time, usually less than 24 hours. TIAs are often a warning sign for a future stroke and should be taken seriously.

Stroke can cause a wide range of symptoms depending on the location and severity of the damage to the brain. Some common symptoms include:

* Weakness or numbness in the face, arm, or leg
* Difficulty speaking or understanding speech
* Sudden vision loss or double vision
* Dizziness, loss of balance, or sudden falls
* Severe headache
* Confusion, disorientation, or difficulty with memory

Stroke is a leading cause of long-term disability and can have a significant impact on the quality of life for survivors. However, with prompt medical treatment and rehabilitation, many people are able to recover some or all of their lost functions and lead active lives.

The medical community has made significant progress in understanding stroke and developing effective treatments. Some of the most important advances include:

* Development of clot-busting drugs and mechanical thrombectomy devices to treat ischemic strokes
* Improved imaging techniques, such as CT and MRI scans, to diagnose stroke and determine its cause
* Advances in surgical techniques for hemorrhagic stroke
* Development of new medications to prevent blood clots and reduce the risk of stroke

Despite these advances, stroke remains a significant public health problem. According to the American Heart Association, stroke is the fifth leading cause of death in the United States and the leading cause of long-term disability. In 2017, there were over 795,000 strokes in the United States alone.

There are several risk factors for stroke that can be controlled or modified. These include:

* High blood pressure
* Diabetes mellitus
* High cholesterol levels
* Smoking
* Obesity
* Lack of physical activity
* Poor diet

In addition to these modifiable risk factors, there are also several non-modifiable risk factors for stroke, such as age (stroke risk increases with age), family history of stroke, and previous stroke or transient ischemic attack (TIA).

The medical community has made significant progress in understanding the causes and risk factors for stroke, as well as developing effective treatments and prevention strategies. However, more research is needed to improve outcomes for stroke survivors and reduce the overall burden of this disease.

In Vfib, the electrical activity of the heart becomes disorganized, leading to a fibrillatory pattern of contraction. This means that the ventricles are contracting in a rapid, unsynchronized manner, rather than the coordinated, synchronized contractions that occur in normal heart function.

Vfib can be caused by a variety of factors, including coronary artery disease, heart attack, cardiomyopathy, and electrolyte imbalances. It can also be triggered by certain medications, such as digoxin, or by electrical shocks to the heart.

Symptoms of Vfib include palpitations, shortness of breath, chest pain, and loss of consciousness. If not treated promptly, Vfib can lead to cardiac arrest and death.

Treatment of Vfib typically involves electrical cardioversion, which involves delivering an electric shock to the heart to restore a normal heart rhythm. In some cases, medications may also be used to help regulate the heart rhythm. In more severe cases, surgery or other interventions may be necessary to address any underlying causes of Vfib.

Overall, ventricular fibrillation is a serious medical condition that requires prompt treatment to prevent complications and ensure effective cardiac function.

The definition of AKI has evolved over time, and it is now defined as a syndrome characterized by an abrupt or rapid decrease in kidney function, with or without oliguria (decreased urine production), and with evidence of tubular injury. The RIFLE (Risk, Injury, Failure, Loss, and End-stage kidney disease) criteria are commonly used to diagnose and stage AKI based on serum creatinine levels, urine output, and other markers of kidney damage.

There are three stages of AKI, with stage 1 representing mild injury and stage 3 representing severe and potentially life-threatening injury. Treatment of AKI typically involves addressing the underlying cause, correcting fluid and electrolyte imbalances, and providing supportive care to maintain blood pressure and oxygenation. In some cases, dialysis may be necessary to remove waste products from the blood.

Early detection and treatment of AKI are crucial to prevent long-term damage to the kidneys and improve outcomes for patients.

Symptoms of PVD may include:

* Cramping pain in the legs during exercise or at rest
* Weakness or numbness in the legs
* Coldness in the lower limbs
* Difficulty healing wounds on the feet or legs
* Poor circulation
* Varicose veins

Treatment for PVD depends on the underlying cause and severity of the condition. Some common treatments include:

* Medications to relieve pain, reduce inflammation, or lower cholesterol levels
* Lifestyle changes such as exercise, smoking cessation, and a healthy diet
* Surgical procedures such as angioplasty or bypass surgery to improve blood flow
* Compression stockings to improve circulation

Prevention of PVD includes:

* Maintaining a healthy lifestyle, including regular exercise, a balanced diet, and not smoking
* Managing underlying conditions such as high blood pressure, high cholesterol, or diabetes
* Regular check-ups with your healthcare provider to monitor your risk factors and detect any early signs of PVD.

There are different types of gangrene, including:

1. Wet gangrene: This type of gangrene is caused by bacterial infection and is characterized by a foul odor. It is often associated with diabetes, peripheral artery disease, and other conditions that affect blood flow.
2. Dry gangrene: This type of gangrene is not caused by infection and is often associated with circulatory problems or nerve damage. It does not have a foul odor like wet gangrene.
3. Gas gangrene: This type of gangrene is caused by the bacterium Clostridium perfringens and is characterized by the presence of gas in the tissue.
4. Necrotizing fasciitis: This is a serious and potentially life-threatening condition that occurs when bacteria infect the tissue under the skin, causing widespread damage to the skin and underlying tissues.

The signs and symptoms of gangrene can vary depending on the type and location of the affected tissue, but they may include:

* Pain or tenderness in the affected area
* Swelling or redness in the affected area
* A foul odor in the case of wet gangrene
* Fever
* Chills
* Weakness or numbness in the affected limb

Gangrene is diagnosed through a combination of physical examination, medical history, and imaging tests such as X-rays, CT scans, or MRI scans. Treatment for gangrene depends on the underlying cause and may include antibiotics, surgical debridement (removal of dead tissue), and amputation in severe cases.

Prevention measures for gangrene include:

* Proper wound care to prevent infection
* Keeping blood sugar levels under control in people with diabetes
* Avoiding smoking and other unhealthy lifestyle habits that can increase the risk of infection and circulatory problems
* Getting prompt medical attention for any injuries or infections to prevent them from spreading and causing gangrene.

Prognosis for gangrene depends on the severity of the condition and the underlying cause. In general, early diagnosis and treatment improve the outlook, while delayed treatment or the presence of underlying health conditions can increase the risk of complications and death.

Some common examples of intraoperative complications include:

1. Bleeding: Excessive bleeding during surgery can lead to hypovolemia (low blood volume), anemia (low red blood cell count), and even death.
2. Infection: Surgical wounds can become infected, leading to sepsis or bacteremia (bacterial infection of the bloodstream).
3. Nerve damage: Surgery can sometimes result in nerve damage, leading to numbness, weakness, or paralysis.
4. Organ injury: Injury to organs such as the liver, lung, or bowel can occur during surgery, leading to complications such as bleeding, infection, or organ failure.
5. Anesthesia-related complications: Problems with anesthesia can include respiratory or cardiac depression, allergic reactions, or awareness during anesthesia (a rare but potentially devastating complication).
6. Hypotension: Low blood pressure during surgery can lead to inadequate perfusion of vital organs and tissues, resulting in organ damage or death.
7. Thromboembolism: Blood clots can form during surgery and travel to other parts of the body, causing complications such as stroke, pulmonary embolism, or deep vein thrombosis.
8. Postoperative respiratory failure: Respiratory complications can occur after surgery, leading to respiratory failure, pneumonia, or acute respiratory distress syndrome (ARDS).
9. Wound dehiscence: The incision site can separate or come open after surgery, leading to infection, fluid accumulation, or hernia.
10. Seroma: A collection of serous fluid that can develop at the surgical site, which can become infected and cause complications.
11. Nerve damage: Injury to nerves during surgery can result in numbness, weakness, or paralysis, sometimes permanently.
12. Urinary retention or incontinence: Surgery can damage the bladder or urinary sphincter, leading to urinary retention or incontinence.
13. Hematoma: A collection of blood that can develop at the surgical site, which can become infected and cause complications.
14. Pneumonia: Inflammation of the lungs after surgery can be caused by bacteria, viruses, or fungi and can lead to serious complications.
15. Sepsis: A systemic inflammatory response to infection that can occur after surgery, leading to organ dysfunction and death if not treated promptly.

It is important to note that these are potential complications, and not all patients will experience them. Additionally, many of these complications are rare, and the vast majority of surgeries are successful with minimal or no complications. However, it is important for patients to be aware of the potential risks before undergoing surgery so they can make an informed decision about their care.

1. Stroke: A stroke occurs when the blood supply to the brain is interrupted, either due to a blockage or a rupture of the blood vessels. This can lead to cell death and permanent brain damage.
2. Cerebral vasospasm: Vasospasm is a temporary constriction of the blood vessels in the brain, which can occur after a subarachnoid hemorrhage (bleeding in the space surrounding the brain).
3. Moyamoya disease: This is a rare condition caused by narrowing or blockage of the internal carotid artery and its branches. It can lead to recurrent transient ischemic attacks (TIs) or stroke.
4. Cerebral amyloid angiopathy: This is a condition where abnormal protein deposits accumulate in the blood vessels of the brain, leading to inflammation and bleeding.
5. Cavernous malformations: These are abnormal collections of blood vessels in the brain that can cause seizures, headaches, and other symptoms.
6. Carotid artery disease: Atherosclerosis (hardening) of the carotid arteries can lead to a stroke or TIAs.
7. Vertebrobasilar insufficiency: This is a condition where the blood flow to the brain is reduced due to narrowing or blockage of the vertebral and basilar arteries.
8. Temporal lobe dementia: This is a type of dementia that affects the temporal lobe of the brain, leading to memory loss and other cognitive symptoms.
9. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL): This is a rare genetic disorder that affects the blood vessels in the brain, leading to recurrent stroke-like events.
10. Moyamoya disease: This is a rare condition caused by narrowing or blockage of the internal carotid artery and its branches, leading to decreased blood flow to the brain and increased risk of stroke.

It's important to note that this list is not exhaustive and there may be other causes of stroke and TIAs that are not included here. A proper diagnosis can only be made by a qualified medical professional after conducting a thorough examination and reviewing the individual's medical history.

The term "intermittent" indicates that the symptoms do not occur all the time, but only during certain activities or situations. This condition can be caused by a variety of factors, such as peripheral artery disease (PAD), arterial occlusive disease, or muscle weakness.

Intermittent claudication can have a significant impact on an individual's quality of life, making it difficult to perform everyday activities like walking or climbing stairs. Treatment options may include medications, lifestyle changes, or surgery, depending on the underlying cause of the condition.

1. Infection: Bacterial or viral infections can develop after surgery, potentially leading to sepsis or organ failure.
2. Adhesions: Scar tissue can form during the healing process, which can cause bowel obstruction, chronic pain, or other complications.
3. Wound complications: Incisional hernias, wound dehiscence (separation of the wound edges), and wound infections can occur.
4. Respiratory problems: Pneumonia, respiratory failure, and atelectasis (collapsed lung) can develop after surgery, particularly in older adults or those with pre-existing respiratory conditions.
5. Cardiovascular complications: Myocardial infarction (heart attack), cardiac arrhythmias, and cardiac failure can occur after surgery, especially in high-risk patients.
6. Renal (kidney) problems: Acute kidney injury or chronic kidney disease can develop postoperatively, particularly in patients with pre-existing renal impairment.
7. Neurological complications: Stroke, seizures, and neuropraxia (nerve damage) can occur after surgery, especially in patients with pre-existing neurological conditions.
8. Pulmonary embolism: Blood clots can form in the legs or lungs after surgery, potentially causing pulmonary embolism.
9. Anesthesia-related complications: Respiratory and cardiac complications can occur during anesthesia, including respiratory and cardiac arrest.
10. delayed healing: Wound healing may be delayed or impaired after surgery, particularly in patients with pre-existing medical conditions.

It is important for patients to be aware of these potential complications and to discuss any concerns with their surgeon and healthcare team before undergoing surgery.

The term "infarction" is derived from the Latin words "in" meaning "into" and "farcire" meaning "to stuff", which refers to the idea that the tissue becomes "stuffed" with blood, leading to cell death and necrosis.

Infarction can be caused by a variety of factors, including atherosclerosis (the buildup of plaque in the blood vessels), embolism (a blood clot or other foreign material that blocks the flow of blood), and vasospasm (constriction of the blood vessels).

The symptoms of infarction vary depending on the location and severity of the blockage, but can include chest pain or discomfort, shortness of breath, numbness or weakness in the affected limbs, and confusion or difficulty speaking or understanding speech.

Diagnosis of infarction typically involves imaging tests such as electrocardiograms (ECGs), echocardiograms, or computerized tomography (CT) scans to confirm the presence of a blockage and assess the extent of the damage. Treatment options for infarction include medications to dissolve blood clots, surgery to restore blood flow, and other interventions to manage symptoms and prevent complications.

Prevention of infarction involves managing risk factors such as high blood pressure, high cholesterol, smoking, and obesity, as well as maintaining a healthy diet and exercise routine. Early detection and treatment of blockages can help reduce the risk of infarction and minimize the damage to affected tissues.

Some examples of pathologic constrictions include:

1. Stenosis: A narrowing or constriction of a blood vessel or other tubular structure, often caused by the buildup of plaque or scar tissue.
2. Asthma: A condition characterized by inflammation and constriction of the airways, which can make breathing difficult.
3. Esophageal stricture: A narrowing of the esophagus that can cause difficulty swallowing.
4. Gastric ring constriction: A narrowing of the stomach caused by a band of tissue that forms in the upper part of the stomach.
5. Anal fissure: A tear in the lining of the anus that can cause pain and difficulty passing stools.

Pathologic constrictions can be caused by a variety of factors, including inflammation, infection, injury, or genetic disorders. They can be diagnosed through imaging tests such as X-rays, CT scans, or endoscopies, and may require surgical treatment to relieve symptoms and improve function.

1. Atrial fibrillation (a type of irregular heartbeat)
2. Heart disease or valve problems
3. Blood clots in the legs or lungs
4. Infective endocarditis (an infection of the heart valves)
5. Cancer and its treatment
6. Trauma to the head or neck
7. High blood pressure
8. Atherosclerosis (the buildup of plaque in the arteries)

When a blockage occurs in one of the blood vessels of the brain, it can deprive the brain of oxygen and nutrients, leading to cell death and potentially causing a range of symptoms including:

1. Sudden weakness or numbness in the face, arm, or leg
2. Sudden confusion or trouble speaking or understanding speech
3. Sudden trouble seeing in one or both eyes
4. Sudden severe headache
5. Dizziness or loss of balance
6. Fainting or falling

Intracranial embolism and thrombosis can be diagnosed through a variety of imaging tests, including:

1. Computed tomography (CT) scan
2. Magnetic resonance imaging (MRI)
3. Magnetic resonance angiography (MRA)
4. Cerebral angiography
5. Doppler ultrasound

Treatment options for intracranial embolism and thrombosis depend on the underlying cause of the blockage, but may include:

1. Medications to dissolve blood clots or prevent further clotting
2. Surgery to remove the blockage or repair the affected blood vessel
3. Endovascular procedures, such as angioplasty and stenting, to open up narrowed or blocked blood vessels
4. Supportive care, such as oxygen therapy and pain management, to help manage symptoms and prevent complications.

There are many different types of nerve degeneration that can occur in various parts of the body, including:

1. Alzheimer's disease: A progressive neurological disorder that affects memory and cognitive function, leading to degeneration of brain cells.
2. Parkinson's disease: A neurodegenerative disorder that affects movement and balance, caused by the loss of dopamine-producing neurons in the brain.
3. Amyotrophic lateral sclerosis (ALS): A progressive neurological disease that affects nerve cells in the brain and spinal cord, leading to muscle weakness, paralysis, and eventually death.
4. Multiple sclerosis: An autoimmune disease that affects the central nervous system, causing inflammation and damage to nerve fibers.
5. Diabetic neuropathy: A complication of diabetes that can cause damage to nerves in the hands and feet, leading to pain, numbness, and weakness.
6. Guillain-Barré syndrome: An autoimmune disorder that can cause inflammation and damage to nerve fibers, leading to muscle weakness and paralysis.
7. Chronic inflammatory demyelinating polyneuropathy (CIDP): An autoimmune disorder that can cause inflammation and damage to nerve fibers, leading to muscle weakness and numbness.

The causes of nerve degeneration are not always known or fully understood, but some possible causes include:

1. Genetics: Some types of nerve degeneration may be inherited from one's parents.
2. Aging: As we age, our nerve cells can become damaged or degenerate, leading to a decline in cognitive and physical function.
3. Injury or trauma: Physical injury or trauma to the nervous system can cause nerve damage and degeneration.
4. Infections: Certain infections, such as viral or bacterial infections, can cause nerve damage and degeneration.
5. Autoimmune disorders: Conditions such as Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy (CIDP) are caused by the immune system attacking and damaging nerve cells.
6. Toxins: Exposure to certain toxins, such as heavy metals or pesticides, can damage and degenerate nerve cells.
7. Poor nutrition: A diet that is deficient in essential nutrients, such as vitamin B12 or other B vitamins, can lead to nerve damage and degeneration.
8. Alcoholism: Long-term alcohol abuse can cause nerve damage and degeneration due to the toxic effects of alcohol on nerve cells.
9. Drug use: Certain drugs, such as chemotherapy drugs and antiviral medications, can damage and degenerate nerve cells.
10. Aging: As we age, our nerve cells can deteriorate and become less functional, leading to a range of cognitive and motor symptoms.

It's important to note that in some cases, nerve damage and degeneration may be irreversible, but there are often strategies that can help manage symptoms and improve quality of life. If you suspect you have nerve damage or degeneration, it's important to seek medical attention as soon as possible to receive an accurate diagnosis and appropriate treatment.

In some cases, hyperemia can be a sign of a more serious underlying condition that requires medical attention. For example, if hyperemia is caused by an inflammatory or infectious process, it may lead to tissue damage or organ dysfunction if left untreated.

Hyperemia can occur in various parts of the body, including the skin, muscles, organs, and other tissues. It is often diagnosed through physical examination and imaging tests such as ultrasound, computed tomography (CT), or magnetic resonance imaging (MRI). Treatment for hyperemia depends on its underlying cause, and may include antibiotics, anti-inflammatory medications, or surgery.

In the context of dermatology, hyperemia is often used to describe a condition called erythema, which is characterized by redness and swelling of the skin due to increased blood flow. Erythema can be caused by various factors, such as sun exposure, allergic reactions, or skin infections. Treatment for erythema may include topical medications, oral medications, or other therapies depending on its underlying cause.

The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the World Health Organization (WHO). In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.

In this article, we will explore the definition and impact of chronic diseases, as well as strategies for managing and living with them. We will also discuss the importance of early detection and prevention, as well as the role of healthcare providers in addressing the needs of individuals with chronic diseases.

What is a Chronic Disease?

A chronic disease is a condition that lasts for an extended period of time, often affecting daily life and activities. Unlike acute diseases, which have a specific beginning and end, chronic diseases are long-term and persistent. Examples of chronic diseases include:

1. Diabetes
2. Heart disease
3. Arthritis
4. Asthma
5. Cancer
6. Chronic obstructive pulmonary disease (COPD)
7. Chronic kidney disease (CKD)
8. Hypertension
9. Osteoporosis
10. Stroke

Impact of Chronic Diseases

The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the WHO. In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.

Chronic diseases can also have a significant impact on an individual's quality of life, limiting their ability to participate in activities they enjoy and affecting their relationships with family and friends. Moreover, the financial burden of chronic diseases can lead to poverty and reduce economic productivity, thus having a broader societal impact.

Addressing Chronic Diseases

Given the significant burden of chronic diseases, it is essential that we address them effectively. This requires a multi-faceted approach that includes:

1. Lifestyle modifications: Encouraging healthy behaviors such as regular physical activity, a balanced diet, and smoking cessation can help prevent and manage chronic diseases.
2. Early detection and diagnosis: Identifying risk factors and detecting diseases early can help prevent or delay their progression.
3. Medication management: Effective medication management is crucial for controlling symptoms and slowing disease progression.
4. Multi-disciplinary care: Collaboration between healthcare providers, patients, and families is essential for managing chronic diseases.
5. Health promotion and disease prevention: Educating individuals about the risks of chronic diseases and promoting healthy behaviors can help prevent their onset.
6. Addressing social determinants of health: Social determinants such as poverty, education, and employment can have a significant impact on health outcomes. Addressing these factors is essential for reducing health disparities and improving overall health.
7. Investing in healthcare infrastructure: Investing in healthcare infrastructure, technology, and research is necessary to improve disease detection, diagnosis, and treatment.
8. Encouraging policy change: Policy changes can help create supportive environments for healthy behaviors and reduce the burden of chronic diseases.
9. Increasing public awareness: Raising public awareness about the risks and consequences of chronic diseases can help individuals make informed decisions about their health.
10. Providing support for caregivers: Chronic diseases can have a significant impact on family members and caregivers, so providing them with support is essential for improving overall health outcomes.

Conclusion

Chronic diseases are a major public health burden that affect millions of people worldwide. Addressing these diseases requires a multi-faceted approach that includes lifestyle changes, addressing social determinants of health, investing in healthcare infrastructure, encouraging policy change, increasing public awareness, and providing support for caregivers. By taking a comprehensive approach to chronic disease prevention and management, we can improve the health and well-being of individuals and communities worldwide.

The buildup of plaque in the coronary arteries is often caused by high levels of low-density lipoprotein (LDL) cholesterol, smoking, high blood pressure, diabetes, and a family history of heart disease. The plaque can also rupture, causing a blood clot to form, which can completely block the flow of blood to the heart muscle, leading to a heart attack.

CAD is the most common type of heart disease and is often asymptomatic until a serious event occurs. Risk factors for CAD include:

* Age (men over 45 and women over 55)
* Gender (men are at greater risk than women, but women are more likely to die from CAD)
* Family history of heart disease
* High blood pressure
* High cholesterol
* Diabetes
* Smoking
* Obesity
* Lack of exercise

Diagnosis of CAD typically involves a physical exam, medical history, and results of diagnostic tests such as:

* Electrocardiogram (ECG or EKG)
* Stress test
* Echocardiogram
* Coronary angiography

Treatment for CAD may include lifestyle changes such as a healthy diet, regular exercise, stress management, and quitting smoking. Medications such as beta blockers, ACE inhibitors, and statins may also be prescribed to manage symptoms and slow the progression of the disease. In severe cases, surgical intervention such as coronary artery bypass grafting (CABG) or percutaneous coronary intervention (PCI) may be necessary.

Prevention of CAD includes managing risk factors such as high blood pressure, high cholesterol, and diabetes, quitting smoking, maintaining a healthy weight, and getting regular exercise. Early detection and treatment of CAD can help to reduce the risk of complications and improve quality of life for those affected by the disease.

There are several possible causes of chest pain, including:

1. Coronary artery disease: The most common cause of chest pain is coronary artery disease, which occurs when the coronary arteries that supply blood to the heart become narrowed or blocked. This can lead to a heart attack if the blood flow to the heart muscle is severely reduced.
2. Heart attack: A heart attack occurs when the heart muscle becomes damaged or dies due to a lack of oxygen and nutrients. This can cause severe chest pain, as well as other symptoms such as shortness of breath, lightheadedness, and fatigue.
3. Acute coronary syndrome: This is a group of conditions that occur when the blood flow to the heart muscle is suddenly blocked or reduced, leading to chest pain or discomfort. In addition to heart attack, acute coronary syndrome can include unstable angina and non-ST-segment elevation myocardial infarction (NSTEMI).
4. Pulmonary embolism: A pulmonary embolism occurs when a blood clot forms in the lungs and blocks the flow of blood to the heart, causing chest pain and shortness of breath.
5. Pneumonia: An infection of the lungs can cause chest pain, fever, and difficulty breathing.
6. Costochondritis: This is an inflammation of the cartilage that connects the ribs to the breastbone (sternum), which can cause chest pain and tenderness.
7. Tietze's syndrome: This is a condition that occurs when the cartilage and muscles in the chest are injured, leading to chest pain and swelling.
8. Heart failure: When the heart is unable to pump enough blood to meet the body's needs, it can cause chest pain, shortness of breath, and fatigue.
9. Pericarditis: An inflammation of the membrane that surrounds the heart (pericardium) can cause chest pain, fever, and difficulty breathing.
10. Precordial catch syndrome: This is a condition that occurs when the muscles and tendons between the ribs become inflamed, causing chest pain and tenderness.

These are just a few of the many possible causes of chest pain. If you are experiencing chest pain, it is important to seek medical attention right away to determine the cause and receive proper treatment.

There are several key features of inflammation:

1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.

Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.

There are several types of inflammation, including:

1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.

There are several ways to reduce inflammation, including:

1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.

It's important to note that chronic inflammation can lead to a range of health problems, including:

1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.

Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.

Paraplegia is classified into two main types:

1. Complete paraplegia: Total loss of motor function in both legs and pelvis.
2. Incomplete paraplegia: Some degree of motor function remains in the affected limbs.

Symptoms of paraplegia can include weakness, paralysis, numbness, or tingling sensations below the level of the spinal cord injury. Loss of bladder and bowel control, sexual dysfunction, and changes in sensation (such as decreased sensitivity to touch and temperature) are also common.

Diagnosis typically involves a physical examination, medical history, neurological tests such as reflexes and muscle strength, and imaging studies like X-rays or MRIs to determine the underlying cause of paraplegia. Treatment depends on the specific cause of the condition and may include medications, rehabilitation therapy, and assistive devices such as braces, canes, or wheelchairs.

There are several potential causes of LVD, including:

1. Coronary artery disease: The buildup of plaque in the coronary arteries can lead to a heart attack, which can damage the left ventricle and impair its ability to function properly.
2. Heart failure: When the heart is unable to pump enough blood to meet the body's needs, it can lead to LVD.
3. Cardiomyopathy: This is a condition where the heart muscle becomes weakened or enlarged, leading to impaired function of the left ventricle.
4. Heart valve disease: Problems with the heart valves can disrupt the normal flow of blood and cause LVD.
5. Hypertension: High blood pressure can cause damage to the heart muscle and lead to LVD.
6. Genetic factors: Some people may be born with genetic mutations that predispose them to developing LVD.
7. Viral infections: Certain viral infections, such as myocarditis, can inflame and damage the heart muscle, leading to LVD.
8. Alcohol or drug abuse: Substance abuse can damage the heart muscle and lead to LVD.
9. Nutritional deficiencies: A diet lacking essential nutrients can lead to damage to the heart muscle and increase the risk of LVD.

Diagnosis of LVD typically involves a physical exam, medical history, and results of diagnostic tests such as electrocardiograms (ECGs), echocardiograms, and stress tests. Treatment options for LVD depend on the underlying cause, but may include medications to improve cardiac function, lifestyle changes, and in severe cases, surgery or other procedures.

Preventing LVD involves taking steps to maintain a healthy heart and reducing risk factors such as high blood pressure, smoking, and obesity. This can be achieved through a balanced diet, regular exercise, stress management, and avoiding substance abuse. Early detection and treatment of underlying conditions that increase the risk of LVD can also help prevent the condition from developing.

Types of cerebral arterial diseases include:

1. Cerebral vasospasm: A temporary constriction of the blood vessels in the brain, often seen after subarachnoid hemorrhage (bleeding in the space surrounding the brain).
2. Moyamoya disease: A rare condition caused by narrowing or blockage of the internal carotid artery and its branches, leading to decreased blood flow to the brain.
3. Cerebral amyloid angiopathy: A condition in which abnormal protein deposits accumulate in the walls of blood vessels supplying the brain, leading to inflammation and damage.
4. Cerebral infarction (stroke): The loss of brain tissue due to reduced blood flow or a blockage in an artery supplying the brain.
5. Cerebral hemorrhage: Bleeding in the brain, often due to rupture of a blood vessel or aneurysm.

Symptoms of cerebral arterial diseases can vary depending on the location and severity of the affected blood vessels, but may include headache, confusion, weakness or numbness in the face or limbs, difficulty speaking or understanding speech, and vision problems.

Diagnosis of cerebral arterial diseases typically involves a combination of physical examination, medical history, neuroimaging studies (such as CT or MRI scans), and angiography (a test that uses dye and X-rays to visualize the blood vessels in the brain).

Treatment options for cerebral arterial diseases depend on the underlying cause and severity of the condition, but may include medications to control blood pressure, cholesterol levels, or inflammation, as well as surgical interventions such as endarterectomy (removing plaque from the affected blood vessel) or aneurysm repair. In some cases, cerebral arterial diseases may be treated with a combination of medical and surgical therapies.

Complications of cerebral arterial diseases can include stroke, seizures, and cognitive decline. With prompt and appropriate treatment, however, many individuals with cerebral arterial diseases can experience significant improvement in symptoms and quality of life.

There are several types of embolism, including:

1. Pulmonary embolism: A blood clot that forms in the lungs and blocks the flow of blood to the heart.
2. Cerebral embolism: A blood clot or other foreign substance that blocks the flow of blood to the brain.
3. Coronary embolism: A blood clot that blocks the flow of blood to the heart muscle, causing a heart attack.
4. Intestinal embolism: A blood clot or other foreign substance that blocks the flow of blood to the intestines.
5. Fat embolism: A condition where fat enters the bloodstream and becomes lodged in a blood vessel, blocking the flow of blood.

The symptoms of embolism can vary depending on the location of the blockage, but may include:

* Pain or tenderness in the affected area
* Swelling or redness in the affected limb
* Difficulty breathing or shortness of breath
* Chest pain or pressure
* Lightheadedness or fainting
* Rapid heart rate or palpitations

Treatment for embolism depends on the underlying cause and the severity of the blockage. In some cases, medication may be used to dissolve blood clots or break up the blockage. In other cases, surgery may be necessary to remove the foreign substance or repair the affected blood vessel.

Prevention is key in avoiding embolism, and this can include:

* Managing underlying conditions such as high blood pressure, diabetes, or heart disease
* Avoiding long periods of immobility, such as during long-distance travel
* Taking blood-thinning medication to prevent blood clots from forming
* Maintaining a healthy weight and diet to reduce the risk of fat embolism.

PAD can be caused by atherosclerosis, the buildup of plaque in the arteries, which can lead to the formation of blood clots and further reduce blood flow. Risk factors for PAD include smoking, age, family history, and certain medical conditions such as diabetes and high blood pressure.

Diagnosis of PAD typically involves a physical examination, medical history, and imaging tests such as angiography or ultrasound. Treatment options for PAD may include lifestyle changes such as exercise and diet, medications to lower cholesterol and blood pressure, and surgery to repair or bypass blocked arteries.

In severe cases, PAD can lead to critical limb ischemia, which can result in tissue death and the need for amputation. Therefore, early detection and treatment of PAD are important to prevent complications and improve quality of life.

Word origin: Greek "anginos" meaning "pain in the neck".

Recurrence can also refer to the re-emergence of symptoms in a previously treated condition, such as a chronic pain condition that returns after a period of remission.

In medical research, recurrence is often studied to understand the underlying causes of disease progression and to develop new treatments and interventions to prevent or delay its return.

There are several possible causes of hyperglycemia, including:

1. Diabetes: This is a chronic condition where the body either does not produce enough insulin or cannot use insulin effectively.
2. Insulin resistance: This occurs when the body's cells become less responsive to insulin, leading to high blood sugar levels.
3. Pancreatitis: This is inflammation of the pancreas, which can lead to high blood sugar levels.
4. Cushing's syndrome: This is a rare hormonal disorder that can cause high blood sugar levels.
5. Medications: Certain medications, such as steroids and some types of antidepressants, can raise blood sugar levels.
6. Stress: Stress can cause the release of hormones such as cortisol and adrenaline, which can raise blood sugar levels.
7. Infections: Certain infections, such as pneumonia or urinary tract infections, can cause high blood sugar levels.
8. Trauma: Traumatic injuries can cause high blood sugar levels due to the release of stress hormones.
9. Surgery: Some types of surgery, such as heart bypass surgery, can cause high blood sugar levels.
10. Pregnancy: High blood sugar levels can occur during pregnancy, especially in women who have a history of gestational diabetes.

Hyperglycemia can cause a range of symptoms, including:

1. Increased thirst and urination
2. Fatigue
3. Blurred vision
4. Headaches
5. Cuts or bruises that are slow to heal
6. Tingling or numbness in the hands and feet
7. Dry, itchy skin
8. Flu-like symptoms, such as weakness, dizziness, and stomach pain
9. Recurring skin, gum, or bladder infections
10. Sexual dysfunction in men and women

If left untreated, hyperglycemia can lead to serious complications, including:

1. Diabetic ketoacidosis (DKA): A life-threatening condition that occurs when the body produces high levels of ketones, which are acidic substances that can cause confusion, nausea, and vomiting.
2. Hypoglycemia: Low blood sugar levels that can cause dizziness, confusion, and even loss of consciousness.
3. Nerve damage: High blood sugar levels over an extended period can damage the nerves, leading to numbness, tingling, and pain in the hands and feet.
4. Kidney damage: The kidneys may become overworked and damaged if they are unable to filter out the excess glucose in the blood.
5. Eye damage: High blood sugar levels can cause damage to the blood vessels in the eyes, leading to vision loss and blindness.
6. Cardiovascular disease: Hyperglycemia can increase the risk of cardiovascular disease, including heart attacks, strokes, and peripheral artery disease.
7. Cognitive impairment: Hyperglycemia has been linked to cognitive impairment and an increased risk of dementia.

It is essential to manage hyperglycemia by making lifestyle changes, such as following a healthy diet, regular exercise, and taking medication if prescribed by a healthcare professional. Monitoring blood sugar levels regularly can help identify the signs of hyperglycemia and prevent long-term complications.

Arteriosclerosis obliterans is often seen as a complication of conditions such as diabetes, hypertension, and atherosclerosis. It can also be caused by other factors such as smoking, high cholesterol levels, and genetic predisposition.

Symptoms of arteriosclerosis obliterans can vary depending on the location and severity of the blockages. They may include:

* Pain or cramping in the legs, feet, or buttocks
* Weakness or fatigue in the affected limbs
* Coldness or numbness in the extremities
* Difficulty healing wounds or ulcers
* Poor circulation in the hands and feet
* High blood pressure
* Heart disease

If you suspect that you may have arteriosclerosis obliterans, it is important to seek medical attention as soon as possible. A healthcare professional can perform a physical examination and order diagnostic tests such as angiography or ultrasound to determine the extent of the blockages and develop an appropriate treatment plan.

Treatment for arteriosclerosis obliterans may include lifestyle modifications such as quitting smoking, exercising regularly, and managing high blood pressure and cholesterol levels. Medications such as vasodilators and antiplatelet agents may also be prescribed to improve blood flow and reduce the risk of further blockages. In severe cases, surgery may be necessary to bypass or remove the blockages.

Preventing arteriosclerosis obliterans involves maintaining a healthy lifestyle, managing any underlying medical conditions, and avoiding risk factors such as smoking and excessive alcohol consumption. Regular check-ups with a healthcare professional can also help to identify early signs of the condition and prevent its progression.

There are several types of edema, including:

1. Pitting edema: This type of edema occurs when the fluid accumulates in the tissues and leaves a pit or depression when it is pressed. It is commonly seen in the skin of the lower legs and feet.
2. Non-pitting edema: This type of edema does not leave a pit or depression when pressed. It is often seen in the face, hands, and arms.
3. Cytedema: This type of edema is caused by an accumulation of fluid in the tissues of the limbs, particularly in the hands and feet.
4. Edema nervorum: This type of edema affects the nerves and can cause pain, numbness, and tingling in the affected area.
5. Lymphedema: This is a condition where the lymphatic system is unable to properly drain fluid from the body, leading to swelling in the arms or legs.

Edema can be diagnosed through physical examination, medical history, and diagnostic tests such as imaging studies and blood tests. Treatment options for edema depend on the underlying cause, but may include medications, lifestyle changes, and compression garments. In some cases, surgery or other interventions may be necessary to remove excess fluid or tissue.

Some common causes of chronic brain damage include:

1. Traumatic brain injury (TBI): A blow to the head or other traumatic injury that causes the brain to bounce or twist inside the skull, leading to damage to brain cells and tissues.
2. Stroke or cerebral vasculature disorders: A loss of blood flow to the brain due to a blockage or rupture of blood vessels, leading to cell death and tissue damage.
3. Infections such as meningitis or encephalitis: Inflammation of the brain and its membranes caused by viral or bacterial infections, which can lead to damage to brain cells and tissues.
4. Chronic exposure to toxins, such as pesticides or heavy metals: Prolonged exposure to these substances can damage brain cells and tissues over time.
5. Neurodegenerative diseases, such as Alzheimer's disease or Parkinson's disease: These conditions are characterized by the progressive loss of brain cells and tissue, leading to cognitive decline and other symptoms.

The effects of chronic brain damage can vary depending on the location and severity of the damage. Some common effects include:

1. Cognitive impairments: Difficulty with memory, attention, problem-solving, and other cognitive functions.
2. Emotional and behavioral changes: Depression, anxiety, irritability, and mood swings.
3. Physical symptoms: Weakness or paralysis on one side of the body, difficulty with balance and coordination, and changes in sensation or perception.
4. Communication difficulties: Slurred speech, difficulty finding the right words, and trouble understanding spoken language.
5. Social and occupational impairments: Difficulty with daily activities, social interactions, and work-related tasks.

The good news is that there are several strategies that can help mitigate the effects of chronic brain damage. These include:

1. Physical exercise: Regular physical activity has been shown to promote brain health and reduce the risk of cognitive decline.
2. Cognitive stimulation: Engaging in mentally challenging activities, such as reading, puzzles, or learning a new skill, can help build cognitive reserve and reduce the risk of cognitive decline.
3. Social engagement: Building and maintaining social connections has been shown to promote brain health and reduce the risk of cognitive decline.
4. Stress management: Chronic stress can exacerbate brain damage, so finding ways to manage stress, such as through meditation or exercise, is important.
5. Proper nutrition: Eating a diet rich in fruits, vegetables, and omega-3 fatty acids can help support brain health and reduce the risk of cognitive decline.
6. Medication and therapy: In some cases, medication or therapy may be necessary to manage the symptoms of chronic brain damage.
7. Neuroplasticity-based interventions: Techniques that promote neuroplasticity, such as non-invasive brain stimulation, can help improve cognitive function and reduce the risk of cognitive decline.

It's important to note that these strategies may not reverse chronic brain damage, but they can help mitigate its effects and improve overall brain health. If you suspect that you or someone you know may be experiencing chronic brain damage, it is important to seek medical attention as soon as possible. Early diagnosis and treatment can help reduce the risk of long-term cognitive decline and improve quality of life.

1. Atherosclerosis: A condition in which plaque builds up inside the arteries, causing them to narrow and harden. This can lead to heart disease, heart attack, or stroke.
2. Hypertension: High blood pressure that can damage blood vessels and increase the risk of heart disease, stroke, and other conditions.
3. Peripheral artery disease (PAD): A condition in which the blood vessels in the legs and arms become narrowed or blocked, leading to pain, cramping, and weakness in the affected limbs.
4. Raynaud's phenomenon: A condition that causes blood vessels in the hands and feet to constrict in response to cold temperatures or stress, leading to discoloration, numbness, and tissue damage.
5. Deep vein thrombosis (DVT): A condition in which a blood clot forms in the deep veins of the legs, often caused by immobility or injury.
6. Varicose veins: Enlarged, twisted veins that can cause pain, swelling, and cosmetic concerns.
7. Angioplasty: A medical procedure in which a balloon is used to open up narrowed blood vessels, often performed to treat peripheral artery disease or blockages in the legs.
8. Stenting: A medical procedure in which a small mesh tube is placed inside a blood vessel to keep it open and improve blood flow.
9. Carotid endarterectomy: A surgical procedure to remove plaque from the carotid arteries, which supply blood to the brain, to reduce the risk of stroke.
10. Bypass surgery: A surgical procedure in which a healthy blood vessel is used to bypass a blocked or narrowed blood vessel, often performed to treat coronary artery disease or peripheral artery disease.

Overall, vascular diseases can have a significant impact on quality of life and can increase the risk of serious complications such as stroke, heart attack, and amputation. It is important to seek medical attention if symptoms persist or worsen over time, as early diagnosis and treatment can help to prevent long-term damage and improve outcomes.

Hypothermia can be mild, moderate, or severe. Mild hypothermia is characterized by shivering and a body temperature of 95 to 97 degrees Fahrenheit (32 to 36.1 degrees Celsius). Moderate hypothermia has a body temperature of 82 to 94 degrees Fahrenheit (28 to 34 degrees Celsius), and the person may appear lethargic, drowsy, or confused. Severe hypothermia is characterized by a body temperature below 82 degrees Fahrenheit (28 degrees Celsius) and can lead to coma and even death if not treated promptly.

Treatment for hypothermia typically involves warming the person up slowly, using blankets or heating pads, and providing warm fluids to drink. In severe cases, medical professionals may use a specialized warm water bath or apply warm packs to specific areas of the body.

Preventing hypothermia is important, especially in cold weather conditions. This can be done by dressing appropriately for the weather, staying dry and avoiding wet clothing, eating regularly to maintain energy levels, and seeking shelter if you become stranded or lost. It's also essential to recognize the signs of hypothermia early on so that treatment can begin promptly.

There are many different types of liver diseases, including:

1. Alcoholic liver disease (ALD): A condition caused by excessive alcohol consumption that can lead to inflammation, scarring, and cirrhosis.
2. Viral hepatitis: Hepatitis A, B, and C are viral infections that can cause inflammation and damage to the liver.
3. Non-alcoholic fatty liver disease (NAFLD): A condition where there is an accumulation of fat in the liver, which can lead to inflammation and scarring.
4. Cirrhosis: A condition where the liver becomes scarred and cannot function properly.
5. Hemochromatosis: A genetic disorder that causes the body to absorb too much iron, which can damage the liver and other organs.
6. Wilson's disease: A rare genetic disorder that causes copper to accumulate in the liver and brain, leading to damage and scarring.
7. Liver cancer (hepatocellular carcinoma): Cancer that develops in the liver, often as a result of cirrhosis or viral hepatitis.

Symptoms of liver disease can include fatigue, loss of appetite, nausea, abdominal pain, dark urine, pale stools, and swelling in the legs. Treatment options for liver disease depend on the underlying cause and may include lifestyle changes, medication, or surgery. In severe cases, a liver transplant may be necessary.

Prevention of liver disease includes maintaining a healthy diet and lifestyle, avoiding excessive alcohol consumption, getting vaccinated against hepatitis A and B, and managing underlying medical conditions such as obesity and diabetes. Early detection and treatment of liver disease can help to prevent long-term damage and improve outcomes for patients.

There are two types of heart arrest:

1. Asystole - This is when the heart stops functioning completely and there is no electrical activity in the heart.
2. Pulseless ventricular tachycardia or fibrillation - This is when the heart is still functioning but there is no pulse and the rhythm is abnormal.

Heart arrest can be diagnosed through various tests such as electrocardiogram (ECG), blood tests, and echocardiography. Treatment options for heart arrest include cardiopulmonary resuscitation (CPR), defibrillation, and medications to restore a normal heart rhythm.

In severe cases of heart arrest, the patient may require advanced life support measures such as mechanical ventilation and cardiac support devices. The prognosis for heart arrest is generally poor, especially if it is not treated promptly and effectively. However, with proper treatment and support, some patients can recover and regain normal heart function.

There are several types of intracranial embolism, including:

1. Cerebral embolism: This occurs when a blood clot or other foreign matter becomes lodged in the brain, blocking the flow of blood and oxygen to brain tissue.
2. Pulmonary embolism: This occurs when a blood clot forms in the lungs and travels to the brain, causing blockage of blood vessels.
3. Aortic embolism: This occurs when a blood clot or other foreign matter becomes lodged in the aorta, the main artery that carries oxygenated blood from the heart to the rest of the body.
4. Atrial myxoma embolism: This occurs when a tumor in the heart, known as an atrial myxoma, breaks loose and travels to the brain, causing blockage of blood vessels.

Intracranial embolism can be diagnosed through various imaging tests such as CT or MRI scans, angiography, and Doppler ultrasound. Treatment options for intracranial embolism depend on the underlying cause and may include medications to dissolve blood clots, surgery to remove the blockage, or endovascular procedures such as stenting or coiling.

Preventive measures for intracranial embolism include managing risk factors for cardiovascular disease, such as high blood pressure, high cholesterol, and smoking cessation, as well as avoiding long periods of immobility during long-distance travel. Early diagnosis and treatment are critical in preventing long-term cognitive and neurological damage.

If you suspect vasospasm, it is essential to seek medical attention immediately. A healthcare professional will perform a physical examination and order imaging tests, such as CT or MRI scans, to confirm the diagnosis. Treatment options may include medications to dilate blood vessels, surgery to relieve pressure on affected areas, or other interventions depending on the severity of the condition.

Preventing vasospasm can be challenging, but some measures can reduce the risk of developing this condition. These include managing underlying conditions such as high blood pressure, diabetes, or high cholesterol levels; avoiding head injuries by wearing protective gear during sports and other activities; and adopting a healthy lifestyle that includes regular exercise and a balanced diet.

Early diagnosis and treatment are critical in managing vasospasm and preventing long-term damage to the brain tissue. If you experience any symptoms suggestive of vasospasm, seek medical attention promptly to receive appropriate care and improve outcomes.

Symptoms of cerebral hemorrhage may include sudden severe headache, confusion, seizures, weakness or numbness in the face or limbs, and loss of consciousness. The condition is diagnosed through a combination of physical examination, imaging tests such as CT or MRI scans, and laboratory tests to determine the cause of the bleeding.

Treatment for cerebral hemorrhage depends on the location and severity of the bleeding, as well as the underlying cause. Medications may be used to control symptoms such as high blood pressure or seizures, while surgery may be necessary to repair the ruptured blood vessel or relieve pressure on the brain. In some cases, the condition may be fatal, and immediate medical attention is essential to prevent long-term damage or death.

Some of the most common complications associated with cerebral hemorrhage include:

1. Rebleeding: There is a risk of rebleeding after the initial hemorrhage, which can lead to further brain damage and increased risk of death.
2. Hydrocephalus: Excess cerebrospinal fluid can accumulate in the brain, leading to increased intracranial pressure and potentially life-threatening complications.
3. Brain edema: Swelling of the brain tissue can occur due to the bleeding, leading to increased intracranial pressure and potentially life-threatening complications.
4. Seizures: Cerebral hemorrhage can cause seizures, which can be a sign of a more severe injury.
5. Cognitive and motor deficits: Depending on the location and severity of the bleeding, cerebral hemorrhage can result in long-term cognitive and motor deficits.
6. Vision loss: Cerebral hemorrhage can cause vision loss or blindness due to damage to the visual cortex.
7. Communication difficulties: Cerebral hemorrhage can cause difficulty with speech and language processing, leading to communication difficulties.
8. Behavioral changes: Depending on the location and severity of the bleeding, cerebral hemorrhage can result in behavioral changes, such as irritability, agitation, or apathy.
9. Infection: Cerebral hemorrhage can increase the risk of infection, particularly if the hemorrhage is caused by a ruptured aneurysm or arteriovenous malformation (AVM).
10. Death: Cerebral hemorrhage can be fatal, particularly if the bleeding is severe or if there are underlying medical conditions that compromise the patient's ability to tolerate the injury.

In this answer, we will explore the definition of 'Kidney Tubular Necrosis, Acute' in more detail, including its causes, symptoms, diagnosis, and treatment options.

What is Kidney Tubular Necrosis, Acute?
------------------------------------------

Kidney Tubular Necrosis, Acute (ATN) is a condition that affects the tubules of the kidneys, leading to inflammation and damage. The condition is often caused by various factors such as sepsis, shock, toxins, or medications.

The term "acute" refers to the sudden and severe nature of the condition, which can progress rapidly within hours or days. The condition can be life-threatening if left untreated, and it is important to seek medical attention immediately if symptoms persist or worsen over time.

Causes of Kidney Tubular Necrosis, Acute
--------------------------------------

There are various factors that can cause Kidney Tubular Necrosis, Acute, including:

### 1. Sepsis

Sepsis is a systemic inflammatory response to an infection, which can lead to damage to the tubules of the kidneys.

### 2. Shock

Shock can cause a decrease in blood flow to the kidneys, leading to damage and inflammation.

### 3. Toxins

Exposure to certain toxins, such as heavy metals or certain medications, can damage the tubules of the kidneys.

### 4. Medications

Certain medications, such as antibiotics and non-steroidal anti-inflammatory drugs (NSAIDs), can cause damage to the tubules of the kidneys.

### 5. Infection

Infections such as pyelonephritis or perinephric abscess can spread to the kidneys and cause inflammation and damage to the tubules.

### 6. Radiation necrosis

Radiation therapy can cause damage to the kidneys, leading to inflammation and scarring.

### 7. Kidney transplant rejection

Rejection of a kidney transplant can lead to inflammation and damage to the tubules of the transplanted kidney.

Symptoms of Kidney Tubular Necrosis, Acute
------------------------------------------

The symptoms of acute tubular necrosis can vary depending on the severity of the condition and the underlying cause. Some common symptoms include:

### 1. Fatigue

Fatigue is a common symptom of acute tubular necrosis, as the condition can lead to a decrease in the kidneys' ability to filter waste products from the blood.

### 2. Nausea and vomiting

Nausea and vomiting can occur due to electrolyte imbalances and changes in fluid levels in the body.

### 3. Decreased urine output

Acute tubular necrosis can cause a decrease in urine production, as the damaged tubules are unable to filter waste products from the blood effectively.

### 4. Swelling (edema)

Swelling in the legs, ankles, and feet can occur due to fluid buildup in the body.

### 5. Abdominal pain

Abdominal pain can be a symptom of acute tubular necrosis, as the condition can cause inflammation and scarring in the kidneys.

### 6. Fever

Fever can occur due to infection or inflammation in the kidneys.

### 7. Blood in urine (hematuria)

Hematuria, or blood in the urine, can be a symptom of acute tubular necrosis, as the damaged tubules can leak blood into the urine.

## Causes and risk factors

The exact cause of acute tubular necrosis is not fully understood, but it is believed to be due to damage to the kidney tubules, which can occur for a variety of reasons. Some possible causes and risk factors include:

1. Sepsis: Bacterial infections can spread to the kidneys and cause inflammation and damage to the tubules.
2. Toxins: Exposure to certain toxins, such as heavy metals or certain medications, can damage the kidney tubules.
3. Medications: Certain medications, such as nonsteroidal anti-inflammatory drugs (NSAIDs) and antibiotics, can cause kidney damage and increase the risk of acute tubular necrosis.
4. Hypotension: Low blood pressure can reduce blood flow to the kidneys and increase the risk of acute tubular necrosis.
5. Shock: Severe shock can lead to damage to the kidney tubules.
6. Burns: Severe burns can cause damage to the kidneys and increase the risk of acute tubular necrosis.
7. Trauma: Traumatic injuries, such as those caused by car accidents or falls, can damage the kidneys and increase the risk of acute tubular necrosis.
8. Surgery: Major surgery can cause damage to the kidneys and increase the risk of acute tubular necrosis.
9. Kidney disease: People with pre-existing kidney disease are at increased risk of developing acute tubular necrosis.
10. Chronic conditions: Certain chronic conditions, such as diabetes and high blood pressure, can increase the risk of developing acute tubular necrosis.

It is important to note that acute tubular necrosis can occur in people with no underlying medical conditions or risk factors, and it is often a diagnosis of exclusion, meaning that other potential causes of the person's symptoms must be ruled out before the diagnosis can be made.

There are several causes of hypotension, including:

1. Dehydration: Loss of fluids and electrolytes can cause a drop in blood pressure.
2. Blood loss: Losing too much blood can lead to hypotension.
3. Medications: Certain medications, such as diuretics and beta-blockers, can lower blood pressure.
4. Heart conditions: Heart failure, cardiac tamponade, and arrhythmias can all cause hypotension.
5. Endocrine disorders: Hypothyroidism (underactive thyroid) and adrenal insufficiency can cause low blood pressure.
6. Vasodilation: A condition where the blood vessels are dilated, leading to low blood pressure.
7. Sepsis: Severe infection can cause hypotension.

Symptoms of hypotension can include:

1. Dizziness and lightheadedness
2. Fainting or passing out
3. Weakness and fatigue
4. Confusion and disorientation
5. Pale, cool, or clammy skin
6. Fast or weak pulse
7. Shortness of breath
8. Nausea and vomiting

If you suspect that you or someone else is experiencing hypotension, it is important to seek medical attention immediately. Treatment will depend on the underlying cause of the condition, but may include fluids, electrolytes, and medication to raise blood pressure. In severe cases, hospitalization may be necessary.

There are several types of diabetic angiopathies, including:

1. Peripheral artery disease (PAD): This occurs when the blood vessels in the legs and arms become narrowed or blocked, leading to reduced blood flow and oxygen supply to the limbs.
2. Peripheral neuropathy: This is damage to the nerves in the hands and feet, which can cause pain, numbness, and weakness.
3. Retinopathy: This is damage to the blood vessels in the retina, which can lead to vision loss and blindness.
4. Nephropathy: This is damage to the kidneys, which can lead to kidney failure and the need for dialysis.
5. Cardiovascular disease: This includes heart attack, stroke, and other conditions that affect the heart and blood vessels.

The risk of developing diabetic angiopathies increases with the duration of diabetes and the level of blood sugar control. Other factors that can increase the risk include high blood pressure, high cholesterol, smoking, and a family history of diabetes-related complications.

Symptoms of diabetic angiopathies can vary depending on the specific type of complication and the location of the affected blood vessels or nerves. Common symptoms include:

* Pain or discomfort in the arms, legs, hands, or feet
* Numbness or tingling sensations in the hands and feet
* Weakness or fatigue in the limbs
* Difficulty healing wounds or cuts
* Vision changes or blindness
* Kidney problems or failure
* Heart attack or stroke

Diagnosis of diabetic angiopathies typically involves a combination of physical examination, medical history, and diagnostic tests such as ultrasound, MRI, or CT scans. Treatment options vary depending on the specific type of complication and may include:

* Medications to control blood sugar levels, high blood pressure, and high cholesterol
* Lifestyle changes such as a healthy diet and regular exercise
* Surgery to repair or bypass affected blood vessels or nerves
* Dialysis for kidney failure
* In some cases, amputation of the affected limb

Preventing diabetic angiopathies involves managing diabetes effectively through a combination of medication, lifestyle changes, and regular medical check-ups. Early detection and treatment can help prevent or delay the progression of complications.

There are several types of coronary occlusion, including:

* Complete coronary occlusion: When all blood flow to the heart is blocked.
* Incomplete coronary occlusion: When only part of the coronary artery is blocked.
* Proximal coronary occlusion: When the blockage occurs closer to the origins of the coronary arteries.
* Distal coronary occlusion: When the blockage occurs further down the coronary arteries, closer to the heart muscle.

The symptoms of coronary occlusion can vary depending on the location and severity of the blockage, but may include:

* Chest pain or discomfort (angina)
* Shortness of breath
* Fatigue
* Dizziness or lightheadedness
* Palpitations

Coronary occlusion can be diagnosed through various tests such as electrocardiogram (ECG), stress test, echocardiogram, and coronary angiography. Treatment options for coronary occlusion include medications to reduce blood pressure and improve blood flow, angioplasty or stenting to open or clear the blockage, and in some cases, coronary artery bypass surgery.

Preventive measures to reduce the risk of coronary occlusion include:

* Maintaining a healthy diet and lifestyle
* Not smoking
* Managing high blood pressure, high cholesterol, and diabetes
* Exercising regularly
* Maintaining a healthy weight

Early diagnosis and treatment of coronary occlusion can help improve outcomes and reduce the risk of complications such as heart attack or death.

An abdominal aortic aneurysm can cause symptoms such as abdominal pain, back pain, and difficulty breathing if it ruptures. It can also be diagnosed through imaging tests such as ultrasound, CT scan, or MRI. Treatment options for an abdominal aortic aneurysm include watchful waiting (monitoring the aneurysm for signs of growth or rupture), endovascular repair (using a catheter to repair the aneurysm from within the blood vessel), or surgical repair (open surgery to repair the aneurysm).

Word Origin and History

The word 'aneurysm' comes from the Greek words 'aneurysma', meaning 'dilation' and 'sma', meaning 'a vessel'. The term 'abdominal aortic aneurysm' was first used in the medical literature in the late 19th century to describe this specific type of aneurysm.


Prevalence and Incidence

Abdominal aortic aneurysms are relatively common, especially among older adults. According to the Society for Vascular Surgery, approximately 2% of people over the age of 65 have an abdominal aortic aneurysm. The prevalence of abdominal aortic aneurysms increases with age, and men are more likely to be affected than women.


Risk Factors

Several risk factors can increase the likelihood of developing an abdominal aortic aneurysm, including:

* High blood pressure
* Atherosclerosis (hardening of the arteries)
* Smoking
* Family history of aneurysms
* Previous heart attack or stroke
* Marfan syndrome or other connective tissue disorders.


Symptoms and Diagnosis

Abdominal aortic aneurysms can be asymptomatic, meaning they do not cause any noticeable symptoms. However, some people may experience symptoms such as:

* Abdominal pain or discomfort
* Back pain
* Weakness or fatigue
* Palpitations
* Shortness of breath

If an abdominal aortic aneurysm is suspected, several diagnostic tests may be ordered, including:

* Ultrasound
* Computed tomography (CT) scan
* Magnetic resonance imaging (MRI)
* Angiography

Treatment and Management

The treatment of choice for an abdominal aortic aneurysm depends on several factors, including the size and location of the aneurysm, as well as the patient's overall health. Treatment options may include:

* Watchful waiting (for small aneurysms that are not causing any symptoms)
* Endovascular repair (using a stent or other device to repair the aneurysm from within the blood vessel)
* Open surgical repair (where the surgeon makes an incision in the abdomen to repair the aneurysm)

In some cases, emergency surgery may be necessary if the aneurysm ruptures or shows signs of impending rupture.

Complications and Risks

Abdominal aortic aneurysms can lead to several complications and risks, including:

* Rupture (which can be life-threatening)
* Infection
* Blood clots or blockages in the blood vessels
* Kidney damage
* Heart problems

Prevention

There is no guaranteed way to prevent an abdominal aortic aneurysm, but several factors may reduce the risk of developing one. These include:

* Maintaining a healthy lifestyle (including a balanced diet and regular exercise)
* Not smoking
* Managing high blood pressure and other medical conditions
* Getting regular check-ups with your healthcare provider

Prognosis and Life Expectancy

The prognosis for abdominal aortic aneurysms depends on several factors, including the size of the aneurysm, its location, and whether it has ruptured. In general, the larger the aneurysm, the poorer the prognosis. If treated before rupture, many people with abdominal aortic aneurysms can expect a good outcome and a normal life expectancy. However, if the aneurysm ruptures, the survival rate is much lower.

In conclusion, abdominal aortic aneurysms are a serious medical condition that can be life-threatening if left untreated. It is important to be aware of the risk factors and symptoms of an aneurysm, and to seek medical attention immediately if any are present. With proper treatment, many people with abdominal aortic aneurysms can expect a good outcome and a normal life expectancy.

Symptoms:

* Chest pain or discomfort
* Shortness of breath
* Coughing up blood
* Pain in the back or shoulders
* Dizziness or fainting

Diagnosis is typically made with imaging tests such as chest X-rays, CT scans, or MRI. Treatment may involve monitoring the aneurysm with regular imaging tests to check for growth, or surgery to repair or replace the affected section of the aorta.

This term is used in the medical field to identify a specific type of aneurysm and differentiate it from other types of aneurysms that occur in different locations.

... of the small bowel is called mesenteric ischemia. Brain ischemia is insufficient blood flow to the brain, and can be ... Ischemia or ischaemia is a restriction in blood supply to any tissue, muscle group, or organ of the body, causing a shortage of ... Inadequate blood supply to a limb may results in acute limb ischemia or chronic limb threatening ischemia. Reduced blood flow ... can result in ischemia of the extremities due to unusual body positions that prevent normal circulation Ischemia results in ...
There are two types of ischemia: focal ischemia, which is confined to a specific region of the brain; and global ischemia, ... "Two Flavors of Ischemia". Brain Ischemia 101. Emergency Medicine Cerebral Resuscitation Lab. Retrieved 2008-10-13. Miettinen, S ... The causes of brain ischemia vary from sickle cell anemia to congenital heart defects. Symptoms of brain ischemia can include ... "Brain Ischemia (Cerebral Ischemia)". Cure Hunter Incorporated. 2003. pp. Relationship Network. Retrieved 2008-11-11. "Clinical ...
... , myocardial ischemia, or cardiac ischemia, is a medical term for a reduced blood flow in the coronary ... This type of ischemia is also known as silent ischemia. Coronary artery disease (CAD) occurs when fatty substances, known as ... "Silent Ischemia - Myocardial Ischemia Without Angina , Beaumont , Beaumont Health". www.beaumont.org. Retrieved 2022-05-28. " ... Coronary artery disease (CAD) is the most common cause of coronary ischemia. Coronary ischemia and coronary artery disease are ...
... also known as nephric ischaemia, is the deficiency of blood in one or both kidneys or nephrons, usually due to ... "Renal ischemia". TheFreeDictionary.com. Retrieved 9 February 2017. v t e (Kidney diseases, Ischemia, All stub articles, Disease ...
... is a disease with a high morbidity and mortality rate. Blood vessels shrink and undergo apoptosis which results ... Moreover, renal ischemia can cause the delay of graft function after renal transplant and can cause rejection of the transplant ... Acute kidney ischemia may result from taking ACEIs due to the alteration of intrarenal hemodynamics. Acute pulmonary edema is ... What causes kidney ischemia is not entirely known, but several pathophysiology relating to this disease have been elucidated. ...
In extensive mesenteric ischemia, bowel may be ischemic but separated from the blood flow such that the byproducts of ischemia ... "Mesenteric ischemia". Mayo Clinic. 2019-04-24. Dr. Rabih A. Chaer. "Mesenteric Ischemia". Society for Vascular Surgery. Higgins ... It can come on suddenly, known as acute intestinal ischemia, or gradually, known as chronic intestinal ischemia. The acute form ... The related term mesenteric ischemia generally defined as ischemia of the small bowel specifically. It has also been defined as ...
Critical limb ischemia is different from acute limb ischemia. Acute limb ischemia is a sudden lack of blood flow to the limb, ... Chronic limb threatening ischemia (CLTI), also known as critical limb ischemia (CLI), is an advanced stage of peripheral artery ... Critical limb ischemia includes rest pain and tissue loss.[citation needed] Rest pain is a continuous burning pain of the lower ... A similar study, BASIL 2 (Bypass Versus Angio plasty in Severe Ischaemia of the Leg), is being conducted in the United Kingdom ...
... nephric ischaemia) Mesenteric ischaemia Cerebral ischaemia Cardiac ischaemia In order to treat acute limb ischaemia there are a ... Acute limb ischaemia (ALI) occurs when there is a sudden lack of blood flow to a limb. Acute limb ischaemia is caused by ... The New Latin term ischaemia as written, is a British version of the word ischemia, and stems from the Greek terms ischein 'to ... In the worst cases, acute limb ischaemia progresses to critical limb ischaemia, and results in death or limb loss. Early ...
"Ischemia": an inadequate blood supply to an organ or part of the body.[citation needed] "Reperfusion": the restoration of blood ... Ischemia-reperfusion (IR) tissue injury is the resultant pathology from a combination of factors, including tissue hypoxia, ... The ischemia-reperfusion injury associated with surgical tourniquets is typically not clinically apparent when used for less ... By design, these devices induce ischemia to the lower extremities (as a secondary effect, or less commonly as their primary use ...
The Myocardial Ischaemia National Audit Project (MINAP) (previously known as the "Myocardial Infarction National Audit Database ...
"ISCHEMIA". Merriam-Webster. Retrieved 2020-03-23. Liang, Cuiping (2019). "Influence of the Distribution of Fibrosis within an ... Katz, Monica Y. (2014). "Three-Dimensional Myocardial Scarring along Myofibers after Coronary Ischemia-Reperfusion Revealed by ... Radauceanu, Anca (2007). "Residual Stress Ischemia Is Associated with Blood Markers of Myocardial Structural Remodeling". ...
Myocardial ischemia. Mayo Clinic (25 July 2015). Retrieved on 28 May 2016. Zvejniece, L; Svalbe, B; Makrecka, M; Liepinsh, E; ... These heart problems may sometimes lead to ischemia, a condition where too little blood flows to the organs in the body, ... "Meldonium cannot improve athletic performance, but it can stop tissue damage in the case of ischemia", the lack of blood flow ... It is primarily distributed in Eastern European countries as an anti-ischemia medication. Since 1 January 2016, it has been on ...
A complete occlusion of the artery can result in cerebral ischemia as the brain is depleted of oxygen-rich blood. Because the ... DeSai C, Hays Shapshak A (2021). "Cerebral Ischemia". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID 32809345. ...
In response to ischemia, the brain degenerates by the process of liquefactive necrosis. There are various classification ... Angioplasty and stenting have begun to be looked at as possible viable options in treatment of acute cerebral ischaemia. In a ... Results of the multi Mechanical Embolus Removal in Cerebral Ischemia (MERCI) trial, part I". AJNR Am J Neuroradiol. 27 (6): ... Another intervention for acute cerebral ischaemia is removal of the offending thrombus directly. This is accomplished by ...
In the context of bowel ischemia in particular ischemic colitis, the splenic flexure is sometimes referred to as Griffith's ... Amini, Afshin; Nagalli, Shivaraj (2021). "Bowel Ischemia". StatPearls. StatPearls Publishing. Retrieved 2 January 2022. Lotti M ...
25 February - Frank Holness, 82, basketball player; cerebral ischemia. 2 March - Telma Barria Pinzón, diplomat (consul of ...
May 2004). "Administration of N-acetylcysteine after focal cerebral ischemia protects brain and reduces inflammation in a rat ... September 2008). "Effectiveness of PSD95 inhibitors in permanent and transient focal ischemia in the rat". Stroke. 39 (9): 2544 ... Deng J, Xiong L, Zuo Z (April 2015). "Trans-sodium crocetinate provides neuroprotection against cerebral ischemia and ... Kalogeris T, Baines CP, Krenz M, Korthuis RJ (December 2016). "Ischemia/Reperfusion". Comprehensive Physiology. 7 (1): 113-170 ...
While in a state of cardiac arrest, the body experiences a unique state of global ischemia. This ischemia results in the ... The kidneys are the third most sensitive organ to ischemia. Prolonged renal ischemia from cardiac arrest leads to acute kidney ... Unlike other causes of ischemia-reperfusion injury, such as organ transplants, PCAS results from global ischemia-reperfusion ... This state of ischemia will continue until ROSC is achieved through CPR, at which time, blood starts to be reperfused ...
As a result, cerebral perfusion pressure (the pressure of blood flow in the brain) is reduced; ischemia results. When the ... Other factors in secondary injury are changes in the blood flow to the brain; ischemia (insufficient blood flow); cerebral ... Microdialysis allows ongoing sampling of extracellular fluid for analysis of metabolites that might indicate ischemia or brain ... June 2005). "Metabolic crisis without brain ischemia is common after traumatic brain injury: a combined microdialysis and ...
... retinal ischemia; and processes linked to rapid eye-movement (REM) sleep or phenomena generated on the border between sleep and ...
Ischemia tolerance:: in order for cells and organs to survive without circulation of the blood, good antioxidant defenses and ...
Nonocclusive ischemia, such as that seen in hypotension secondary to heart failure, may also contribute, but usually results in ... Haglund, Ulf, M.D (2001). "Mesenteric ischemia". National Center for Biotechnology Information, U.S. National Library of ... or an area especially vulnerable to ischemia during periods of systemic hypoperfusion, such as in shock.[citation needed] Acute ... Acute appendicitis Acute peptic ulcer and its complications Acute cholecystitis Acute pancreatitis Acute intestinal ischemia ( ...
For severe symptoms, the signs are usually visible and lead to ischemia. The clinical presentation of ischemia consists of the ... An occlusion of arteries disrupts oxygen and blood supply to tissues, leading to ischemia. Depending on the extent of ischemia ... Depending on the severity of ischemia, MIs are categorized as NSTEMI or STEMI. NSTEMI stands for 'Non-ST Elevation Myocardial ... Peripheral artery disease (PAD), or limb ischemia, affects the femoral, popliteal, or iliac arteries. PAD is caused by ...
36-. ISBN 978-0-306-48644-9. Eugene I. Gusev; Veronika I. Skvortsova (30 April 2003). Brain Ischemia. Springer Science & ... It was under investigation by Acea Pharmaceuticals as a neuroprotective agent for the treatment of cerebral ischemia associated ...
Liepzig: Ischemia Verlagsgesellschaft. Puustinen A, Wikström M. (1991). "The heme groups of cytochrome o from Escherichia coli ...
Cerebral ischemia occurs when the brain is not receiving adequate oxygen to continue normal functions. When this occurs, the ... Ischemia causes anoxic cell depolarizations and it is this increase in membrane potential at the presynaptic cell that triggers ... Ulegyria develops as a result of a brain injury called cerebral ischemia surrounding the time of an infant's birth. Oftentimes ... The cause of perinatal brain injuries includes: 1. cerebral ischemia 2. cerebral hemorrhage 3. ascending intrauterine ...
Silent Myocardial Ischemia. Springer: 29-36. doi:10.1007/978-3-642-69589-6_6. ISBN 978-3-540-13193-9. The SoS Investigators: ...
For example, in a feline model of intestinal ischemia, four hours of ischemia resulted in less injury than three hours of ... With reperfusion comes ischemia/reperfusion (IR) injury (IRI), which paradoxically causes cell death in reperfused tissue and ... This can be due to ischemia, thrombus, embolus (a lodged particle) or hemorrhage (a bleed). In thrombotic stroke, a thrombus ( ... Creager, Mark A.; Kaufman, John A.; Conte, Michael S. (7 June 2012). "Acute Limb Ischemia". New England Journal of Medicine. ...
"Acute Limb Ischemia". The Lecturio Medical Concept Library. Retrieved 11 August 2021. Light, RW (2013). "Chapter 1: Anatomy of ... where clots involve at a minimum the common iliac vein Acute limb ischaemia Clotted hemothorax Thrombolysis is usually ...
"Ischemia Reperfusion Research , BMG LABTECH". BMGLabtech.com. Retrieved 2021-11-26. Keeley EC, Boura JA, Grines CL (2003). " ... Thrombolysis in Myocardial Ischemia". Circulation. 89 (4): 1545-56. April 1994. doi:10.1161/01.cir.89.4.1545. PMID 8149520. ... Perfusion scanning Reperfusion injury Revascularization TIMI Ischemia-reperfusion injury of the appendicular musculoskeletal ...
Mesenteric ischemia is characterized by inadequate blood flow to or from the involved mesenteric vessels supplying a particular ... Mesenteric ischemia can be acute or chronic. [1] Most cases of mesenteric ischemia are due to an acute event leading to ... Chronic mesenteric ischemia is uncommon, accounting for less than 5% of cases of mesenteric ischemia, and is almost always ... encoded search term (Mesenteric Ischemia Imaging) and Mesenteric Ischemia Imaging What to Read Next on Medscape ...
... Review clinical trials at Sutter Health. ... International Study of Comparative Health Effectiveness With Medical and Invasive Approaches (ISCHEMIA). To determine whether a ...
Hepatic ischemia is a condition in which the liver does not get enough blood or oxygen. This causes injury to liver cells. ... Hepatic ischemia is a condition in which the liver does not get enough blood or oxygen. This causes injury to liver cells. ... Blood tests to check liver function (AST and ALT). These readings can be very high (in the thousands) with ischemia. ... People generally recover if the illness causing hepatic ischemia can be treated. Death from liver failure due to hepatic ...
Effects of spinal cord stimulation on myocardial ischaemia during daily life in patients with severe coronary artery disease. A ...
JavaScript is disabled for your browser. Some features of this site may not work without it ...
Downloading a figure as powerpoint requires a browser with javascript support. Enable javascript and try again For help please contact [email protected] ...
Ischemia-modified albumin was a risk marker for peripheral arterial disease. Taken together, these result … ... The baseline ischemia-modified albumin levels were significantly higher and positively associated with HbA1c and homocysteine ... Ischemia-modified albumin in type 2 diabetic patients with and without peripheral arterial disease Clinics (Sao Paulo). 2011;66 ... Ischemia-modified albumin was a risk marker for peripheral arterial disease. Taken together, these results might be helpful for ...
Acute mesenteric ischemia. Surgery. 1993; 114:489-490.. *Adaba F, Askari A, Dastur J et al. Mortality after acute primary ... Zalcman M, Sy M, Donckier V et al. Helical CT signs in the diagnosis of intestinal ischemia in small-bowel obstruction. AJR. Am ... Acute mesenteric ischemia (AMI), a surgical emergency, is an uncommon but serious condition that accounts for 1 in 1000 ... Acute mesenteric ischemia is a rare but life-threatening condition that requires timely recognition and intervention. The role ...
Ischaemia/reperfusion, inflammatory responses and acute lung injury. Message subject: (Your Name) has forwarded a page to you ...
Reduction of liver ischemia reperfusion injury by silencing of TNF-α gene with shRNA. Download Prime PubMed App to iPhone, iPad ... GdCl3 abates hepatic ischemia-reperfusion injury by inhibiting apoptosis in rats.. *[TLR4 is involved in hepatic ischemia/ ... Alpha-lipoic acid protects against hepatic ischemia-reperfusion injury in rats.. *Attenuation of liver ischemia/reperfusion ... Reduction of liver ischemia reperfusion injury by silencing of TNF-α gene with shRNA.. J Surg Res. 2012 Aug; 176(2):614-20.JS ...
Unwell for 2 days. Initially vague abdominal discomfort. Now profoundly septic.. ...
... at specific members of these various pathways have been instrumental in demonstrating the importance of neutrophils in ischemia ... cell adhesion glycoproteins were effective in limiting the myocardial necrosis that developed in response to an ischemia- ...
Scientific Video Article | Oclusão carotídea bilateral juntamente com hipotensão sistêmica produz isquemia cerebral em ratos, resultando em danos ao hipocampo com ...
To induce ischemia of the median and left lobes of the liver, a micro clip was used to clamp the left branches of the portal ... Zhao J, Ming Y, Wan Q, Ye S, Xie S, Zhu Y, Wang Y, Zhong Z, Li L, Ye Q, Ye Q, et al: Gypenoside attenuates hepatic ischemia/ ... Qi G, Zhang L, Xie WL, Chen XY and Li JS: Protective effect of gypenosides on DNA and RNA of rat neurons in cerebral ischemia- ... Ischemia/reperfusion (I/R) is a predominant cause of hepatic injury, which is of clinical significance following liver surgery ...
Ischemia-induced retinal neovascularization was markedly suppressed in 17-day-old leptin-deficient ob/ob mice. Western blot ... Ischemia-induced retinal neovascularization model was performed as described (1,16). Briefly, litters of 7-day-old (postnatal ... The ischemia-induced retinal neovascularization often results in catastrophic loss of vision in the final stage of various ... Leptin Stimulates Ischemia-Induced Retinal Neovascularization: Possible Role of Vascular Endothelial Growth Factor Expressed in ...
Myocardial Ischemia Market Analysis by Type, End-Use and Region , Myocardial Ischemia Industry , Market Research Future (MRFR) ... Myocardial Ischemia Market Size to register a CAGR of 5.70% By 2030. ... Myocardial Ischemia Market Myocardial Ischemia Market Research Report Information by Type (Symptomatic and Asymptomatic), ... FIGURE 7 PORTERS FIVE FORCES MODEL: GLOBAL MYOCARDIAL ISCHEMIA MARKET: 28 FIGURE 8 GLOBAL MYOCARDIAL ISCHEMIA MARKET: BY TYPE ...
Moreover, tissue ischemia was considered to be the main causative factor of post-operative adhesions, which represent vascular ... It is obvious that the production of oxygen free radicals is closely related to the duration of ischemia. This is the reason ... In this study hepatic ischemia and reperfusion were created in dogs in order to evaluate: a) the hepatic injury caused by OFRs ... In the first group hepatic ischemia lasted for 90 minutes; in the second group for 120 minutes; in the third 10 minutes prior ...
We present a case of a 15-year-old teenage girl presenting with typical purpuric rash of HSP, developed DAH, bowel ischaemia ... Life-threatening complications of Henoch-Schönlein purpura: diffuse alveolar haemorrhage, venous thrombosis and bowel ischaemia ... Diffuse alveolar haemorrhage (DAH), bowel ischaemia and venous thrombosis are rare complications of this disorder. ... Life-threatening complications of Henoch-Schönlein purpura: diffuse alveolar haemorrhage, venous thrombosis and bowel ischaemia ...
... ischemia-normothermia, or ischemia-hypothermia. Brain sections were immunohistochemically labeled to assess neurons, microglia ... Persistent cortical and white matter inflammation after therapeutic hypothermia for ischemia in near-term fetal sheep.. Login ... Persistent cortical and white matter inflammation after therapeutic hypothermia for ischemia in near-term fetal sheep.. Zhou, ... RNAscope,sup,®,/sup, was used to assess microglial phenotype markers CD86 and CD206.,h4,Results,/h4,Ischemia-normothermia was ...
Finally, studies of either myocardial or cerebral ischemia and reperfusion indicate that leukotriene signaling in addition may ... Leukotriene signaling in atherosclerosis and ischemia.. Cardiovascular Drugs and Therapy, 2009, 23 (1), pp.41-8. ⟨10.1007/ ... Finally, studies of either myocardial or cerebral ischemia and reperfusion indicate that leukotriene signaling in addition may ...
The effect of the calcium antagonist, nimodipine, on local cerebral blood flow, glucose use and focal cerebral ischaemia ... and this has stimulated interest in its effect on normal cerebral circulation and its use in cerebral ischaemia. In the studies ... glucose use and focal cerebral ischaemia. PhD thesis, University of Glasgow. ...
To explore the role of perioperative hyperglycemia in ischemia reperfusion injury, we conducted a prospective study of 40 ... Diabetes is a risk factor for delayed graft function in kidney transplantation, and hyperglycemia increases ischemia ... warm ischemia time >30 minutes (β 0.11, P-value 0.13), and recipient age (β 0.05, P-value 0.05) were associated with ... a protein whose expression is increased with renal ischemia, was then used to determine the extent of injury. Results. In a ...
Lipid-Lowering Therapy is Related to Inflammatory Markers and 3-Year Mortality in Patients With Critical Limb Ischemia. I: ... Lipid-Lowering Therapy is Related to Inflammatory Markers and 3-Year Mortality in Patients With Critical Limb Ischemia. / Isma ... Lipid-Lowering Therapy is Related to Inflammatory Markers and 3-Year Mortality in Patients With Critical Limb Ischemia. ... Lipid-Lowering Therapy is Related to Inflammatory Markers and 3-Year Mortality in Patients With Critical Limb Ischemia.. ...
This study was performed to evaluate the bilateral effects of focal permanent ischemia (FPI) on glial metabolism in the ...
keywords = "Functional recovery, Ischemia time, Ischemia type, Parenchymal mass preservation, Partial nephrectomy", ... each additional 10 min of warm ischemia was associated with only a 2.5% decline in recovery from ischemia. Limitations include ... each additional 10 min of warm ischemia was associated with only a 2.5% decline in recovery from ischemia. Limitations include ... each additional 10 min of warm ischemia was associated with only a 2.5% decline in recovery from ischemia. Limitations include ...
PreClinical Research Ischemia/Reperfusion Nervous system learn more Reproductive system learn more Go back to Preclinical ...
This study analyzes the role of the TLR system in an established murine model of liver warm ischemia followed by reperfusion. ... This study analyzes the role of the TLR system in an established murine model of liver warm ischemia followed by reperfusion. ... This study analyzes the role of the TLR system in an established murine model of liver warm ischemia followed by reperfusion. ... This study analyzes the role of the TLR system in an established murine model of liver warm ischemia followed by reperfusion. ...
This can happen in a number of ways, and ischemia is one of them. ... Ischemia: Too much and too little is destructive Savitha S, 11 ... Ischemia - "isch" means restraint or suppression and "emia" refers to blood. So ischemia means some kind of suppression or ... Tags #Anemia #arteries #Blood #defrination #etiology #heart #hypoxia #Ischemia #lack #leukemia #oxygen #pathogenesis #pathology ... Ischemia may result from occlusion of arterioles, capillaries, and venules. The causes are as under:. *By red cells- in sickle ...
Follow JFIM on your favorite social network. ...
Dive into the research topics of Responses of the SVZ to hypoxia and hypoxia/ischemia. Together they form a unique ...
  • Calpain: the regulatory point of myocardial ischemia-reperfusion injury. (bvsalud.org)
  • Abnormally elevation of Ca2+ promotes the abnormal activation of calpain during myocardial ischemia - reperfusion , resulting in myocardial injury and cardiac dysfunction. (bvsalud.org)
  • In this paper , we mainly reviewed the effects of calpain in various programmed cell death (such as apoptosis , mitochondrial-mediated necrosis , autophagy-dependent cell death , and parthanatos ) in myocardial ischemia - reperfusion . (bvsalud.org)
  • In addition, we also discussed the abnormal activation of calpain during myocardial ischemia - reperfusion , the effect of calpain on myocardial repair, and the possible future research directions of calpain . (bvsalud.org)
  • Silent myocardial ischemia and infarction / Peter F. Cohn. (who.int)
  • metabolic acidosis, arrhythmias, myocardial ischemia or infarction, and noncardiogenic pulmonary edema, although any organ system might be involved. (cdc.gov)
  • Cold and warm ischemia were utilized in 151 and 250 patients, and the median ischemia time was 27 and 21 min, respectively. (umn.edu)
  • However, each additional 10 min of warm ischemia was associated with only a 2.5% decline in recovery from ischemia. (umn.edu)
  • Longer duration of warm ischemia was associated with poorer recovery, although the incremental changes were modest. (umn.edu)
  • This study analyzes the role of the TLR system in an established murine model of liver warm ischemia followed by reperfusion. (houstonmethodist.org)
  • 4 Studies employing monoclonal antibodies (MAbs) directed at specific members of these various pathways have been instrumental in demonstrating the importance of neutrophils in ischemia-reperfusion injury. (neurology.org)
  • Intraoperative hyperglycemia augments ischemia reperfusion injury in renal transplantation: a prospective study. (escholarship.org)
  • Diabetes is a risk factor for delayed graft function in kidney transplantation, and hyperglycemia increases ischemia reperfusion injury in animal models. (escholarship.org)
  • To explore the role of perioperative hyperglycemia in ischemia reperfusion injury, we conducted a prospective study of 40 patients undergoing living donor renal transplantation. (escholarship.org)
  • The triggering molecular mechanism of ischemia-reperfusion injury (IRI), which in clinical settings results in excessive and detrimental inflammatory responses, remains unclear. (houstonmethodist.org)
  • This study tested the hypotheses that compared to drinking water, consumption of a caffeinated soft drink sweetened with high-fructose corn syrup (HFCS) attenuates the cutaneous vasodilatory response to local skin heating without (Protocol 1) and following ischemia-reperfusion injury (Protocol 2). (cdc.gov)
  • The cutaneous microvascular vasodilator response to local heating with or without prior ischemia-reperfusion injury is not affected by acute consumption of a caffeinated soft drink sweetened with HFCS. (cdc.gov)
  • Brain sections were immunohistochemically labeled to assess neurons, microglia and their interactions with neurons, astrocytes, myelination, and gitter cells (microglia with cytoplasmic lipid granules) 7 days after cerebral ischemia. (auckland.ac.nz)
  • Hypothermia prevented lesions after cerebral ischemia, but only partially suppressed microglial wrapping and M1 marker expression. (auckland.ac.nz)
  • Finally, studies of either myocardial or cerebral ischemia and reperfusion indicate that leukotriene signaling in addition may be involved in the development of ischemic injury. (inserm.fr)
  • Nimodipine is a potent dilator of cerebral vessels in vitro and in situ, and this has stimulated interest in its effect on normal cerebral circulation and its use in cerebral ischaemia. (gla.ac.uk)
  • Cortical Bilateral Adaptations in Rats Submitted to Focal Cerebral Ischemia: Emphasis on Glial Metabolism. (unil.ch)
  • Hepatic ischemia is a condition in which the liver does not get enough blood or oxygen. (medlineplus.gov)
  • Low blood pressure from any condition can lead to hepatic ischemia. (medlineplus.gov)
  • People generally recover if the illness causing hepatic ischemia can be treated. (medlineplus.gov)
  • Death from liver failure due to hepatic ischemia is very rare. (medlineplus.gov)
  • Quickly treating the causes of low blood pressure may prevent hepatic ischemia. (medlineplus.gov)
  • Tumor necrosis factor-alpha (TNF-α) is a central mediator in the hepatic response to ischemia/reperfusion. (unboundmedicine.com)
  • However, the effect of GP on ischemia/reperfusion (I/R)-induced hepatic injury has, to the best of our knowledge, not previously been investigated. (spandidos-publications.com)
  • Ischemia/reperfusion (I/R) is a predominant cause of hepatic injury, which is of clinical significance following liver surgery, hemorrhagic shock and liver transplantation ( 1 ). (spandidos-publications.com)
  • For example, in canine gastric dilatation-volvulus or diaphragmatic hernia, the epithelial hepatic cells could be irreversibly damaged not only due to ischemia but also to the large quantities of OFRs that are produced. (vin.com)
  • In this study hepatic ischemia and reperfusion were created in dogs in order to evaluate: a) the hepatic injury caused by OFRs, and b) the effectiveness of ascorbic acid and mannitol in neutralizing the deleterious effects of OFRs as far as lipid peroxidation, hepatic function, hepatic structure and ultrastructure are concerned. (vin.com)
  • In order to create hepatic ischemia, each dog was anesthetized and anesthesia was maintained with a mixture of halothane in oxygen. (vin.com)
  • Through midline laparotomy the left hepatic artery was occluded temporarily with Bulldog artery forceps in order to create left lobe ischemia. (vin.com)
  • in the third 10 minutes prior to hepatic artery occlusion a combination of vitamin C (25 IU/kg iv) and mannitol (0,2 mg/kg iv) was administered and ischemia lasted for 120 minutes. (vin.com)
  • 10,11 Alternatively, after a prolonged period of ischemia, progressive vasoconstriction is established in the obstructed vascular territory, which can persist even after blood flow returns, leading to persistent ischemia, full-thickness necrosis of the bowel wall, and perforation. (appliedradiology.com)
  • 6 (anti-CD11a, anti-CD18, anti-ICAM-1) were among the first to demonstrate that MAbs directed against either leukocyte or endothelial cell adhesion glycoproteins were effective in limiting the myocardial necrosis that developed in response to an ischemia-reperfusion protocol. (neurology.org)
  • To evaluate relationships between lipid-lowering therapy, inflammation, and 3-year mortality in critical limb ischemia (CLI), 259 consecutive CLI patients underwent evaluation of medication, tumor necrosis factor-alpha, interleukin-6 (IL6), neopterin, high-sensitivity C-reactive protein (hs-CRP), 8-epi-PGF2alpha, and endothelin-1. (lu.se)
  • Ischemic damage can range from reversible ischemia, including mucosal infarction and mural infarction involving the mucosa and submucosa, to irreversible transmural infarction and perforation. (appliedradiology.com)
  • Mesenteric ischemia can be acute or chronic. (medscape.com)
  • [ 1 ] Most cases of mesenteric ischemia are due to an acute event leading to decreased blood supply to the splanchnic vasculature. (medscape.com)
  • Acute mesenteric ischemia (AMI) may be classified as either arterial or venous. (medscape.com)
  • Acute insufficiency of mesenteric blood flow accounts for 60-70% of cases of mesenteric ischemia 4 , with the remainder related to chronic mesenteric ischemia, which is not a focus of this review. (appliedradiology.com)
  • Ischaemia/reperfusion, inflammatory responses and acute lung injury. (bmj.com)
  • IMSEAR at SEARO: A 10-year experience of managing acute limb ischaemia in India. (who.int)
  • Acute limb ischaemia is threatening to both limb and life. (who.int)
  • We did a retrospective analysis of the clinical profile of patients presenting with non-traumatic acute limb ischaemia to our department (a tertiary care centre in India) from January 1998 to December 2007. (who.int)
  • Acute limb ischaemia is a catastrophic event. (who.int)
  • To determine whether there is an association between serum ischemia-modified albumin and the risk factor profile in type 2 diabetic patients with peripheral arterial disease and to identify the risk markers for peripheral arterial disease. (nih.gov)
  • Multiple logistic analyses indicated that HbA1c, systolic blood pressure, homocysteine and ischemia-modified albumin were independent risk factors for peripheral arterial disease in the diabetic subjects. (nih.gov)
  • The baseline ischemia-modified albumin levels were significantly higher and positively associated with HbA1c and homocysteine levels in type 2 diabetic patients with peripheral arterial disease. (nih.gov)
  • Ischemia-modified albumin was a risk marker for peripheral arterial disease. (nih.gov)
  • The major causes of AMI include mesenteric arterial occlusion (embolism or thrombosis), non-occlusive mesenteric ischemia due to intestinal hypoperfusion, and mesenteric venous occlusion (thrombosis). (appliedradiology.com)
  • This mismatch can result from mesenteric arterial occlusion (MAO), mesenteric venous congestion/occlusion (MVO), or non-occlusive mesenteric ischemia (NOMI), as discussed below. (appliedradiology.com)
  • A super important and well-known example of this arterial ischemia is atherosclerosis. (doctor29.com)
  • The most common and most important causes of ischaemia are due to obstruction in arterial blood supply. (doctor29.com)
  • Blockage of venous drainage may lead to engorgement and obstruction to arterial blood supply resulting in ischemia. (doctor29.com)
  • Venous type resulting from impaired venous drainage (most commonly seen as the mechanism for ischemia in setting of mesenteric strangulation or venous thrombosis). (appliedradiology.com)
  • Diffuse alveolar haemorrhage (DAH), bowel ischaemia and venous thrombosis are rare complications of this disorder. (bmj.com)
  • We present a case of a 15-year-old teenage girl presenting with typical purpuric rash of HSP, developed DAH, bowel ischaemia and venous thrombosis. (bmj.com)
  • Development of intestinal ischemia depends on the following factors: systemic perfusion, number and caliber of affected vessels, available collateral circulation, and duration of the ischemic insult. (appliedradiology.com)
  • Moreover, tissue ischemia was considered to be the main causative factor of post-operative adhesions, which represent vascular bridging between healthy tissue and ischemic area. (vin.com)
  • Mesenteric ischemia is characterized by inadequate blood flow to or from the involved mesenteric vessels supplying a particular segment of bowel (see the images below). (medscape.com)
  • Effects of spinal cord stimulation on myocardial ischaemia during daily life in patients with severe coronary artery disease. (bmj.com)
  • Lipid-Lowering Therapy is Related to Inflammatory Markers and 3-Year Mortality in Patients With Critical Limb Ischemia. (lu.se)
  • Ischemia may result from occlusion of arterioles, capillaries, and venules. (doctor29.com)
  • Leukotriene signaling in atherosclerosis and ischemia. (inserm.fr)
  • Persistent cortical and white matter inflammation after therapeutic hypothermia for ischemia in near-term fetal sheep. (auckland.ac.nz)
  • Near-term fetal sheep (n = 24) were randomized to sham control, ischemia-normothermia, or ischemia-hypothermia. (auckland.ac.nz)
  • The percentage change in neutrophil gelatinase-associated lipocalin (NGAL), a protein whose expression is increased with renal ischemia, was then used to determine the extent of injury. (escholarship.org)
  • A secondary clinical entity of mesenteric ischemia occurs as a consequence of mechanical obstruction (eg, from internal hernia with strangulation, volvulus, or intussusception). (medscape.com)
  • The basal ischemia-modified albumin levels and clinical parameters were measured and analyzed. (nih.gov)
  • Chronic mesenteric ischemia is uncommon, accounting for less than 5% of cases of mesenteric ischemia, and is almost always associated with diffuse atherosclerotic disease. (medscape.com)
  • Thirty minutes following beverage consumption local skin heating commenced on the right forearm (Protocol 1), while on the left forearm ischemia-reperfusion commenced with 20 min of ischemia followed by 20 min of reperfusion and then local skin heating (Protocol 2). (cdc.gov)
  • Ischemia resulting from something outside the blood vessel is a traumatic injury, which can cause inflammation and swelling. (doctor29.com)
  • Design, setting, and participants: A total of 401 patients managed with PN with necessary studies were analyzed for function and nephron mass preserved specifically within the kidney exposed to ischemia. (umn.edu)
  • Background: Nephron mass preservation is a key determinant of functional outcomes after partial nephrectomy (PN), while ischemia plays a secondary role. (umn.edu)
  • The diagnosis of mesenteric ischemia often is a challenge to both clinicians and radiologists. (medscape.com)
  • So ischemia means some kind of suppression or reduction of blood flow to an organ or tissue. (doctor29.com)
  • Using the retinopathy of prematurity model, a mouse model of ischemia-induced retinal neovascularization, we have demonstrated more pronounced retinal neovascularization in 17-day-old transgenic mice overexpressing leptin than in age-matched wild-type littermates. (diabetesjournals.org)
  • Cette étude a permis de déterminer la fréquence et l'étiologie de l'insuffisance rénale aiguë chez des patients hospitalisés en Arabie saoudite sur une période de 2 ans. (who.int)
  • The "M1" marker CD86 and "M2" marker CD206 were upregulated after ischemia. (auckland.ac.nz)
  • In cases of a short period ischemia, the intra-cellular defense mechanisms are capable to neutralize the OFRs. (vin.com)
  • During the last two decades the main area of concern has been the deleterious effect of OFRs following ischemia and reperfusion in various organs. (vin.com)
  • Pearson correlation was used to evaluate relationships between functional recovery and nephron mass preservation or ischemia time. (umn.edu)