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.
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.
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.
NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).
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.
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 circulation of blood through the CORONARY VESSELS of the HEART.
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.
Surgical removal of an obstructing clot or foreign material from a blood vessel at the point of its formation. Removal of a clot arising from a distant site is called EMBOLECTOMY.
The removal of secretions, gas or fluid from hollow or tubular organs or cavities by means of a tube and a device that acts on negative pressure.
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.
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).
Dilation of an occluded coronary artery (or arteries) by means of a balloon catheter to restore myocardial blood supply.
Solutions which, upon administration, will temporarily arrest cardiac activity. They are used in the performance of heart surgery.
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.
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.
Radiography of the vascular system of the heart muscle after injection of a contrast medium.
Use of infusions of FIBRINOLYTIC AGENTS to destroy or dissolve thrombi in blood vessels or bypass grafts.
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).
Elements of limited time intervals, contributing to particular results or situations.
The veins and arteries of the HEART.
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.
MYOCARDIAL INFARCTION in which the anterior wall of the heart is involved. Anterior wall myocardial infarction is often caused by occlusion of the left anterior descending coronary artery. It can be categorized as anteroseptal or anterolateral wall myocardial infarction.
Coagulation of blood in any of the CORONARY VESSELS. The presence of a blood clot (THROMBUS) often leads to MYOCARDIAL INFARCTION.
An isoenzyme of creatine kinase found in the CARDIAC MUSCLE.
A family of percutaneous techniques that are used to manage CORONARY OCCLUSION, including standard balloon angioplasty (PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY), the placement of intracoronary STENTS, and atheroablative technologies (e.g., ATHERECTOMY; ENDARTERECTOMY; THROMBECTOMY; PERCUTANEOUS TRANSLUMINAL LASER ANGIOPLASTY). PTCA was the dominant form of PCI, before the widespread use of stenting.
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.
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).
Treatment process involving the injection of fluid into an organ or tissue.
The hollow, muscular organ that maintains the circulation of the blood.
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 movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.
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.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
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.
Proteins involved in the transport of specific substances across the membranes of the MITOCHONDRIA.
Contractile activity of the MYOCARDIUM.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
The mitochondria of the myocardium.
Cell adhesion molecule and CD antigen that mediates the adhesion of neutrophils and monocytes to activated platelets and endothelial cells.
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.
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.
The circulation of the BLOOD through the MICROVASCULAR NETWORK.
Univalent antigen-binding fragments composed of one entire IMMUNOGLOBULIN LIGHT CHAIN and the amino terminal end of one of the IMMUNOGLOBULIN HEAVY CHAINS from the hinge region, linked to each other by disulfide bonds. Fab contains the IMMUNOGLOBULIN VARIABLE REGIONS, which are part of the antigen-binding site, and the first IMMUNOGLOBULIN CONSTANT REGIONS. This fragment can be obtained by digestion of immunoglobulins with the proteolytic enzyme PAPAIN.
Platelet membrane glycoprotein complex important for platelet adhesion and aggregation. It is an integrin complex containing INTEGRIN ALPHAIIB and INTEGRIN BETA3 which recognizes the arginine-glycine-aspartic acid (RGD) sequence present on several adhesive proteins. As such, it is a receptor for FIBRINOGEN; VON WILLEBRAND FACTOR; FIBRONECTIN; VITRONECTIN; and THROMBOSPONDINS. A deficiency of GPIIb-IIIa results in GLANZMANN THROMBASTHENIA.
Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).
Ultrasonic recording of the size, motion, and composition of the heart and surrounding tissues. The standard approach is transthoracic.
Granular leukocytes having a nucleus with three to five lobes connected by slender threads of chromatin, and cytoplasm containing fine inconspicuous granules and stainable by neutral dyes.
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 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.
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.
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).
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.
Devices that provide support for tubular structures that are being anastomosed or for body cavities during skin grafting.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
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.
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.
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.
Antibodies produced by a single clone of cells.
Prolonged dysfunction of the myocardium after a brief episode of severe ischemia, with gradual return of contractile activity.
The dialdehyde of malonic acid.
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.
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)
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 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).
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.
The act of constricting.
10-carbon saturated monocarboxylic acids.
Organic compounds containing both the hydroxyl and carboxyl radicals.
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).
Sulfhydryl acylated derivative of GLYCINE.
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.
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.
Inbred C57BL mice are a strain of laboratory mice that have been produced by many generations of brother-sister matings, resulting in a high degree of genetic uniformity and homozygosity, making them widely used for biomedical research, including studies on genetics, immunology, cancer, and neuroscience.
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.
Fibrinolysin or agents that convert plasminogen to FIBRINOLYSIN.
Solutions used to store organs and minimize tissue damage, particularly while awaiting implantation.
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.
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.
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.
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.
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.
Non-human animals, selected because of specific characteristics, for use in experimental research, teaching, or testing.
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.
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.
The process by which chemical compounds provide protection to cells against harmful agents.
The circulation of blood through the BLOOD VESSELS of the BRAIN.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
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.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
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.
A XANTHINE OXIDASE inhibitor that decreases URIC ACID production. It also acts as an antimetabolite on some simpler organisms.
A proteolytic enzyme in the serine protease family found in many tissues which converts PLASMINOGEN to FIBRINOLYSIN. It has fibrin-binding activity and is immunologically different from UROKINASE-TYPE PLASMINOGEN ACTIVATOR. The primary sequence, composed of 527 amino acids, is identical in both the naturally occurring and synthetic proteases.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
Streptococcal fibrinolysin . An enzyme produced by hemolytic streptococci. It hydrolyzes amide linkages and serves as an activator of plasminogen. It is used in thrombolytic therapy and is used also in mixtures with streptodornase (STREPTODORNASE AND STREPTOKINASE). EC 3.4.-.
Enzymes of the transferase class that catalyze the conversion of L-aspartate and 2-ketoglutarate to oxaloacetate and L-glutamate. EC 2.6.1.1.
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 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.
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.
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).
An enzyme that catalyzes the conversion of L-alanine and 2-oxoglutarate to pyruvate and L-glutamate. (From Enzyme Nomenclature, 1992) EC 2.6.1.2.

Effect of coronary occlusion on left ventricular function with and without collateral supply during beating heart coronary artery surgery. (1/1442)

OBJECTIVE: To study the effects of coronary occlusion and collateral supply on left ventricular (LV) function during beating heart coronary artery surgery. DESIGN: Prospective intraoperative study, performed at baseline, during wall stabilisation, coronary artery occlusion, and 2 and 10 minutes after reperfusion. Transoesophageal M mode echocardiograms, simultaneous high fidelity LV pressure, and thermodilution cardiac output were measured. LV anterior wall thickening, thinning velocities, thickening fraction, regional work, and power production were derived. Asynchrony during the isovolumic periods was quantified as cycle efficiency. SETTING: Tertiary referral cardiac centre. PATIENTS: 14 patients with stable angina, mean (SD) age 62 (7) years, undergoing left anterior descending artery grafting using the "Octopus" device. RESULTS: Collaterals were absent in nine patients and present in five. Epicardial stabilisation did not affect LV function. Results are expressed as mean (SD). Coronary occlusion (15.6 (2) minutes) depressed anterior wall thickening (1.4 (0.6) v 2.6 (0.6) cm/s) and thinning velocities (1.4 (0.5) v 3.0 (0.6) cm/s), regional work (2.2 (0.8) v 4.6 (0.6) mJ/cm2), and power (21 (4) v 33 (5) mW/cm2) in patients without collaterals (p < 0.05 for all), but only wall thinning (3.5 (0.5) v 4.8 (0.5) cm/s, p < 0.05) in patients with collaterals. All returned to baseline within 10 minutes of reperfusion. Cycle efficiency and regional work were impaired at baseline and fell during occlusion, regardless of collaterals. Within 10 minutes of reperfusion both had increased above baseline. CONCLUSIONS: Coronary occlusion for up to 15 minutes during beating heart coronary artery surgery depressed standard measurements of systolic and diastolic anterior wall function in patients without collaterals, but only those of diastolic function in patients with collaterals. Regional synchrony decreased in both groups. All disturbances regressed within 10 minutes of reperfusion.  (+info)

Bradykinin promotes ischemic norepinephrine release in guinea pig and human hearts. (2/1442)

We previously reported that bradykinin (BK; 1-1000 nM) facilitates norepinephrine (NE) release from cardiac sympathetic nerves. Because BK production increases in myocardial ischemia, endogenous BK could foster NE release and associated arrhythmias. We tested this hypothesis in guinea pig and human myocardial ischemia models. BK administration (100 nM) markedly enhanced exocytotic and carrier-mediated NE overflow from guinea pig hearts subjected to 10- and 20-min ischemia/reperfusion, respectively. Ventricular fibrillation invariably occurred after 20-min global ischemia; BK prolonged its duration 3-fold. The BK B2 receptor antagonist HOE140 (30 nM) blocked the effects of BK, whereas the B1 receptor antagonist des-Arg9-Leu8-BK (1 microM; i.e., 2.5 x pA2) did not. When serine proteinase inhibitors (500 KIU/ml aprotinin and 100 microg/ml soybean trypsin inhibitor) were used to prevent the formation of endogenous BK, NE overflow and reperfusion arrhythmias were diminished. In contrast, when kininase I and II inhibitors (DL-2-mercaptomethyl-3-guanidinoethylthiopropanoic acid and enalaprilat, each 1 microM) were used to prevent the degradation of endogenous BK, NE overflow and reperfusion arrhythmias were enhanced. B2 receptor blockade abolished these effects but was ineffective if kininases were not inhibited. B2 receptor stimulation, by either exogenous or endogenous BK, also markedly enhanced carrier-mediated NE release in the human myocardial ischemia model; conversely, inhibition of BK biosynthesis diminished ischemic NE release. Because atherosclerotic heart disease impairs endothelial BK production, in myocardial ischemia BK could accumulate at sympathetic nerve endings, thus augmenting exocytotic and carrier-mediated NE release and favoring coronary vasoconstriction and arrhythmias.  (+info)

Regional electrophysiological effects of hypokalaemia, hypomagnesaemia and hyponatraemia in isolated rabbit hearts in normal and ischaemic conditions. (3/1442)

OBJECTIVE: The aims of this study were to establish an isolated working heart model for electrophysiological recordings from the epicardium and endocardium and to examine regional effects of changes in ion concentrations in normal and ischaemic conditions. METHODS: Monophasic action potential duration (MAPD90), effective refractory period (ERP) and conduction delay were measured simultaneously in the epicardium and endocardium of rabbit hearts paced at 3.3 Hz, subjected to 30 min of regional ischaemia and 15 min of reperfusion. The hearts were exposed before and throughout ischaemia and reperfusion to hypokalaemia (K+ = 2 mM), hypomagnesaemia (Mg2+ = 0.5 mM) or hyponatraemia (Na+ = 110 mM). RESULTS: In the control hearts, no regional electrophysiological differences were seen before ischaemia, but ischaemia-induced MAPD90 shortening and postrepolarisation refractoriness were greater in the epicardium than in the endocardium and conduction delay increased only in the epicardium. Hypokalaemia shortened ERP in the epicardium (but not endocardium) and increased conduction delay in all areas before ischaemia, but it had no effects during ischaemia. During reperfusion hypokalaemia increased the incidence of recurrent tachyarrhythmias. Hypomagnesaemia had no effect before ischaemia, increased epicardial (but not endocardial) MAPD90 shortening during ischaemia, although it had no pro-arrhythmic action. Hyponatraemia increased conduction delay in all areas before ischaemia and produced asystole or severe bradycardia in all hearts. During ischaemia, hyponatraemia decreased ERP shortening and inducibility of arrhythmias in the epicardium (but not endocardium). CONCLUSIONS: We conclude that the more pronounced effect of ischaemia upon the epicardium than the endocardium can be explained by the contact of the endocardium with intracavitary perfusate. We also conclude that changes in ion concentrations may have differential regional electrical effects in normal or ischaemic conditions.  (+info)

Myocardial temperature reduction attenuates necrosis after prolonged ischemia in rabbits. (4/1442)

OBJECTIVE: Previously we observed that a large reduction in infarct size was attained by cooling the risk region of the heart, either before or early after the onset of a 30-min coronary artery occlusion. While this is a standard duration of ischemia used in the rabbit model of infarction, it may not reflect the situation of patients who are reperfused late. The effects of regional hypothermia with a longer duration of ischemia, and when the intervention is applied later, are unknown. This study tests the hypothesis that a local reduction in cardiac temperature protects myocardium during prolonged ischemia (2 h) even if begun well after coronary artery occlusion. METHODS: Anesthetized rabbits received 2 h of coronary artery occlusion and 3 h of reperfusion. Rabbits were randomly assigned to a treated group: topical myocardial cooling starting 30 min after coronary occlusion (n = 14), or control group, no intervention (n = 12). Myocardial temperature in the risk zone, hemodynamics and regional myocardial blood flow were measured. RESULTS: Ischemic zone temperature was similar in both groups at 30 min post occlusion, but the cooling maneuver produced a reduction in temperature in the risk region of the treated group such that myocardial temperature was reduced an average of 10 degrees C between 30 and 60 min of coronary artery occlusion. Myocardial temperature in the control group remained within 0.3 degree C of baseline during coronary artery occlusion and into reperfusion. Core temperatures were similar in both groups. Hemodynamic parameters and collateral blood flow during occlusion were also equivalent in both groups. After 120 min of coronary occlusion, necrosis in the control group comprised 72 +/- 3% of the ischemic risk region. However, in cooled hearts, infarct size, expressed as a fraction of the risk region was significantly lower. Infarct size in this group averaged 59 +/- 3% of the risk region (p < 0.004 vs. controls), and thus cooling resulted in a salvage of approximately 18% of the risk region. CONCLUSION: These results show that reducing myocardial temperature protects ischemic myocardium during a long duration of ischemia even if initiated after coronary artery occlusion.  (+info)

Intravenous magnesium reduces infarct size after ischemia/reperfusion injury combined with a thrombogenic lesion in the left anterior descending artery. (5/1442)

Experimental studies have demonstrated that intravenous magnesium (Mg) can protect the ischemic myocardium and has an antithrombotic effect. In patients with myocardial infarction, the reperfusion injury is complicated by the presence of a thrombogenic area in the affected coronary artery that may cause repetitive thrombus formation and embolization. We investigated the effect of Mg on infarct size in a randomized study in pigs. Myocardial infarction was induced by a 50-minute mechanical occlusion of the left anterior descending artery combined with an arterial injury, which stimulated a dynamic thrombus formation with emboli shedding on reperfusion. Magnesium sulfate (6 mmol/20 min plus 3 mmol/h) or saline was started at 30 minutes after coronary occlusion. Real-time ventricular pressure-volume loops were generated from the left ventricle by using a microtip pressure manometer and a conductance catheter. Platelet accumulation in the myocardium was evaluated by using 111In-labeled platelets. After 4 hours of reperfusion, the infarct size/area at risk ratio in the placebo group was 46+/-0.06% (n=8) compared with 22+/-0.07% (n=6) in the Mg-treated animals (P=0. 03). Ejection fraction decreased significantly in the control group but not in the Mg-treated animals (P=0.03). Platelet accumulation in the myocardium did not change significantly between the Mg- and placebo-treated animals (placebo group, 191+/-19%; Mg group, 177+/-29%; NS). The present study demonstrates that intravenous Mg infusion is able to reduce infarct size by >50% and preserve the ejection fraction in this model where ischemia/reperfusion injury was evaluated in the presence of a thrombogenic area in the nutrient artery.  (+info)

Repeated administration of vasopressin but not epinephrine maintains coronary perfusion pressure after early and late administration during prolonged cardiopulmonary resuscitation in pigs. (6/1442)

BACKGROUND: It is unknown whether repeated dosages of vasopressin or epinephrine given early or late during basic life support cardiopulmonary resuscitation (CPR) may be able to increase coronary perfusion pressure above a threshold between 20 and 30 mm Hg that renders defibrillation successful. METHODS AND RESULTS: After 4 minutes of cardiac arrest, followed by 3 minutes of basic life support CPR, 12 animals were randomly assigned to receive, every 5 minutes, either vasopressin (early vasopressin: 0.4, 0.4, and 0.8 U/kg, respectively; n=6) or epinephrine (early epinephrine: 45, 45, and 200 microg/kg, respectively; n=6). Another 12 animals were randomly allocated after 4 minutes of cardiac arrest, followed by 8 minutes of basic life support CPR, to receive, every 5 minutes, either vasopressin (late vasopressin: 0.4 and 0.8 U/kg, respectively; n=6), or epinephrine (late epinephrine: 45 and 200 microg/kg, respectively; n=6). Defibrillation was attempted after 22 minutes of cardiac arrest. Mean+/-SEM coronary perfusion pressure was significantly higher 90 seconds after early vasopressin compared with early epinephrine (50+/-4 versus 34+/-3 mm Hg, P<0.02; 42+/-5 versus 15+/-3 mm Hg, P<0.0008; and 37+/-5 versus 11+/-3 mm Hg, P<0. 002, respectively). Mean+/-SEM coronary perfusion pressure was significantly higher 90 seconds after late vasopressin compared with late epinephrine (40+/-3 versus 22+/-4 mm Hg, P<0.004, and 32+/-4 versus 15+/-4 mm Hg, P<0.01, respectively). All vasopressin animals survived 60 minutes, whereas no epinephrine pig had return of spontaneous circulation (P<0.05). CONCLUSIONS: Repeated administration of vasopressin but only the first epinephrine dose given early and late during basic life support CPR maintained coronary perfusion pressure above the threshold that is needed for successful defibrillation.  (+info)

Effects of the prostanoid EP3-receptor agonists M&B 28767 and GR 63799X on infarct size caused by regional myocardial ischaemia in the anaesthetized rat. (7/1442)

1. This study investigates the effects of two agonists of the prostanoid EP3-receptor (M&B 28767 and GR 63799X) on the infarct size caused by regional myocardial ischaemia and reperfusion in the anaesthetized rat. 2. One hundred and sixty-seven, male Wistar rats were anaesthetized (thiopentone, 120 mg kg(-1) i.p.), ventilated (8-10 ml kg(-1), 70 strokes min(-1), inspiratory oxygen concentration: 30%; PEEP: 1-2 mmHg) and subjected to occlusion of the left anterior descending coronary artery (LAD, for 7.5, 15, 25, 35, 45 or 60 min) followed by reperfusion (2 h). Infarct size was determined by staining of viable myocardium with a tetrazolium stain (NBT), histological evaluation by light and electron microscopy and determination of the plasma levels of cardiac troponin T. 3. M&B 28767 (0.5 microg kg(-1) min(-1), i.v., n=7) or GR 63799X (3 microg kg(-1) min(-1), i.v., n=7) caused significant reductions in infarct size from 60+/-3% (25 min ischaemia and 2 h reperfusion; saline-control, n=8) to 39+/-6 and 38+/-4% of the area at risk, without causing a significant fall in blood pressure. Pretreatment of rats with 5-hydroxydecanoate (5-HD), an inhibitor of ATP-sensitive potassium channels, attenuated the cardioprotective effects of both EP3-receptor agonists. The reduction in infarct size afforded by M&B 28767 was also abolished by glibenclamide and the protein kinase C (PKC) inhibitors staurosporine and chelerythrine. 4. Thus, M&B 28767 and GR 63799X reduce myocardial infarct size in the rat by a mechanism(s) which involves the activation of PKC and the opening of ATP-sensitive potassium channels.  (+info)

Enhanced role for the opening of potassium channels in relaxant responses to acetylcholine after myocardial ischaemia and reperfusion in dog coronary arteries. (8/1442)

1. Anaesthetized dogs were subjected to 1 h occlusion of the left circumflex coronary artery followed by 2 h of reperfusion. Relaxant responses were examined in coronary artery rings removed proximal (nonischaemic) or distal (ischaemic) to the site of occlusion. 2. Relaxant responses to acetylcholine (ACh) were similar in nonischaemic and ischaemic artery rings. In addition ACh-induced relaxation of nonischaemic and ischaemic artery rings was equally susceptible to inhibition of nitric oxide (NO) synthase using L-N(G)-nitroarginine (L-NOARG, 10(-4) M), or to inhibition of soluble guanylate cyclase using 1H-[1,2,4]oxadiazolo[4,3-a]quinoxaline-1-one (ODQ, 10(-5) M). 3. In nonischaemic arteries, the relaxation to ACh was unaffected by high K+ (67 mM) but in ischaemic arteries, the maximum relaxation to ACh was significantly reduced from 113+/-6 to 60+/-2% (ANOVA, P<0.05). Tetraethylammonium (TEA, 10(-3) M), an inhibitor of large conductance calcium activated potassium (BK(Ca)) channels did not inhibit the response to ACh in nonischaemic arteries but in ischaemic arteries TEA significantly shifted the concentration response curve to ACh to the right (pEC(50); nonischaemic, 7.07+/-0.25; ischaemic, 6.54+/-0.21, P<0.01, ANOVA) without decreasing the maximum relaxation. TEA did not affect the responses to sodium nitroprusside in either nonischaemic or ischaemic arteries. 4. In conclusion, ischaemia/reperfusion did not change the sensitivity of endothelium-dependent relaxation to L-NOARG or ODQ indicating that ischaemia did not affect the contribution of NO or cyclic GMP to ACh-induced relaxation. However, in ischaemic arteries the opening of the BK(Ca) channels contributed to relaxation caused by ACh whereas TEA had no effect in nonischaemic arteries. The factor responsible for the opening of this potassium channel was a factor other than NO and may be endothelium derived hyperpolarizing factor (EDHF).  (+info)

Myocardial reperfusion injury is a pathological process that occurs when blood flow is restored to the heart muscle (myocardium) after a period of ischemia or reduced oxygen supply, such as during a myocardial infarction (heart attack). The restoration of blood flow, although necessary to salvage the dying tissue, can itself cause further damage to the heart muscle. This paradoxical phenomenon is known as myocardial reperfusion injury.

The mechanisms behind myocardial reperfusion injury are complex and involve several processes, including:

1. Oxidative stress: The sudden influx of oxygen into the previously ischemic tissue leads to an overproduction of reactive oxygen species (ROS), which can damage cellular structures, such as proteins, lipids, and DNA.
2. Calcium overload: During reperfusion, there is an increase in calcium influx into the cardiomyocytes (heart muscle cells). This elevated intracellular calcium level can disrupt normal cellular functions, leading to further damage.
3. Inflammation: Reperfusion triggers an immune response, with the recruitment of inflammatory cells, such as neutrophils and monocytes, to the site of injury. These cells release cytokines and other mediators that can exacerbate tissue damage.
4. Mitochondrial dysfunction: The restoration of blood flow can cause mitochondria, the powerhouses of the cell, to malfunction, leading to the release of pro-apoptotic factors and contributing to cell death.
5. Vasoconstriction and microvascular obstruction: During reperfusion, there may be vasoconstriction of the small blood vessels (microvasculature) in the heart, which can further limit blood flow and contribute to tissue damage.

Myocardial reperfusion injury is a significant concern because it can negate some of the benefits of early reperfusion therapy, such as thrombolysis or primary percutaneous coronary intervention (PCI), used to treat acute myocardial infarction. Strategies to minimize myocardial reperfusion injury are an area of active research and include pharmacological interventions, ischemic preconditioning, and remote ischemic conditioning.

Myocardial reperfusion is the restoration of blood flow to the heart muscle (myocardium), usually after a period of ischemia or reduced oxygen supply, such as during a myocardial infarction (heart attack). This can be achieved through various medical interventions, including thrombolytic therapy, percutaneous coronary intervention (PCI), or coronary artery bypass surgery (CABG). The goal of myocardial reperfusion is to salvage the jeopardized myocardium, preserve cardiac function, and reduce the risk of complications like heart failure or arrhythmias. However, it's important to note that while reperfusion is crucial for treating ischemic heart disease, it can also lead to additional injury to the heart muscle, known as reperfusion injury.

Reperfusion injury is a complex pathophysiological process that occurs when blood flow is restored to previously ischemic tissues, leading to further tissue damage. This phenomenon can occur in various clinical settings such as myocardial infarction (heart attack), stroke, or peripheral artery disease after an intervention aimed at restoring perfusion.

The restoration of blood flow leads to the generation of reactive oxygen species (ROS) and inflammatory mediators, which can cause oxidative stress, cellular damage, and activation of the immune system. This results in a cascade of events that may lead to microvascular dysfunction, capillary leakage, and tissue edema, further exacerbating the injury.

Reperfusion injury is an important consideration in the management of ischemic events, as interventions aimed at restoring blood flow must be carefully balanced with potential harm from reperfusion injury. Strategies to mitigate reperfusion injury include ischemic preconditioning (exposing the tissue to short periods of ischemia before a prolonged ischemic event), ischemic postconditioning (applying brief periods of ischemia and reperfusion after restoring blood flow), remote ischemic preconditioning (ischemia applied to a distant organ or tissue to protect the target organ), and pharmacological interventions that scavenge ROS, reduce inflammation, or improve microvascular function.

Myocardial infarction (MI), also known as a heart attack, is a medical condition characterized by the death of a segment of heart muscle (myocardium) due to the interruption of its blood supply. This interruption is most commonly caused by the blockage of a coronary artery by a blood clot formed on the top of an atherosclerotic plaque, which is a buildup of cholesterol and other substances in the inner lining of the artery.

The lack of oxygen and nutrients supply to the heart muscle tissue results in damage or death of the cardiac cells, causing the affected area to become necrotic. The extent and severity of the MI depend on the size of the affected area, the duration of the occlusion, and the presence of collateral circulation.

Symptoms of a myocardial infarction may include chest pain or discomfort, shortness of breath, nausea, lightheadedness, and sweating. Immediate medical attention is necessary to restore blood flow to the affected area and prevent further damage to the heart muscle. Treatment options for MI include medications, such as thrombolytics, antiplatelet agents, and pain relievers, as well as procedures such as percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG).

Reperfusion, in medical terms, refers to the restoration of blood flow to tissues or organs that have been deprived of adequate oxygen supply, usually as a result of ischemia (lack of blood flow). This process is often initiated through therapeutic interventions such as thrombolysis (breaking up blood clots), angioplasty (opening narrowed or blocked blood vessels using a balloon or stent), or surgical procedures.

Reperfusion aims to salvage the affected tissues and prevent further damage; however, it can also lead to reperfusion injury. This injury occurs when the return of oxygen-rich blood to previously ischemic tissues results in the overproduction of free radicals and inflammatory mediators, which can cause additional cellular damage and organ dysfunction.

Managing reperfusion injury involves using various strategies such as antioxidants, anti-inflammatory agents, and other protective treatments to minimize its negative impact on the recovering tissues or organs.

Ischemic postconditioning is a medical/physiological term that refers to a cardioprotective strategy used to mitigate the damage caused by ischemia-reperfusion injury, which occurs during myocardial infarction (heart attack) or other conditions involving restricted blood flow to the heart muscle.

The technique involves applying brief, intermittent periods of reduced blood flow (ischemia) and reflow (reperfusion) to the heart immediately after a prolonged period of ischemia. This process triggers a complex intracellular signaling cascade that helps protect the heart tissue from further damage during reperfusion.

The protective effects of ischemic postconditioning are attributed to various cellular and molecular mechanisms, such as reducing oxidative stress, inhibiting inflammation, preserving mitochondrial function, and modulating calcium homeostasis. These combined actions help minimize the infarct size (area of damaged heart tissue) and improve overall cardiac function following an ischemic event.

Ischemic postconditioning has been explored as a potential therapeutic approach to treat ischemia-reperfusion injuries in various clinical settings, including heart attacks, cardiac surgery, and organ transplantation. However, its translation into clinical practice has been challenging due to the complexity of the intervention and the need for precise timing and control over the ischemic and reperfusion periods.

Coronary circulation refers to the circulation of blood in the coronary vessels, which supply oxygenated blood to the heart muscle (myocardium) and drain deoxygenated blood from it. The coronary circulation system includes two main coronary arteries - the left main coronary artery and the right coronary artery - that branch off from the aorta just above the aortic valve. These arteries further divide into smaller branches, which supply blood to different regions of the heart muscle.

The left main coronary artery divides into two branches: the left anterior descending (LAD) artery and the left circumflex (LCx) artery. The LAD supplies blood to the front and sides of the heart, while the LCx supplies blood to the back and sides of the heart. The right coronary artery supplies blood to the lower part of the heart, including the right ventricle and the bottom portion of the left ventricle.

The veins that drain the heart muscle include the great cardiac vein, the middle cardiac vein, and the small cardiac vein, which merge to form the coronary sinus. The coronary sinus empties into the right atrium, allowing deoxygenated blood to enter the right side of the heart and be pumped to the lungs for oxygenation.

Coronary circulation is essential for maintaining the health and function of the heart muscle, as it provides the necessary oxygen and nutrients required for proper contraction and relaxation of the myocardium. Any disruption or blockage in the coronary circulation system can lead to serious consequences, such as angina, heart attack, or even death.

The myocardium is the middle layer of the heart wall, composed of specialized cardiac muscle cells that are responsible for pumping blood throughout the body. It forms the thickest part of the heart wall and is divided into two sections: the left ventricle, which pumps oxygenated blood to the rest of the body, and the right ventricle, which pumps deoxygenated blood to the lungs.

The myocardium contains several types of cells, including cardiac muscle fibers, connective tissue, nerves, and blood vessels. The muscle fibers are arranged in a highly organized pattern that allows them to contract in a coordinated manner, generating the force necessary to pump blood through the heart and circulatory system.

Damage to the myocardium can occur due to various factors such as ischemia (reduced blood flow), infection, inflammation, or genetic disorders. This damage can lead to several cardiac conditions, including heart failure, arrhythmias, and cardiomyopathy.

A thrombectomy is a medical procedure that involves the removal of a blood clot (thrombus) from a blood vessel. This is typically performed to restore blood flow in cases where the clot is causing significant blockage, which can lead to serious complications such as tissue damage or organ dysfunction.

During a thrombectomy, a surgeon makes an incision and accesses the affected blood vessel, often with the help of imaging guidance. Specialized tools are then used to extract the clot, after which the blood vessel is usually repaired. Thrombectomies can be performed on various blood vessels throughout the body, including those in the brain, heart, lungs, and limbs.

This procedure may be recommended for patients with deep vein thrombosis (DVT), pulmonary embolism (PE), or certain types of stroke, depending on the specific circumstances and the patient's overall health. It is generally considered when anticoagulation therapy or clot-dissolving medications are not sufficient or appropriate to treat the blood clot.

In medical terms, suction refers to the process of creating and maintaining a partial vacuum in order to remove fluids or gases from a body cavity or wound. This is typically accomplished using specialized medical equipment such as a suction machine, which uses a pump to create the vacuum, and a variety of different suction tips or catheters that can be inserted into the area being treated.

Suction is used in a wide range of medical procedures and treatments, including wound care, surgical procedures, respiratory therapy, and diagnostic tests. It can help to remove excess fluids such as blood or pus from a wound, clear secretions from the airways during mechanical ventilation, or provide a means of visualizing internal structures during endoscopic procedures.

It is important to use proper technique when performing suctioning, as excessive or improperly applied suction can cause tissue damage or bleeding. Medical professionals are trained in the safe and effective use of suction equipment and techniques to minimize risks and ensure optimal patient outcomes.

Creatine kinase (CK) is a muscle enzyme that is normally present in small amounts in the blood. It is primarily found in tissues that require a lot of energy, such as the heart, brain, and skeletal muscles. When these tissues are damaged or injured, CK is released into the bloodstream, causing the levels to rise.

Creatine kinase exists in several forms, known as isoenzymes, which can be measured in the blood to help identify the location of tissue damage. The three main isoenzymes are:

1. CK-MM: Found primarily in skeletal muscle
2. CK-MB: Found primarily in heart muscle
3. CK-BB: Found primarily in the brain

Elevated levels of creatine kinase, particularly CK-MB, can indicate damage to the heart muscle, such as occurs with a heart attack. Similarly, elevated levels of CK-BB may suggest brain injury or disease. Overall, measuring creatine kinase levels is a useful diagnostic tool for assessing tissue damage and determining the severity of injuries or illnesses.

Myocardial ischemia is a condition in which the blood supply to the heart muscle (myocardium) is reduced or blocked, leading to insufficient oxygen delivery and potential damage to the heart tissue. This reduction in blood flow typically results from the buildup of fatty deposits, called plaques, in the coronary arteries that supply the heart with oxygen-rich blood. The plaques can rupture or become unstable, causing the formation of blood clots that obstruct the artery and limit blood flow.

Myocardial ischemia may manifest as chest pain (angina pectoris), shortness of breath, fatigue, or irregular heartbeats (arrhythmias). In severe cases, it can lead to myocardial infarction (heart attack) if the oxygen supply is significantly reduced or cut off completely, causing permanent damage or death of the heart muscle. Early diagnosis and treatment of myocardial ischemia are crucial for preventing further complications and improving patient outcomes.

Coronary balloon angioplasty is a minimally invasive medical procedure used to widen narrowed or obstructed coronary arteries (the blood vessels that supply oxygen-rich blood to the heart muscle) and improve blood flow to the heart. This procedure is typically performed in conjunction with the insertion of a stent, a small mesh tube that helps keep the artery open.

During coronary balloon angioplasty, a thin, flexible catheter with a deflated balloon at its tip is inserted into a blood vessel, usually through a small incision in the groin or arm. The catheter is then guided to the narrowed or obstructed section of the coronary artery. Once in position, the balloon is inflated to compress the plaque against the artery wall and widen the lumen (the inner space) of the artery. This helps restore blood flow to the heart muscle.

The procedure is typically performed under local anesthesia and conscious sedation to minimize discomfort. Coronary balloon angioplasty is a relatively safe and effective treatment for many people with coronary artery disease, although complications such as bleeding, infection, or re-narrowing of the artery (restenosis) can occur in some cases.

Cardioplegic solutions are specially formulated liquids used in medical procedures to induce cardiac arrest and protect the heart muscle during open-heart surgery. These solutions typically contain a combination of electrolytes, such as potassium and magnesium, which stop the heart from beating by interrupting its electrical activity. They may also include energy substrates, buffers, and other components to maintain the health and function of the heart cells during the period of arrest. The specific formulation of cardioplegic solutions can vary depending on the needs of the patient and the preferences of the medical team.

Ischemic preconditioning, myocardial is a phenomenon in cardiac physiology where the heart muscle (myocardium) is made more resistant to the damaging effects of a prolonged period of reduced blood flow (ischemia) or oxygen deprivation (hypoxia), followed by reperfusion (restoration of blood flow). This resistance is developed through a series of brief, controlled episodes of ischemia and reperfusion, which act as "preconditioning" stimuli, protecting the myocardium from subsequent more severe ischemic events. The adaptive responses triggered during preconditioning include the activation of various protective signaling pathways, release of protective factors, and modulation of cellular metabolism, ultimately leading to reduced infarct size, improved contractile function, and attenuated reperfusion injury in the myocardium.

Electrocardiography (ECG or EKG) is a medical procedure that records the electrical activity of the heart. It provides a graphic representation of the electrical changes that occur during each heartbeat. The resulting tracing, called an electrocardiogram, can reveal information about the heart's rate and rhythm, as well as any damage to its cells or abnormalities in its conduction system.

During an ECG, small electrodes are placed on the skin of the chest, arms, and legs. These electrodes detect the electrical signals produced by the heart and transmit them to a machine that amplifies and records them. The procedure is non-invasive, painless, and quick, usually taking only a few minutes.

ECGs are commonly used to diagnose and monitor various heart conditions, including arrhythmias, coronary artery disease, heart attacks, and electrolyte imbalances. They can also be used to evaluate the effectiveness of certain medications or treatments.

Coronary angiography is a medical procedure that uses X-ray imaging to visualize the coronary arteries, which supply blood to the heart muscle. During the procedure, a thin, flexible catheter is inserted into an artery in the arm or groin and threaded through the blood vessels to the heart. A contrast dye is then injected through the catheter, and X-ray images are taken as the dye flows through the coronary arteries. These images can help doctors diagnose and treat various heart conditions, such as blockages or narrowing of the arteries, that can lead to chest pain or heart attacks. It is also known as coronary arteriography or cardiac catheterization.

Thrombolytic therapy, also known as thrombolysis, is a medical treatment that uses medications called thrombolytics or fibrinolytics to dissolve or break down blood clots (thrombi) in blood vessels. These clots can obstruct the flow of blood to vital organs such as the heart, lungs, or brain, leading to serious conditions like myocardial infarction (heart attack), pulmonary embolism, or ischemic stroke.

The goal of thrombolytic therapy is to restore blood flow as quickly and efficiently as possible to prevent further damage to the affected organ and potentially save lives. Commonly used thrombolytic drugs include alteplase (tPA), reteplase, and tenecteplase. It's essential to administer these medications as soon as possible after the onset of symptoms for optimal treatment outcomes. However, there are risks associated with thrombolytic therapy, such as an increased chance of bleeding complications, which must be carefully weighed against its benefits in each individual case.

Cardiotonic agents are a type of medication that have a positive inotropic effect on the heart, meaning they help to improve the contractility and strength of heart muscle contractions. These medications are often used to treat heart failure, as they can help to improve the efficiency of the heart's pumping ability and increase cardiac output.

Cardiotonic agents work by increasing the levels of calcium ions inside heart muscle cells during each heartbeat, which in turn enhances the force of contraction. Some common examples of cardiotonic agents include digitalis glycosides (such as digoxin), which are derived from the foxglove plant, and synthetic medications such as dobutamine and milrinone.

While cardiotonic agents can be effective in improving heart function, they can also have potentially serious side effects, including arrhythmias, electrolyte imbalances, and digestive symptoms. As a result, they are typically used under close medical supervision and their dosages may need to be carefully monitored to minimize the risk of adverse effects.

In the field of medicine, "time factors" refer to the duration of symptoms or time elapsed since the onset of a medical condition, which can have significant implications for diagnosis and treatment. Understanding time factors is crucial in determining the progression of a disease, evaluating the effectiveness of treatments, and making critical decisions regarding patient care.

For example, in stroke management, "time is brain," meaning that rapid intervention within a specific time frame (usually within 4.5 hours) is essential to administering tissue plasminogen activator (tPA), a clot-busting drug that can minimize brain damage and improve patient outcomes. Similarly, in trauma care, the "golden hour" concept emphasizes the importance of providing definitive care within the first 60 minutes after injury to increase survival rates and reduce morbidity.

Time factors also play a role in monitoring the progression of chronic conditions like diabetes or heart disease, where regular follow-ups and assessments help determine appropriate treatment adjustments and prevent complications. In infectious diseases, time factors are crucial for initiating antibiotic therapy and identifying potential outbreaks to control their spread.

Overall, "time factors" encompass the significance of recognizing and acting promptly in various medical scenarios to optimize patient outcomes and provide effective care.

Coronary vessels refer to the network of blood vessels that supply oxygenated blood and nutrients to the heart muscle, also known as the myocardium. The two main coronary arteries are the left main coronary artery and the right coronary artery.

The left main coronary artery branches off into the left anterior descending artery (LAD) and the left circumflex artery (LCx). The LAD supplies blood to the front of the heart, while the LCx supplies blood to the side and back of the heart.

The right coronary artery supplies blood to the right lower part of the heart, including the right atrium and ventricle, as well as the back of the heart.

Coronary vessel disease (CVD) occurs when these vessels become narrowed or blocked due to the buildup of plaque, leading to reduced blood flow to the heart muscle. This can result in chest pain, shortness of breath, or a heart attack.

Left ventricular function refers to the ability of the left ventricle (the heart's lower-left chamber) to contract and relax, thereby filling with and ejecting blood. The left ventricle is responsible for pumping oxygenated blood to the rest of the body. Its function is evaluated by measuring several parameters, including:

1. Ejection fraction (EF): This is the percentage of blood that is pumped out of the left ventricle with each heartbeat. A normal ejection fraction ranges from 55% to 70%.
2. Stroke volume (SV): The amount of blood pumped by the left ventricle in one contraction. A typical SV is about 70 mL/beat.
3. Cardiac output (CO): The total volume of blood that the left ventricle pumps per minute, calculated as the product of stroke volume and heart rate. Normal CO ranges from 4 to 8 L/minute.

Assessment of left ventricular function is crucial in diagnosing and monitoring various cardiovascular conditions such as heart failure, coronary artery disease, valvular heart diseases, and cardiomyopathies.

An anterior wall myocardial infarction (AMI) is a type of heart attack that occurs when there is a significant reduction or complete blockage of blood flow to the front wall of the heart muscle, also known as the anterior wall of the left ventricle. This reduction or blockage in blood flow is typically caused by a buildup of fatty deposits, called plaques, in the coronary arteries that supply oxygen-rich blood to the heart muscle.

When a plaque ruptures or breaks open, a blood clot forms around it, which can completely block the flow of blood to the heart muscle. This lack of blood flow causes the heart muscle to start to die, leading to a myocardial infarction or heart attack.

An anterior wall myocardial infarction is often associated with more severe symptoms and a higher risk of complications than other types of heart attacks because it affects a larger area of the heart muscle. Symptoms may include chest pain, shortness of breath, nausea, vomiting, sweating, and anxiety.

Immediate medical attention is necessary for an anterior wall myocardial infarction to restore blood flow to the heart muscle as quickly as possible and prevent further damage. Treatment options may include medications, such as clot-busting drugs or blood thinners, as well as procedures such as angioplasty or coronary artery bypass surgery.

Coronary thrombosis is a medical condition that refers to the formation of a blood clot (thrombus) inside a coronary artery, which supplies oxygenated blood to the heart muscle. The development of a thrombus can partially or completely obstruct blood flow, leading to insufficient oxygen supply to the heart muscle. This can cause chest pain (angina) or a heart attack (myocardial infarction), depending on the severity and duration of the blockage.

Coronary thrombosis often results from the rupture of an atherosclerotic plaque, a buildup of cholesterol, fat, calcium, and other substances in the inner lining (endothelium) of the coronary artery. The ruptured plaque exposes the underlying tissue to the bloodstream, triggering the coagulation cascade and resulting in the formation of a thrombus.

Immediate medical attention is crucial for managing coronary thrombosis, as timely treatment can help restore blood flow, prevent further damage to the heart muscle, and reduce the risk of complications such as heart failure or life-threatening arrhythmias. Treatment options may include medications, such as antiplatelet agents, anticoagulants, and thrombolytic drugs, or interventional procedures like angioplasty and stenting to open the blocked artery. In some cases, surgical intervention, such as coronary artery bypass grafting (CABG), may be necessary.

Creatine kinase (CK) is an enzyme found in various cells throughout the body, including heart muscle cells and skeletal muscle fibers. The CK enzyme exists in different forms, depending on the type of tissue where it is found. One such form is creatine kinase MB (CK-MB), which is primarily found in cardiac muscle cells.

An increase in the levels of CK-MB in the blood can indicate damage to the heart muscle, such as that caused by a heart attack or myocardial infarction. When heart muscle cells are damaged, they release their contents, including CK-MB, into the bloodstream. Therefore, measuring CK-MB levels is a useful diagnostic tool for detecting and monitoring heart muscle damage.

It's important to note that while an elevated CK-MB level can suggest heart muscle damage, it is not specific to the heart and can also be elevated in other conditions such as skeletal muscle damage or certain muscle disorders. Therefore, CK-MB levels should be interpreted in conjunction with other clinical findings and diagnostic tests.

Percutaneous Coronary Intervention (PCI), also known as coronary angioplasty, is a non-surgical procedure that opens up clogged coronary arteries to improve blood flow to the heart. It involves inserting a thin, flexible catheter into an artery in the groin or wrist and guiding it to the blocked artery in the heart. A small balloon is then inflated to widen the narrowed or blocked artery, and sometimes a stent (a tiny mesh tube) is placed to keep the artery open. This procedure helps to restore and maintain blood flow to the heart muscle, reducing symptoms of angina and improving overall cardiac function.

Peroxidase is a type of enzyme that catalyzes the chemical reaction in which hydrogen peroxide (H2O2) is broken down into water (H2O) and oxygen (O2). This enzymatic reaction also involves the oxidation of various organic and inorganic compounds, which can serve as electron donors.

Peroxidases are widely distributed in nature and can be found in various organisms, including bacteria, fungi, plants, and animals. They play important roles in various biological processes, such as defense against oxidative stress, breakdown of toxic substances, and participation in metabolic pathways.

The peroxidase-catalyzed reaction can be represented by the following chemical equation:

H2O2 + 2e- + 2H+ → 2H2O

In this reaction, hydrogen peroxide is reduced to water, and the electron donor is oxidized. The peroxidase enzyme facilitates the transfer of electrons between the substrate (hydrogen peroxide) and the electron donor, making the reaction more efficient and specific.

Peroxidases have various applications in medicine, industry, and research. For example, they can be used for diagnostic purposes, as biosensors, and in the treatment of wastewater and medical wastes. Additionally, peroxidases are involved in several pathological conditions, such as inflammation, cancer, and neurodegenerative diseases, making them potential targets for therapeutic interventions.

Induced heart arrest, also known as controlled cardiac arrest or planned cardiac arrest, is a deliberate medical intervention where cardiac activity is temporarily stopped through the use of medications or electrical disruption. This procedure is typically carried out during a surgical procedure, such as open-heart surgery, where the heart needs to be stilled to allow surgeons to work on it safely.

The most common method used to induce heart arrest is by administering a medication called potassium chloride, which stops the heart's electrical activity. Alternatively, an electrical shock may be delivered to the heart to achieve the same effect. Once the procedure is complete, the heart can be restarted using various resuscitation techniques, such as defibrillation or medication administration.

It's important to note that induced heart arrest is a carefully monitored and controlled medical procedure carried out by trained healthcare professionals in a hospital setting. It should not be confused with sudden cardiac arrest, which is an unexpected and often unpredictable event that occurs outside of a medical setting.

Perfusion, in medical terms, refers to the process of circulating blood through the body's organs and tissues to deliver oxygen and nutrients and remove waste products. It is a measure of the delivery of adequate blood flow to specific areas or tissues in the body. Perfusion can be assessed using various methods, including imaging techniques like computed tomography (CT) scans, magnetic resonance imaging (MRI), and perfusion scintigraphy.

Perfusion is critical for maintaining proper organ function and overall health. When perfusion is impaired or inadequate, it can lead to tissue hypoxia, acidosis, and cell death, which can result in organ dysfunction or failure. Conditions that can affect perfusion include cardiovascular disease, shock, trauma, and certain surgical procedures.

In medical terms, the heart is a muscular organ located in the thoracic cavity that functions as a pump to circulate blood throughout the body. It's responsible for delivering oxygen and nutrients to the tissues and removing carbon dioxide and other wastes. The human heart is divided into four chambers: two atria on the top and two ventricles on the bottom. The right side of the heart receives deoxygenated blood from the body and pumps it to the lungs, while the left side receives oxygenated blood from the lungs and pumps it out to the rest of the body. The heart's rhythmic contractions and relaxations are regulated by a complex electrical conduction system.

I believe there might be a misunderstanding in your question. "Dogs" is not a medical term or condition. It is the common name for a domesticated carnivore of the family Canidae, specifically the genus Canis, which includes wolves, foxes, and other extant and extinct species of mammals. Dogs are often kept as pets and companions, and they have been bred in a wide variety of forms and sizes for different purposes, such as hunting, herding, guarding, assisting police and military forces, and providing companionship and emotional support.

If you meant to ask about a specific medical condition or term related to dogs, please provide more context so I can give you an accurate answer.

Hemodynamics is the study of how blood flows through the cardiovascular system, including the heart and the vascular network. It examines various factors that affect blood flow, such as blood volume, viscosity, vessel length and diameter, and pressure differences between different parts of the circulatory system. Hemodynamics also considers the impact of various physiological and pathological conditions on these variables, and how they in turn influence the function of vital organs and systems in the body. It is a critical area of study in fields such as cardiology, anesthesiology, and critical care medicine.

Animal disease models are specialized animals, typically rodents such as mice or rats, that have been genetically engineered or exposed to certain conditions to develop symptoms and physiological changes similar to those seen in human diseases. These models are used in medical research to study the pathophysiology of diseases, identify potential therapeutic targets, test drug efficacy and safety, and understand disease mechanisms.

The genetic modifications can include knockout or knock-in mutations, transgenic expression of specific genes, or RNA interference techniques. The animals may also be exposed to environmental factors such as chemicals, radiation, or infectious agents to induce the disease state.

Examples of animal disease models include:

1. Mouse models of cancer: Genetically engineered mice that develop various types of tumors, allowing researchers to study cancer initiation, progression, and metastasis.
2. Alzheimer's disease models: Transgenic mice expressing mutant human genes associated with Alzheimer's disease, which exhibit amyloid plaque formation and cognitive decline.
3. Diabetes models: Obese and diabetic mouse strains like the NOD (non-obese diabetic) or db/db mice, used to study the development of type 1 and type 2 diabetes, respectively.
4. Cardiovascular disease models: Atherosclerosis-prone mice, such as ApoE-deficient or LDLR-deficient mice, that develop plaque buildup in their arteries when fed a high-fat diet.
5. Inflammatory bowel disease models: Mice with genetic mutations affecting intestinal barrier function and immune response, such as IL-10 knockout or SAMP1/YitFc mice, which develop colitis.

Animal disease models are essential tools in preclinical research, but it is important to recognize their limitations. Differences between species can affect the translatability of results from animal studies to human patients. Therefore, researchers must carefully consider the choice of model and interpret findings cautiously when applying them to human diseases.

"Wistar rats" are a strain of albino rats that are widely used in laboratory research. They were developed at the Wistar Institute in Philadelphia, USA, and were first introduced in 1906. Wistar rats are outbred, which means that they are genetically diverse and do not have a fixed set of genetic characteristics like inbred strains.

Wistar rats are commonly used as animal models in biomedical research because of their size, ease of handling, and relatively low cost. They are used in a wide range of research areas, including toxicology, pharmacology, nutrition, cancer, cardiovascular disease, and behavioral studies. Wistar rats are also used in safety testing of drugs, medical devices, and other products.

Wistar rats are typically larger than many other rat strains, with males weighing between 500-700 grams and females weighing between 250-350 grams. They have a lifespan of approximately 2-3 years. Wistar rats are also known for their docile and friendly nature, making them easy to handle and work with in the laboratory setting.

Sprague-Dawley rats are a strain of albino laboratory rats that are widely used in scientific research. They were first developed by researchers H.H. Sprague and R.C. Dawley in the early 20th century, and have since become one of the most commonly used rat strains in biomedical research due to their relatively large size, ease of handling, and consistent genetic background.

Sprague-Dawley rats are outbred, which means that they are genetically diverse and do not suffer from the same limitations as inbred strains, which can have reduced fertility and increased susceptibility to certain diseases. They are also characterized by their docile nature and low levels of aggression, making them easier to handle and study than some other rat strains.

These rats are used in a wide variety of research areas, including toxicology, pharmacology, nutrition, cancer, and behavioral studies. Because they are genetically diverse, Sprague-Dawley rats can be used to model a range of human diseases and conditions, making them an important tool in the development of new drugs and therapies.

Mitochondrial membrane transport proteins are a type of integral membrane proteins located in the inner and outer mitochondrial membranes. They play a crucial role in the regulation of molecule exchange between the cytosol and the mitochondrial matrix, allowing only specific ions and molecules to pass through while maintaining the structural and functional integrity of the mitochondria.

The inner mitochondrial membrane transport proteins, also known as the mitochondrial carrier proteins or the solute carriers, are a family of about 50 different types of proteins that facilitate the passage of various metabolites, such as nucleotides, amino acids, fatty acids, and inorganic ions (like calcium, sodium, and potassium). These transport proteins usually function as exchangers or uniporters, moving one type of solute in one direction in exchange for another type of solute or a proton.

The outer mitochondrial membrane is more permeable than the inner membrane due to the presence of voltage-dependent anion channels (VDACs) and other porins that allow small molecules, ions, and metabolites to pass through. VDACs are the most abundant proteins in the outer mitochondrial membrane and play a significant role in controlling the flow of metabolites between the cytosol and the intermembrane space.

In summary, mitochondrial membrane transport proteins are essential for maintaining the proper functioning of mitochondria by regulating the movement of molecules across the inner and outer membranes. They facilitate the exchange of nutrients, metabolites, and ions required for oxidative phosphorylation, energy production, and other cellular processes.

Myocardial contraction refers to the rhythmic and forceful shortening of heart muscle cells (myocytes) in the myocardium, which is the muscular wall of the heart. This process is initiated by electrical signals generated by the sinoatrial node, causing a wave of depolarization that spreads throughout the heart.

During myocardial contraction, calcium ions flow into the myocytes, triggering the interaction between actin and myosin filaments, which are the contractile proteins in the muscle cells. This interaction causes the myofilaments to slide past each other, resulting in the shortening of the sarcomeres (the functional units of muscle contraction) and ultimately leading to the contraction of the heart muscle.

Myocardial contraction is essential for pumping blood throughout the body and maintaining adequate circulation to vital organs. Any impairment in myocardial contractility can lead to various cardiac disorders, such as heart failure, cardiomyopathy, and arrhythmias.

Treatment outcome is a term used to describe the result or effect of medical treatment on a patient's health status. It can be measured in various ways, such as through symptoms improvement, disease remission, reduced disability, improved quality of life, or survival rates. The treatment outcome helps healthcare providers evaluate the effectiveness of a particular treatment plan and make informed decisions about future care. It is also used in clinical research to compare the efficacy of different treatments and improve patient care.

I'm happy to help! However, it seems like there are two terms combined into one request: "Mitochondria" and "Heart." I will provide separate definitions for each.

Mitochondrion (singular) or Mitochondria (plural): These are specialized structures found in the cytoplasm of most eukaryotic cells (cells with a true nucleus), including human cells. They are often referred to as the "powerhouse" of the cell because they generate energy in the form of ATP (adenosine triphosphate) through a process called oxidative phosphorylation. Mitochondria contain their own DNA, which is distinct from the nuclear DNA, and are believed to have originated from ancient bacteria that established a symbiotic relationship with primitive eukaryotic cells.

Heart: In human anatomy, the heart is a muscular organ responsible for pumping blood throughout the body. It is located in the thoracic cavity, slightly left of the center, and is enclosed by the pericardium, a double-walled sac that provides protection and lubrication for the heart's movement. The human heart is divided into four chambers: two atria on the top and two ventricles on the bottom. The right side of the heart receives deoxygenated blood from the body and pumps it to the lungs, while the left side receives oxygenated blood from the lungs and pumps it to the rest of the body. The heart's pumping action is regulated by electrical signals that originate in a group of specialized cardiac muscle cells called the sinoatrial node (SA node).

P-Selectin is a type of cell adhesion molecule, specifically a member of the selectin family, that is involved in the inflammatory response. It is primarily expressed on the surface of activated platelets and endothelial cells. P-Selectin plays a crucial role in the initial interaction between leukocytes (white blood cells) and the vascular endothelium, which is an essential step in the recruitment of leukocytes to sites of inflammation or injury. This process helps to mediate the rolling and adhesion of leukocytes to the endothelial surface, facilitating their extravasation into the surrounding tissue. P-Selectin's function is regulated by its interaction with specific ligands on the surface of leukocytes, such as PSGL-1 (P-Selectin Glycoprotein Ligand-1).

Necrosis is the premature death of cells or tissues due to damage or injury, such as from infection, trauma, infarction (lack of blood supply), or toxic substances. It's a pathological process that results in the uncontrolled and passive degradation of cellular components, ultimately leading to the release of intracellular contents into the extracellular space. This can cause local inflammation and may lead to further tissue damage if not treated promptly.

There are different types of necrosis, including coagulative, liquefactive, caseous, fat, fibrinoid, and gangrenous necrosis, each with distinct histological features depending on the underlying cause and the affected tissues or organs.

"Random allocation," also known as "random assignment" or "randomization," is a process used in clinical trials and other research studies to distribute participants into different intervention groups (such as experimental group vs. control group) in a way that minimizes selection bias and ensures the groups are comparable at the start of the study.

In random allocation, each participant has an equal chance of being assigned to any group, and the assignment is typically made using a computer-generated randomization schedule or other objective methods. This process helps to ensure that any differences between the groups are due to the intervention being tested rather than pre-existing differences in the participants' characteristics.

Microcirculation is the circulation of blood in the smallest blood vessels, including arterioles, venules, and capillaries. It's responsible for the delivery of oxygen and nutrients to the tissues and the removal of waste products. The microcirculation plays a crucial role in maintaining tissue homeostasis and is regulated by various physiological mechanisms such as autonomic nervous system activity, local metabolic factors, and hormones.

Impairment of microcirculation can lead to tissue hypoxia, inflammation, and organ dysfunction, which are common features in several diseases, including diabetes, hypertension, sepsis, and ischemia-reperfusion injury. Therefore, understanding the structure and function of the microcirculation is essential for developing new therapeutic strategies to treat these conditions.

Immunoglobulin (Ig) Fab fragments are the antigen-binding portions of an antibody that result from the digestion of the whole antibody molecule by enzymes such as papain. An antibody, also known as an immunoglobulin, is a Y-shaped protein produced by the immune system to identify and neutralize foreign substances like bacteria, viruses, or toxins. The antibody has two identical antigen-binding sites, located at the tips of the two shorter arms, which can bind specifically to a target antigen.

Fab fragments are formed when an antibody is cleaved by papain, resulting in two Fab fragments and one Fc fragment. Each Fab fragment contains one antigen-binding site, composed of a variable region (Fv) and a constant region (C). The Fv region is responsible for the specificity and affinity of the antigen binding, while the C region contributes to the effector functions of the antibody.

Fab fragments are often used in various medical applications, such as immunodiagnostics and targeted therapies, due to their ability to bind specifically to target antigens without triggering an immune response or other effector functions associated with the Fc region.

The platelet glycoprotein GPIIb-IIIa complex, also known as integrin αIIbβ3 or CD41/CD61, is a heterodimeric transmembrane receptor found on the surface of platelets and megakaryocytes. It plays a crucial role in platelet aggregation and thrombus formation during hemostasis and pathological conditions such as arterial thrombosis.

The GPIIb-IIIa complex is composed of two non-covalently associated subunits, GPIIb (αIIb or CD41) and IIIa (β3 or CD61). Upon platelet activation by various agonists like ADP, thrombin, or collagen, the GPIIb-IIIa complex undergoes a conformational change that allows it to bind fibrinogen, von Willebrand factor, and other adhesive proteins. This binding event leads to platelet aggregation and the formation of a hemostatic plug or pathological thrombus.

Inhibition of the GPIIb-IIIa complex has been a target for antiplatelet therapy in the prevention and treatment of arterial thrombosis, such as myocardial infarction and stroke. Several pharmacological agents, including monoclonal antibodies and small molecule antagonists, have been developed to block this complex and reduce platelet aggregation.

Cardiac myocytes are the muscle cells that make up the heart muscle, also known as the myocardium. These specialized cells are responsible for contracting and relaxing in a coordinated manner to pump blood throughout the body. They differ from skeletal muscle cells in several ways, including their ability to generate their own electrical impulses, which allows the heart to function as an independent rhythmical pump. Cardiac myocytes contain sarcomeres, the contractile units of the muscle, and are connected to each other by intercalated discs that help coordinate contraction and ensure the synchronous beating of the heart.

Echocardiography is a medical procedure that uses sound waves to produce detailed images of the heart's structure, function, and motion. It is a non-invasive test that can help diagnose various heart conditions, such as valve problems, heart muscle damage, blood clots, and congenital heart defects.

During an echocardiogram, a transducer (a device that sends and receives sound waves) is placed on the chest or passed through the esophagus to obtain images of the heart. The sound waves produced by the transducer bounce off the heart structures and return to the transducer, which then converts them into electrical signals that are processed to create images of the heart.

There are several types of echocardiograms, including:

* Transthoracic echocardiography (TTE): This is the most common type of echocardiogram and involves placing the transducer on the chest.
* Transesophageal echocardiography (TEE): This type of echocardiogram involves passing a specialized transducer through the esophagus to obtain images of the heart from a closer proximity.
* Stress echocardiography: This type of echocardiogram is performed during exercise or medication-induced stress to assess how the heart functions under stress.
* Doppler echocardiography: This type of echocardiogram uses sound waves to measure blood flow and velocity in the heart and blood vessels.

Echocardiography is a valuable tool for diagnosing and managing various heart conditions, as it provides detailed information about the structure and function of the heart. It is generally safe, non-invasive, and painless, making it a popular choice for doctors and patients alike.

Neutrophils are a type of white blood cell that are part of the immune system's response to infection. They are produced in the bone marrow and released into the bloodstream where they circulate and are able to move quickly to sites of infection or inflammation in the body. Neutrophils are capable of engulfing and destroying bacteria, viruses, and other foreign substances through a process called phagocytosis. They are also involved in the release of inflammatory mediators, which can contribute to tissue damage in some cases. Neutrophils are characterized by the presence of granules in their cytoplasm, which contain enzymes and other proteins that help them carry out their immune functions.

Ischemic preconditioning is a phenomenon in which brief, non-lethal episodes of ischemia (restriction or interruption of blood supply to an organ or tissue) render the tissue more resistant to subsequent prolonged ischemia and reperfusion injury. This adaptive response involves a complex series of cellular and molecular changes that protect the myocardium, brain, kidney, or other organs from ischemic damage. The underlying mechanisms include the activation of various signaling pathways, such as adenosine, opioid, and kinase pathways, which lead to the production of protective factors and the modulation of cellular responses to ischemia and reperfusion injury. Ischemic preconditioning has been extensively studied in the context of cardiovascular medicine, where it has been shown to reduce infarct size and improve cardiac function after myocardial infarction. However, this protective phenomenon has also been observed in other organs and systems, including the brain, kidney, liver, and skeletal muscle.

Ischemia is the medical term used to describe a lack of blood flow to a part of the body, often due to blocked or narrowed blood vessels. This can lead to a shortage of oxygen and nutrients in the tissues, which can cause them to become damaged or die. Ischemia can affect many different parts of the body, including the heart, brain, legs, and intestines. Symptoms of ischemia depend on the location and severity of the blockage, but they may include pain, cramping, numbness, weakness, or coldness in the affected area. In severe cases, ischemia can lead to tissue death (gangrene) or organ failure. Treatment for ischemia typically involves addressing the underlying cause of the blocked blood flow, such as through medication, surgery, or lifestyle changes.

I believe there may be some confusion in your question. "Rabbits" is a common name used to refer to the Lagomorpha species, particularly members of the family Leporidae. They are small mammals known for their long ears, strong legs, and quick reproduction.

However, if you're referring to "rabbits" in a medical context, there is a term called "rabbit syndrome," which is a rare movement disorder characterized by repetitive, involuntary movements of the fingers, resembling those of a rabbit chewing. It is also known as "finger-chewing chorea." This condition is usually associated with certain medications, particularly antipsychotics, and typically resolves when the medication is stopped or adjusted.

"Swine" is a common term used to refer to even-toed ungulates of the family Suidae, including domestic pigs and wild boars. However, in a medical context, "swine" often appears in the phrase "swine flu," which is a strain of influenza virus that typically infects pigs but can also cause illness in humans. The 2009 H1N1 pandemic was caused by a new strain of swine-origin influenza A virus, which was commonly referred to as "swine flu." It's important to note that this virus is not transmitted through eating cooked pork products; it spreads from person to person, mainly through respiratory droplets produced when an infected person coughs or sneezes.

Coronary artery disease, often simply referred to as coronary disease, is a condition in which the blood vessels that supply oxygen-rich blood to the heart become narrowed or blocked due to the buildup of fatty deposits called plaques. This can lead to chest pain (angina), shortness of breath, or in severe cases, a heart attack.

The medical definition of coronary artery disease is:

A condition characterized by the accumulation of atheromatous plaques in the walls of the coronary arteries, leading to decreased blood flow and oxygen supply to the myocardium (heart muscle). This can result in symptoms such as angina pectoris, shortness of breath, or arrhythmias, and may ultimately lead to myocardial infarction (heart attack) or heart failure.

Risk factors for coronary artery disease include age, smoking, high blood pressure, high cholesterol, diabetes, obesity, physical inactivity, and a family history of the condition. Lifestyle changes such as quitting smoking, exercising regularly, eating a healthy diet, and managing stress can help reduce the risk of developing coronary artery disease. Medical treatments may include medications to control blood pressure, cholesterol levels, or irregular heart rhythms, as well as procedures such as angioplasty or bypass surgery to improve blood flow to the heart.

A stent is a small mesh tube that's used to treat narrow or weak arteries. Arteries are blood vessels that carry blood away from your heart to other parts of your body. A stent is placed in an artery as part of a procedure called angioplasty. Angioplasty restores blood flow through narrowed or blocked arteries by inflating a tiny balloon inside the blocked artery to widen it.

The stent is then inserted into the widened artery to keep it open. The stent is usually made of metal, but some are coated with medication that is slowly and continuously released to help prevent the formation of scar tissue in the artery. This can reduce the chance of the artery narrowing again.

Stents are also used in other parts of the body, such as the neck (carotid artery) and kidneys (renal artery), to help maintain blood flow and prevent blockages. They can also be used in the urinary system to treat conditions like ureteropelvic junction obstruction or narrowing of the urethra.

The endothelium is a thin layer of simple squamous epithelial cells that lines the interior surface of blood vessels, lymphatic vessels, and heart chambers. The vascular endothelium, specifically, refers to the endothelial cells that line the blood vessels. These cells play a crucial role in maintaining vascular homeostasis by regulating vasomotor tone, coagulation, platelet activation, inflammation, and permeability of the vessel wall. They also contribute to the growth and repair of the vascular system and are involved in various pathological processes such as atherosclerosis, hypertension, and diabetes.

The Predictive Value of Tests, specifically the Positive Predictive Value (PPV) and Negative Predictive Value (NPV), are measures used in diagnostic tests to determine the probability that a positive or negative test result is correct.

Positive Predictive Value (PPV) is the proportion of patients with a positive test result who actually have the disease. It is calculated as the number of true positives divided by the total number of positive results (true positives + false positives). A higher PPV indicates that a positive test result is more likely to be a true positive, and therefore the disease is more likely to be present.

Negative Predictive Value (NPV) is the proportion of patients with a negative test result who do not have the disease. It is calculated as the number of true negatives divided by the total number of negative results (true negatives + false negatives). A higher NPV indicates that a negative test result is more likely to be a true negative, and therefore the disease is less likely to be present.

The predictive value of tests depends on the prevalence of the disease in the population being tested, as well as the sensitivity and specificity of the test. A test with high sensitivity and specificity will generally have higher predictive values than a test with low sensitivity and specificity. However, even a highly sensitive and specific test can have low predictive values if the prevalence of the disease is low in the population being tested.

Prospective studies, also known as longitudinal studies, are a type of cohort study in which data is collected forward in time, following a group of individuals who share a common characteristic or exposure over a period of time. The researchers clearly define the study population and exposure of interest at the beginning of the study and follow up with the participants to determine the outcomes that develop over time. This type of study design allows for the investigation of causal relationships between exposures and outcomes, as well as the identification of risk factors and the estimation of disease incidence rates. Prospective studies are particularly useful in epidemiology and medical research when studying diseases with long latency periods or rare outcomes.

Brain ischemia is the medical term used to describe a reduction or interruption of blood flow to the brain, leading to a lack of oxygen and glucose delivery to brain tissue. This can result in brain damage or death of brain cells, known as infarction. Brain ischemia can be caused by various conditions such as thrombosis (blood clot formation), embolism (obstruction of a blood vessel by a foreign material), or hypoperfusion (reduced blood flow). The severity and duration of the ischemia determine the extent of brain damage. Symptoms can range from mild, such as transient ischemic attacks (TIAs or "mini-strokes"), to severe, including paralysis, speech difficulties, loss of consciousness, and even death. Immediate medical attention is required for proper diagnosis and treatment to prevent further damage and potential long-term complications.

Monoclonal antibodies are a type of antibody that are identical because they are produced by a single clone of cells. They are laboratory-produced molecules that act like human antibodies in the immune system. They can be designed to attach to specific proteins found on the surface of cancer cells, making them useful for targeting and treating cancer. Monoclonal antibodies can also be used as a therapy for other diseases, such as autoimmune disorders and inflammatory conditions.

Monoclonal antibodies are produced by fusing a single type of immune cell, called a B cell, with a tumor cell to create a hybrid cell, or hybridoma. This hybrid cell is then able to replicate indefinitely, producing a large number of identical copies of the original antibody. These antibodies can be further modified and engineered to enhance their ability to bind to specific targets, increase their stability, and improve their effectiveness as therapeutic agents.

Monoclonal antibodies have several mechanisms of action in cancer therapy. They can directly kill cancer cells by binding to them and triggering an immune response. They can also block the signals that promote cancer growth and survival. Additionally, monoclonal antibodies can be used to deliver drugs or radiation directly to cancer cells, increasing the effectiveness of these treatments while minimizing their side effects on healthy tissues.

Monoclonal antibodies have become an important tool in modern medicine, with several approved for use in cancer therapy and other diseases. They are continuing to be studied and developed as a promising approach to treating a wide range of medical conditions.

Myocardial stunning is a condition in cardiovascular medicine where the heart muscle (myocardium) temporarily loses its ability to contract effectively after being exposed to a brief, severe episode of ischemia (restriction of blood supply) or reperfusion injury (damage that occurs when blood flow is restored to an organ or tissue after a period of ischemia). This results in a reduction in the heart's pumping function, which can be detected using imaging techniques such as echocardiography.

The stunning phenomenon is believed to be caused by complex biochemical and cellular processes that occur during ischemia-reperfusion injury, including the generation of free radicals, calcium overload, inflammation, and activation of various signaling pathways. These changes can lead to the dysfunction of contractile proteins, mitochondrial damage, and altered gene expression in cardiomyocytes (heart muscle cells).

Myocardial stunning is often observed following procedures such as coronary angioplasty or bypass surgery, where blood flow is temporarily interrupted and then restored to the heart. It can also occur during episodes of unstable angina, acute myocardial infarction, or cardiac arrest. Although the stunning itself is usually reversible within a few days to several weeks, it may contribute to short-term hemodynamic instability and increased risk of adverse events such as heart failure, arrhythmias, or even death.

Management of myocardial stunning typically involves supportive care, optimizing hemodynamics, and addressing any underlying conditions that may have contributed to the ischemic episode. In some cases, medications like inotropes or vasopressors might be used to support cardiac function temporarily. Preventive strategies, such as maintaining adequate blood pressure, heart rate, and oxygenation during procedures, can help reduce the risk of myocardial stunning.

Malondialdehyde (MDA) is a naturally occurring organic compound that is formed as a byproduct of lipid peroxidation, a process in which free radicals or reactive oxygen species react with polyunsaturated fatty acids. MDA is a highly reactive aldehyde that can modify proteins, DNA, and other biomolecules, leading to cellular damage and dysfunction. It is often used as a marker of oxidative stress in biological systems and has been implicated in the development of various diseases, including cancer, cardiovascular disease, and neurodegenerative disorders.

Middle Cerebral Artery (MCA) infarction is a type of ischemic stroke that occurs when there is an obstruction in the blood supply to the middle cerebral artery, which is one of the major blood vessels that supplies oxygenated blood to the brain. The MCA supplies blood to a large portion of the brain, including the motor and sensory cortex, parts of the temporal and parietal lobes, and the basal ganglia.

An infarction is the death of tissue due to the lack of blood supply, which can lead to damage or loss of function in the affected areas of the brain. Symptoms of MCA infarction may include weakness or numbness on one side of the body, difficulty speaking or understanding speech, vision problems, and altered levels of consciousness.

MCA infarctions can be caused by various factors, including embolism (a blood clot that travels to the brain from another part of the body), thrombosis (a blood clot that forms in the MCA itself), or stenosis (narrowing of the artery due to atherosclerosis or other conditions). Treatment for MCA infarction may include medications to dissolve blood clots, surgery to remove the obstruction, or rehabilitation to help regain lost function.

A Transient Ischemic Attack (TIA), also known as a "mini-stroke," is a temporary period of symptoms similar to those you'd get if you were having a stroke. A TIA doesn't cause permanent damage and is often caused by a temporary decrease in blood supply to part of your brain, which may last as little as five minutes.

Like an ischemic stroke, a TIA occurs when a clot or debris blocks blood flow to part of your nervous system. However, unlike a stroke, a TIA doesn't leave lasting damage because the blockage is temporary.

Symptoms of a TIA can include sudden onset of weakness, numbness or paralysis in your face, arm or leg, typically on one side of your body. You could also experience slurred or garbled speech, or difficulty understanding others. Other symptoms can include blindness in one or both eyes, dizziness, or a severe headache with no known cause.

Even though TIAs usually last only a few minutes, they are a serious condition and should not be ignored. If you suspect you or someone else is experiencing a TIA, seek immediate medical attention. TIAs can be a warning sign that a full-blown stroke is imminent.

Warm ischemia, also known as warm injury or warm hypoxia, refers to the damage that occurs to tissues when there is an inadequate blood supply at body temperature. This can happen during surgical procedures, trauma, or other medical conditions that restrict blood flow to a specific area of the body. The lack of oxygen and nutrients, combined with the buildup of waste products, can cause cells to become damaged or die, leading to tissue dysfunction or failure.

The term "warm" is used to distinguish this type of ischemia from cold ischemia, which occurs when tissues are cooled and blood flow is restricted. Cold ischemia is often used in organ transplantation to preserve the organ until it can be transplanted. Warm ischemia is generally more damaging to tissues than cold ischemia because the metabolic demands of the cells are not being met, leading to a more rapid onset of cellular damage.

The severity and duration of warm ischemia can affect the extent of tissue damage and the likelihood of recovery. In some cases, warm ischemia may be reversible if blood flow is restored quickly enough, but in other cases it may lead to permanent tissue damage or loss of function. Treatment for warm ischemia typically involves restoring blood flow to the affected area as soon as possible, along with supportive care to manage any complications that may arise.

Organ preservation is a medical technique used to maintain the viability and functionality of an organ outside the body for a certain period, typically for transplantation purposes. This process involves cooling the organ to slow down its metabolic activity and prevent tissue damage, while using specialized solutions that help preserve the organ's structure and function. Commonly preserved organs include hearts, livers, kidneys, lungs, and pancreases. The goal of organ preservation is to ensure that the transplanted organ remains in optimal condition until it can be successfully implanted into a recipient.

L-Lactate Dehydrogenase (LDH) is an enzyme found in various tissues within the body, including the heart, liver, kidneys, muscles, and brain. It plays a crucial role in the process of energy production, particularly during anaerobic conditions when oxygen levels are low.

In the presence of the coenzyme NADH, LDH catalyzes the conversion of pyruvate to lactate, generating NAD+ as a byproduct. Conversely, in the presence of NAD+, LDH can convert lactate back to pyruvate using NADH. This reversible reaction is essential for maintaining the balance between lactate and pyruvate levels within cells.

Elevated blood levels of LDH may indicate tissue damage or injury, as this enzyme can be released into the circulation following cellular breakdown. As a result, LDH is often used as a nonspecific biomarker for various medical conditions, such as myocardial infarction (heart attack), liver disease, muscle damage, and certain types of cancer. However, it's important to note that an isolated increase in LDH does not necessarily pinpoint the exact location or cause of tissue damage, and further diagnostic tests are usually required for confirmation.

In medical terms, constriction refers to the narrowing or tightening of a body part or passageway. This can occur due to various reasons such as spasms of muscles, inflammation, or abnormal growths. It can lead to symptoms like difficulty in breathing, swallowing, or blood flow, depending on where it occurs. For example, constriction of the airways in asthma, constriction of blood vessels in hypertension, or constriction of the esophagus in certain digestive disorders.

Decanoic acids are a type of medium-chain fatty acid with a chain length of 10 carbon atoms. The most common decanoic acid is decanoic acid or capric acid. It is found in various animal and plant sources, such as coconut oil and cow's milk. Decanoic acids have a variety of uses, including as ingredients in cosmetics and food products, and as a potential treatment for medical conditions such as epilepsy and bacterial infections. In the body, decanoic acids are metabolized in the liver and used for energy production.

Hydroxy acids are a class of chemical compounds that contain both a carboxylic acid group and a hydroxyl group. They are commonly used in dermatology and cosmetic products for their exfoliating, moisturizing, and anti-aging properties. The two main types of hydroxy acids used in skincare are alpha-hydroxy acids (AHAs) and beta-hydroxy acids (BHAs).

Alpha-hydroxy acids include compounds such as glycolic acid, lactic acid, malic acid, tartaric acid, and citric acid. They work by breaking down the "glue" that holds dead skin cells together, promoting cell turnover and helping to improve the texture and tone of the skin. AHAs are also known for their ability to improve the appearance of fine lines, wrinkles, and age spots.

Beta-hydroxy acids, on the other hand, are primarily represented by salicylic acid. BHAs are oil-soluble, which allows them to penetrate deeper into the pores and exfoliate dead skin cells and excess sebum that can lead to clogged pores and acne breakouts.

It is important to note that hydroxy acids can cause skin irritation and sensitivity to sunlight, so it is recommended to use sunscreen and start with lower concentrations when first incorporating them into a skincare routine.

Oxidative stress is defined as an imbalance between the production of reactive oxygen species (free radicals) and the body's ability to detoxify them or repair the damage they cause. This imbalance can lead to cellular damage, oxidation of proteins, lipids, and DNA, disruption of cellular functions, and activation of inflammatory responses. Prolonged or excessive oxidative stress has been linked to various health conditions, including cancer, cardiovascular diseases, neurodegenerative disorders, and aging-related diseases.

Tiopronin is a medication that belongs to a class of drugs called mucolytic agents. It works by breaking down mucus in the respiratory tract, making it easier to cough up and clear the airways. Tiopronin is also known as tiopronin sodium or Thiola®.

In addition to its use as a mucolytic agent, tiopronin has been found to be effective in reducing the formation of cystine kidney stones in patients with a rare genetic disorder called cystinuria. It works by binding to cystine in the urine and preventing it from forming into crystals or stones.

Tiopronin is available as a tablet or oral solution and is typically taken several times a day, with dosing adjusted based on the patient's individual needs and response to treatment. Common side effects of tiopronin include stomach upset, loss of appetite, and rash.

In the context of medicine and toxicology, protective agents are substances that provide protection against harmful or damaging effects of other substances. They can work in several ways, such as:

1. Binding to toxic substances: Protective agents can bind to toxic substances, rendering them inactive or less active, and preventing them from causing harm. For example, activated charcoal is sometimes used in the emergency treatment of certain types of poisoning because it can bind to certain toxins in the stomach and intestines and prevent their absorption into the body.
2. Increasing elimination: Protective agents can increase the elimination of toxic substances from the body, for example by promoting urinary or biliary excretion.
3. Reducing oxidative stress: Antioxidants are a type of protective agent that can reduce oxidative stress caused by free radicals and reactive oxygen species (ROS). These agents can protect cells and tissues from damage caused by oxidation.
4. Supporting organ function: Protective agents can support the function of organs that have been damaged by toxic substances, for example by improving blood flow or reducing inflammation.

Examples of protective agents include chelating agents, antidotes, free radical scavengers, and anti-inflammatory drugs.

Apoptosis is a programmed and controlled cell death process that occurs in multicellular organisms. It is a natural process that helps maintain tissue homeostasis by eliminating damaged, infected, or unwanted cells. During apoptosis, the cell undergoes a series of morphological changes, including cell shrinkage, chromatin condensation, and fragmentation into membrane-bound vesicles called apoptotic bodies. These bodies are then recognized and engulfed by neighboring cells or phagocytic cells, preventing an inflammatory response. Apoptosis is regulated by a complex network of intracellular signaling pathways that involve proteins such as caspases, Bcl-2 family members, and inhibitors of apoptosis (IAPs).

C57BL/6 (C57 Black 6) is an inbred strain of laboratory mouse that is widely used in biomedical research. The term "inbred" refers to a strain of animals where matings have been carried out between siblings or other closely related individuals for many generations, resulting in a population that is highly homozygous at most genetic loci.

The C57BL/6 strain was established in 1920 by crossing a female mouse from the dilute brown (DBA) strain with a male mouse from the black strain. The resulting offspring were then interbred for many generations to create the inbred C57BL/6 strain.

C57BL/6 mice are known for their robust health, longevity, and ease of handling, making them a popular choice for researchers. They have been used in a wide range of biomedical research areas, including studies of cancer, immunology, neuroscience, cardiovascular disease, and metabolism.

One of the most notable features of the C57BL/6 strain is its sensitivity to certain genetic modifications, such as the introduction of mutations that lead to obesity or impaired glucose tolerance. This has made it a valuable tool for studying the genetic basis of complex diseases and traits.

Overall, the C57BL/6 inbred mouse strain is an important model organism in biomedical research, providing a valuable resource for understanding the genetic and molecular mechanisms underlying human health and disease.

Medical Definition:

Superoxide dismutase (SOD) is an enzyme that catalyzes the dismutation of superoxide radicals (O2-) into oxygen (O2) and hydrogen peroxide (H2O2). This essential antioxidant defense mechanism helps protect the body's cells from damage caused by reactive oxygen species (ROS), which are produced during normal metabolic processes and can lead to oxidative stress when their levels become too high.

There are three main types of superoxide dismutase found in different cellular locations:
1. Copper-zinc superoxide dismutase (CuZnSOD or SOD1) - Present mainly in the cytoplasm of cells.
2. Manganese superoxide dismutase (MnSOD or SOD2) - Located within the mitochondrial matrix.
3. Extracellular superoxide dismutase (EcSOD or SOD3) - Found in the extracellular spaces, such as blood vessels and connective tissues.

Imbalances in SOD levels or activity have been linked to various pathological conditions, including neurodegenerative diseases, cancer, and aging-related disorders.

Fibrinolytic agents are medications that dissolve or break down blood clots by activating plasminogen, which is converted into plasmin. Plasmin is a proteolytic enzyme that degrades fibrin, the structural protein in blood clots. Fibrinolytic agents are used medically to treat conditions such as acute ischemic stroke, deep vein thrombosis, pulmonary embolism, and myocardial infarction (heart attack) by restoring blood flow in occluded vessels. Examples of fibrinolytic agents include alteplase, reteplase, and tenecteplase. It is important to note that these medications carry a risk of bleeding complications and should be administered with caution.

Organ preservation solutions are specialized fluids used to maintain the viability and functionality of organs ex vivo (outside the body) during the process of transplantation. These solutions are designed to provide optimal conditions for the organ by preventing tissue damage, reducing metabolic activity, and minimizing ischemic injuries that may occur during the time between organ removal from the donor and implantation into the recipient.

The composition of organ preservation solutions typically includes various ingredients such as:

1. Cryoprotectants: These help prevent ice crystal formation and damage to cell membranes during freezing and thawing processes, especially for organs like the heart and lungs that require deep hypothermia for preservation.
2. Buffers: They maintain physiological pH levels and counteract acidosis caused by anaerobic metabolism in the absence of oxygen supply.
3. Colloids: These substances, such as hydroxyethyl starch or dextran, help preserve oncotic pressure and prevent cellular edema.
4. Electrolytes: Balanced concentrations of ions like sodium, potassium, calcium, magnesium, chloride, and bicarbonate are essential for maintaining physiological osmolarity and membrane potentials.
5. Energy substrates: Glucose, lactate, or other energy-rich compounds can serve as fuel sources to support the metabolic needs of the organ during preservation.
6. Antioxidants: These agents protect against oxidative stress and lipid peroxidation induced by ischemia-reperfusion injuries.
7. Anti-inflammatory agents and immunosuppressants: Some solutions may contain substances that mitigate the inflammatory response and reduce immune activation in the transplanted organ.

Examples of commonly used organ preservation solutions include University of Wisconsin (UW) solution, Histidine-Tryptophan-Ketoglutarate (HTK) solution, Custodiol HTK solution, and Euro-Collins solution. The choice of preservation solution depends on the specific organ being transplanted and the duration of preservation required.

Neuroprotective agents are substances that protect neurons or nerve cells from damage, degeneration, or death caused by various factors such as trauma, inflammation, oxidative stress, or excitotoxicity. These agents work through different mechanisms, including reducing the production of free radicals, inhibiting the release of glutamate (a neurotransmitter that can cause cell damage in high concentrations), promoting the growth and survival of neurons, and preventing apoptosis (programmed cell death). Neuroprotective agents have been studied for their potential to treat various neurological disorders, including stroke, traumatic brain injury, Parkinson's disease, Alzheimer's disease, and multiple sclerosis. However, more research is needed to fully understand their mechanisms of action and to develop effective therapies.

Ventricular pressure refers to the pressure within the ventricles, which are the lower chambers of the heart. In the left ventricle, the pressure measures the force that the blood exerts on the walls as it is pumped out to the rest of the body. In the right ventricle, the pressure measures the force of the blood being pumped into the pulmonary artery and ultimately to the lungs for oxygenation.

Normally, the left ventricular pressure ranges from 8-12 mmHg at rest when the heart is relaxed (diastolic pressure) and can increase up to 120-140 mmHg during contraction (systolic pressure). The right ventricular pressure is lower than the left, with a normal diastolic pressure of 0-6 mmHg and a systolic pressure ranging from 15-30 mmHg.

Abnormal ventricular pressures can indicate various heart conditions, such as heart failure, hypertension, or valvular heart disease. Regular monitoring of ventricular pressure is essential in managing these conditions and ensuring proper heart function.

Free radicals are molecules or atoms that have one or more unpaired electrons in their outermost shell, making them highly reactive. They can be formed naturally in the body through processes such as metabolism and exercise, or they can come from external sources like pollution, radiation, and certain chemicals. Free radicals can cause damage to cells and contribute to the development of various diseases, including cancer, cardiovascular disease, and neurodegenerative disorders. Antioxidants are substances that can neutralize free radicals and help protect against their harmful effects.

Nitric oxide (NO) is a molecule made up of one nitrogen atom and one oxygen atom. In the body, it is a crucial signaling molecule involved in various physiological processes such as vasodilation, immune response, neurotransmission, and inhibition of platelet aggregation. It is produced naturally by the enzyme nitric oxide synthase (NOS) from the amino acid L-arginine. Inhaled nitric oxide is used medically to treat pulmonary hypertension in newborns and adults, as it helps to relax and widen blood vessels, improving oxygenation and blood flow.

Free radical scavengers, also known as antioxidants, are substances that neutralize or stabilize free radicals. Free radicals are highly reactive atoms or molecules with unpaired electrons, capable of causing damage to cells and tissues in the body through a process called oxidative stress. Antioxidants donate an electron to the free radical, thereby neutralizing it and preventing it from causing further damage. They can be found naturally in foods such as fruits, vegetables, and nuts, or they can be synthesized and used as dietary supplements. Examples of antioxidants include vitamins C and E, beta-carotene, and selenium.

An animal model in medicine refers to the use of non-human animals in experiments to understand, predict, and test responses and effects of various biological and chemical interactions that may also occur in humans. These models are used when studying complex systems or processes that cannot be easily replicated or studied in human subjects, such as genetic manipulation or exposure to harmful substances. The choice of animal model depends on the specific research question being asked and the similarities between the animal's and human's biological and physiological responses. Examples of commonly used animal models include mice, rats, rabbits, guinea pigs, and non-human primates.

Neutrophil infiltration is a pathological process characterized by the accumulation of neutrophils, a type of white blood cell, in tissue. It is a common feature of inflammation and occurs in response to infection, injury, or other stimuli that trigger an immune response. Neutrophils are attracted to the site of tissue damage by chemical signals called chemokines, which are released by damaged cells and activated immune cells. Once they reach the site of inflammation, neutrophils help to clear away damaged tissue and microorganisms through a process called phagocytosis. However, excessive or prolonged neutrophil infiltration can also contribute to tissue damage and may be associated with various disease states, including cancer, autoimmune disorders, and ischemia-reperfusion injury.

Reactive Oxygen Species (ROS) are highly reactive molecules containing oxygen, including peroxides, superoxide, hydroxyl radical, and singlet oxygen. They are naturally produced as byproducts of normal cellular metabolism in the mitochondria, and can also be generated by external sources such as ionizing radiation, tobacco smoke, and air pollutants. At low or moderate concentrations, ROS play important roles in cell signaling and homeostasis, but at high concentrations, they can cause significant damage to cell structures, including lipids, proteins, and DNA, leading to oxidative stress and potential cell death.

Cytoprotection refers to the protection of cells, particularly from harmful agents or damaging conditions. This can be achieved through various mechanisms, such as:

1. Activation of cellular defense pathways that help cells resist damage.
2. Inhibition of oxidative stress and inflammation, which can cause cellular damage.
3. Enhancement of cell repair processes, enabling cells to recover from damage more effectively.
4. Prevention of apoptosis (programmed cell death) or promotion of cell survival signals.

In the medical context, cytoprotective agents are often used to protect tissues and organs from injury due to various factors like chemotherapy, radiation therapy, ischemia-reperfusion injury, or inflammation. These agents can include antioxidants, anti-inflammatory drugs, growth factors, and other compounds that help maintain cellular integrity and function.

Cerebrovascular circulation refers to the network of blood vessels that supply oxygenated blood and nutrients to the brain tissue, and remove waste products. It includes the internal carotid arteries, vertebral arteries, circle of Willis, and the intracranial arteries that branch off from them.

The internal carotid arteries and vertebral arteries merge to form the circle of Willis, a polygonal network of vessels located at the base of the brain. The anterior cerebral artery, middle cerebral artery, posterior cerebral artery, and communicating arteries are the major vessels that branch off from the circle of Willis and supply blood to different regions of the brain.

Interruptions or abnormalities in the cerebrovascular circulation can lead to various neurological conditions such as stroke, transient ischemic attack (TIA), and vascular dementia.

The liver is a large, solid organ located in the upper right portion of the abdomen, beneath the diaphragm and above the stomach. It plays a vital role in several bodily functions, including:

1. Metabolism: The liver helps to metabolize carbohydrates, fats, and proteins from the food we eat into energy and nutrients that our bodies can use.
2. Detoxification: The liver detoxifies harmful substances in the body by breaking them down into less toxic forms or excreting them through bile.
3. Synthesis: The liver synthesizes important proteins, such as albumin and clotting factors, that are necessary for proper bodily function.
4. Storage: The liver stores glucose, vitamins, and minerals that can be released when the body needs them.
5. Bile production: The liver produces bile, a digestive juice that helps to break down fats in the small intestine.
6. Immune function: The liver plays a role in the immune system by filtering out bacteria and other harmful substances from the blood.

Overall, the liver is an essential organ that plays a critical role in maintaining overall health and well-being.

Antioxidants are substances that can prevent or slow damage to cells caused by free radicals, which are unstable molecules that the body produces as a reaction to environmental and other pressures. Antioxidants are able to neutralize free radicals by donating an electron to them, thus stabilizing them and preventing them from causing further damage to the cells.

Antioxidants can be found in a variety of foods, including fruits, vegetables, nuts, and grains. Some common antioxidants include vitamins C and E, beta-carotene, and selenium. Antioxidants are also available as dietary supplements.

In addition to their role in protecting cells from damage, antioxidants have been studied for their potential to prevent or treat a number of health conditions, including cancer, heart disease, and age-related macular degeneration. However, more research is needed to fully understand the potential benefits and risks of using antioxidant supplements.

A kidney, in medical terms, is one of two bean-shaped organs located in the lower back region of the body. They are essential for maintaining homeostasis within the body by performing several crucial functions such as:

1. Regulation of water and electrolyte balance: Kidneys help regulate the amount of water and various electrolytes like sodium, potassium, and calcium in the bloodstream to maintain a stable internal environment.

2. Excretion of waste products: They filter waste products from the blood, including urea (a byproduct of protein metabolism), creatinine (a breakdown product of muscle tissue), and other harmful substances that result from normal cellular functions or external sources like medications and toxins.

3. Endocrine function: Kidneys produce several hormones with important roles in the body, such as erythropoietin (stimulates red blood cell production), renin (regulates blood pressure), and calcitriol (activated form of vitamin D that helps regulate calcium homeostasis).

4. pH balance regulation: Kidneys maintain the proper acid-base balance in the body by excreting either hydrogen ions or bicarbonate ions, depending on whether the blood is too acidic or too alkaline.

5. Blood pressure control: The kidneys play a significant role in regulating blood pressure through the renin-angiotensin-aldosterone system (RAAS), which constricts blood vessels and promotes sodium and water retention to increase blood volume and, consequently, blood pressure.

Anatomically, each kidney is approximately 10-12 cm long, 5-7 cm wide, and 3 cm thick, with a weight of about 120-170 grams. They are surrounded by a protective layer of fat and connected to the urinary system through the renal pelvis, ureters, bladder, and urethra.

Adenosine is a purine nucleoside that is composed of a sugar (ribose) and the base adenine. It plays several important roles in the body, including serving as a precursor for the synthesis of other molecules such as ATP, NAD+, and RNA.

In the medical context, adenosine is perhaps best known for its use as a pharmaceutical agent to treat certain cardiac arrhythmias. When administered intravenously, it can help restore normal sinus rhythm in patients with paroxysmal supraventricular tachycardia (PSVT) by slowing conduction through the atrioventricular node and interrupting the reentry circuit responsible for the arrhythmia.

Adenosine can also be used as a diagnostic tool to help differentiate between narrow-complex tachycardias of supraventricular origin and those that originate from below the ventricles (such as ventricular tachycardia). This is because adenosine will typically terminate PSVT but not affect the rhythm of VT.

It's worth noting that adenosine has a very short half-life, lasting only a few seconds in the bloodstream. This means that its effects are rapidly reversible and generally well-tolerated, although some patients may experience transient symptoms such as flushing, chest pain, or shortness of breath.

Allopurinol is a medication used to treat chronic gout and certain types of kidney stones. It works by reducing the production of uric acid in the body, which is the substance that can cause these conditions when it builds up in high levels. Allopurinol is a xanthine oxidase inhibitor, meaning it blocks an enzyme called xanthine oxidase from converting purines into uric acid. By doing this, allopurinol helps to lower the levels of uric acid in the body and prevent the formation of new kidney stones or gout attacks.

It is important to note that allopurinol can have side effects, including rash, stomach upset, and liver or kidney problems. It may also interact with other medications, so it is essential to inform your healthcare provider of any other drugs you are taking before starting allopurinol. Your healthcare provider will determine the appropriate dosage and monitoring schedule based on your individual needs and medical history.

Tissue Plasminogen Activator (tPA) is a thrombolytic enzyme, which means it dissolves blood clots. It is naturally produced by the endothelial cells that line the interior surface of blood vessels. tPA activates plasminogen, a zymogen, to convert it into plasmin, a protease that breaks down fibrin, the structural protein in blood clots. This enzyme is used medically as a thrombolytic drug under various brand names, such as Activase and Alteplase, to treat conditions like acute ischemic stroke, pulmonary embolism, and deep vein thrombosis by dissolving the clots and restoring blood flow.

Enzyme inhibitors are substances that bind to an enzyme and decrease its activity, preventing it from catalyzing a chemical reaction in the body. They can work by several mechanisms, including blocking the active site where the substrate binds, or binding to another site on the enzyme to change its shape and prevent substrate binding. Enzyme inhibitors are often used as drugs to treat various medical conditions, such as high blood pressure, abnormal heart rhythms, and bacterial infections. They can also be found naturally in some foods and plants, and can be used in research to understand enzyme function and regulation.

Streptokinase is a thrombolytic or clot-busting enzyme produced by certain strains of streptococcus bacteria. It functions by converting plasminogen to plasmin, which then degrades fibrin, a protein that forms the structural framework of blood clots. This activity helps in dissolving blood clots and restoring blood flow in areas obstructed by them. In a medical context, streptokinase is often used as a medication to treat conditions associated with abnormal blood clotting, such as heart attacks, pulmonary embolisms, and deep vein thromboses. However, its use carries the risk of bleeding complications due to excessive fibrinolysis or clot dissolution.

Aspartate aminotransferases (ASTs) are a group of enzymes found in various tissues throughout the body, including the heart, liver, and muscles. They play a crucial role in the metabolic process of transferring amino groups between different molecules.

In medical terms, AST is often used as a blood test to measure the level of this enzyme in the serum. Elevated levels of AST can indicate damage or injury to tissues that contain this enzyme, such as the liver or heart. For example, liver disease, including hepatitis and cirrhosis, can cause elevated AST levels due to damage to liver cells. Similarly, heart attacks can also result in increased AST levels due to damage to heart muscle tissue.

It is important to note that an AST test alone cannot diagnose a specific medical condition, but it can provide valuable information when used in conjunction with other diagnostic tests and clinical evaluation.

Induced hypothermia is a medically controlled lowering of the core body temperature to around 89.6-93.2°F (32-34°C) for therapeutic purposes. It is intentionally induced to reduce the metabolic rate and oxygen demand of organs, thereby offering protection during periods of low blood flow or inadequate oxygenation, such as during cardiac bypass surgery, severe trauma, or after a cardiac arrest. The deliberate induction and maintenance of hypothermia can help minimize tissue damage and improve outcomes in specific clinical scenarios. Once the risk has passed, the body temperature is gradually rewarmed to normal levels under controlled conditions.

Cold ischemia is a medical term that refers to the loss of blood flow and subsequent lack of oxygen delivery to an organ or tissue, which is then cooled and stored in a solution at temperatures between 0-4°C (32-39°F) for the purpose of transplantation. The term "cold" indicates the temperature range, while "ischemia" refers to the lack of blood flow and oxygen delivery to the tissue.

During cold ischemia, the metabolic activity of the organ or tissue slows down significantly, which helps to reduce the rate of cellular damage that would otherwise occur due to the absence of oxygen and nutrients. However, even with cold storage, there is still some degree of injury to the organ or tissue, and this can affect its function after transplantation.

The duration of cold ischemia time is an important factor in determining the success of a transplant procedure. Prolonged cold ischemia times are associated with increased risk of poor organ function and rejection, as well as decreased graft survival rates. Therefore, it is essential to minimize the cold ischemia time as much as possible during organ transplantation to ensure optimal outcomes for the recipient.

Oxygen is a colorless, odorless, tasteless gas that constitutes about 21% of the earth's atmosphere. It is a crucial element for human and most living organisms as it is vital for respiration. Inhaled oxygen enters the lungs and binds to hemoglobin in red blood cells, which carries it to tissues throughout the body where it is used to convert nutrients into energy and carbon dioxide, a waste product that is exhaled.

Medically, supplemental oxygen therapy may be provided to patients with conditions such as chronic obstructive pulmonary disease (COPD), pneumonia, heart failure, or other medical conditions that impair the body's ability to extract sufficient oxygen from the air. Oxygen can be administered through various devices, including nasal cannulas, face masks, and ventilators.

Cerebral infarction, also known as a "stroke" or "brain attack," is the sudden death of brain cells caused by the interruption of their blood supply. It is most commonly caused by a blockage in one of the blood vessels supplying the brain (an ischemic stroke), but can also result from a hemorrhage in or around the brain (a hemorrhagic stroke).

Ischemic strokes occur when a blood clot or other particle blocks a cerebral artery, cutting off blood flow to a part of the brain. The lack of oxygen and nutrients causes nearby brain cells to die. Hemorrhagic strokes occur when a weakened blood vessel ruptures, causing bleeding within or around the brain. This bleeding can put pressure on surrounding brain tissues, leading to cell death.

Symptoms of cerebral infarction depend on the location and extent of the affected brain tissue but may include sudden weakness or numbness in the face, arm, or leg; difficulty speaking or understanding speech; vision problems; loss of balance or coordination; and severe headache with no known cause. Immediate medical attention is crucial for proper diagnosis and treatment to minimize potential long-term damage or disability.

Alanine transaminase (ALT) is a type of enzyme found primarily in the cells of the liver and, to a lesser extent, in the cells of other tissues such as the heart, muscles, and kidneys. Its primary function is to catalyze the reversible transfer of an amino group from alanine to another alpha-keto acid, usually pyruvate, to form pyruvate and another amino acid, usually glutamate. This process is known as the transamination reaction.

When liver cells are damaged or destroyed due to various reasons such as hepatitis, alcohol abuse, nonalcoholic fatty liver disease, or drug-induced liver injury, ALT is released into the bloodstream. Therefore, measuring the level of ALT in the blood is a useful diagnostic tool for evaluating liver function and detecting liver damage. Normal ALT levels vary depending on the laboratory, but typically range from 7 to 56 units per liter (U/L) for men and 6 to 45 U/L for women. Elevated ALT levels may indicate liver injury or disease, although other factors such as muscle damage or heart disease can also cause elevations in ALT.

  • Worldwide morbidity and mortality from acute myocardial infarction (AMI) and related heart failure remain high. (hindawi.com)
  • Among clinical emergency events, ST-segment elevation (STE) or the non-STE electrocardiogram diagnosis of acute myocardial infarction (AMI) is particularly common worldwide, with a staggering number of annual first episodes as well as recurrent ones [ 1 ]. (hindawi.com)
  • Paris, France - Aug. 30, 2011: Primary PCI is the best reperfusion therapy for patients presenting with acute ST-elevation myocardial infarction. (escardio.org)
  • A survey from 2007/8 showed that only 40% of European patients with ST-elevation myocardial infarction are treated with primary PCI. (escardio.org)
  • OPTIMAL REPERFUSION IN STEMI (presentation on Stent for Life and abstract 83408: CJ Terkelsen et al, Primary percutaneous coronary intervention as a national reperfusion strategy in patients with ST-elevation myocardial infarction: eleven years of experience from the Western Denmark Heart Registry. (escardio.org)
  • Segment-Elevation Myocardial Infarction," published in the February 1, 2019, issue of the American Journal of Cardiology. (cdc.gov)
  • management of ST-segment-elevation myocardial infarction (STEMI) patients, and primary percutaneous coronary intervention (PCI) is the preferred reperfusion therapy when first-medical-contact-to-balloon time is within 90 minutes for patients admitted directly to a PCI-capable hospital and 2 hours for patients transferred to a PCI-capable hospital. (cdc.gov)
  • Pre-hospital transport times and outcomes after different reperfusion strategies for ST-elevation myocardial infarction. (cdc.gov)
  • Patients' data for the study were obtained from the EARLY-MYO-CMR (Early Assessment of Myocardial Tissue Characteristics by CMR in STEMI) registry, which was a prospective, multicenter registry of patients with ST-segment elevation myocardial infarction (STEMI) who underwent cardiac magnetic resonance (CMR) imaging after reperfusion therapy. (physiciansweekly.com)
  • A recent study discovered that shift employment causes myocardial infarction reperfusion damage. (physiciansweekly.com)
  • GRh2 reduced the area of myocardial infarction and the histological changes in the myocardium and improved cardiac functions. (spandidos-publications.com)
  • Despite improvements in revascularization after a myocardial infarction, coronary disease remains a major contributor to global mortality. (ku.dk)
  • The treatment strategy in acute myocardial infarction (AMI) has changed substantially in recent decades. (revespcardiol.org)
  • Background: Up to 40% of patients with ST-segment elevation myocardial infarction (STEMI) present later than 12 hours after symptom onset. (lu.se)
  • Following myocardial infarction (MI), elderly patients have a poorer prognosis than younger patients, which may be linked to increased coronary microvessel susceptibility to injury. (jci.org)
  • Background Suboptimal myocardial reperfusion is common in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). (jgc301.com)
  • Outcomes of interest were thrombolysis in myocardial infarction myocardial perfusion grade (TMPG), infarct size (IS) assessed by cardiac magnetic resonance imaging, left ventricular ejection fraction (LVEF), major adverse cardiac events (MACE) at short-term (≤ 1 month) and long-term (6?12 months) follow-up, and bleeding complications during the hospital stay. (jgc301.com)
  • Inhibitors of free fatty acid metabolism have been shown experimentally to decrease the size of myocardial infarction and lessen postischemic cardiac dysfunction in animal models of regional and global ischemia. (elsevierpure.com)
  • A diagnosis of myocardial infarction is created by integrating the history of the presenting illness and physical examination with electrocardiogram findings and cardiac markers (blood tests for heart muscle cell damage). (wikipedia.org)
  • At autopsy, a pathologist can diagnose a myocardial infarction based on anatomopathological findings. (wikipedia.org)
  • New regional wall motion abnormalities on an echocardiogram are also suggestive of a myocardial infarction. (wikipedia.org)
  • In particular, acute myocardial infarction in the distribution of the circumflex artery is likely to produce a nondiagnostic ECG. (wikipedia.org)
  • The use of additional ECG leads like right-sided leads V3R and V4R and posterior leads V7, V8, and V9 may improve sensitivity for right ventricular and posterior myocardial infarction. (wikipedia.org)
  • A normal ECG does not rule out acute myocardial infarction. (wikipedia.org)
  • It should be determined if a person is at high risk for myocardial infarction before conducting imaging tests to make a diagnosis. (wikipedia.org)
  • Myocardial infarction (MI) denotes the death of cardiac myocytes due to extended ischemia. (aku.edu)
  • Hashmi, S & Al-Salam, S 2015, ' Acute myocardial infarction and myocardial ischemia-reperfusion injury: A comparison ', International Journal of Clinical and Experimental Pathology , vol. 8, no. 8, pp. 8786-8796. (uaeu.ac.ae)
  • [ 2 ] In 1958, streptokinase was first used in patients with acute myocardial infarction (AMI), and this changed the focus of treatment. (medscape.com)
  • Twenty-one patients with acute myocardial infarction received only heparin and aspirin. (elsevierpure.com)
  • Spontaneous reperfusion of the IRA occurs frequently in patients with acute myocardial infarction and is associated with significant myocardial salvage. (elsevierpure.com)
  • Platelets play a crucial role in ischemic diseases, which can lead to myocardial infarction (MI), the most leading cause of death in Western countries. (isth.org)
  • In the acute phase of myocardial infarction (AMI) in patients antiplatelet intervention inhibits inflammatory cell recruitment into the infarcted myocardium. (isth.org)
  • Thrombocytopenia in mice leads to reduced infarct size and an improved left ventricular function 24 hours and 21 days after myocardial infarction. (isth.org)
  • Our results show that platelets modulate inflammation and cell-survival after myocardial infarction indicating platelet interaction with inflammatory and endothelial cells and migration into the infarcted border zone to induce cell apoptosis of cardiomyocytes and / or inflammatory leukocyte. (isth.org)
  • Long-Term Prognosis of Different Reperfusion Strategies for ST-Segment Elevation Myocardial Infarction in Chinese County-Level Hospitals: Insight from China Acute Myocardial Infarction Registry. (bvsalud.org)
  • To evaluate the long-term prognosis of patients with ST-segment elevation myocardial infarction ( STEMI ) treated with different reperfusion strategies in Chinese county-level hospitals . (bvsalud.org)
  • A total of 2,514 patients with STEMI from 32 hospitals participated in the China Acute Myocardial Infarction registry between January 2013 and September 2014. (bvsalud.org)
  • AIM: Prompt access to cardiac defibrillation and reperfusion therapy improves outcomes in patients with ST-segment elevation myocardial infarction (STEMI). (ox.ac.uk)
  • The study aim was to describe the 'patient' and 'system' delay in patients who receive acute reperfusion therapy for ST-elevation myocardial infarction (STEMI) in New Zealand. (ox.ac.uk)
  • Diabetes mellitus is strongly associated with increased cardiovascular morbidity and mortality in patients with ST-segment elevation myocardial infarction. (elsevierpure.com)
  • We compared myocardial perfusion and infarct sizes between diabetic and nondiabetic patients undergoing PCI for acute ST-segment elevation myocardial infarction in the EMERALD trial. (elsevierpure.com)
  • EMERALD was a prospective, randomized, multicenter study evaluating distal embolic protection during primary PCI in ST-segment elevation myocardial infarction. (elsevierpure.com)
  • In conclusion, in patients with ST-segment elevation myocardial infarction undergoing primary PCI, diabetes is independently associated with decreased myocardial reperfusion, larger infarct, development of congestive heart failure, and decreased survival. (elsevierpure.com)
  • Comparison of Myocardial Reperfusion in Patients With Fasting Blood Glucose 125 mg/dl and ST-Elevation Myocardial Infarction With Percutaneous Coronary Intervention. (wustl.edu)
  • 125 mg/dl and ST-Elevation Myocardial Infarction With Percutaneous Coronary Intervention. (wustl.edu)
  • Diabetes and impaired fasting glucose (FG) were associated with worse outcomes in patients with acute myocardial infarction (MI). (wustl.edu)
  • Acute myocardial infarction (MI) is a global issue with high incidence and mortality. (edu.iq)
  • Rapid recovery of the blocked coronary flow represents the most effective strategy to reduce the size of myocardial infarction and improve the cardiac function. (edu.iq)
  • Background The circadian clock influences a number of cardiovascular (patho)physiological processes including the incidence of acute myocardial infarction. (bmj.com)
  • Objective To determine the impact of time-of-day onset of ST segment elevation myocardial infarction (STEMI) on infarct size. (bmj.com)
  • The study aims to examine the effects of coenzyme Q10, (a bioenergetic antioxidant), on the indexes of left ventricular remodeling, oxidative damage, and angiotensin-converting enzyme (ACE) level after acute myocardial infarction (AMI) with left ventricular dysfunction. (mdpi.com)
  • Acute myocardial infarction is myocardial necrosis resulting from acute obstruction of a coronary artery. (msdmanuals.com)
  • For non-ST-segment-elevation myocardial infarction, reperfusion is via percutaneous intervention or coronary artery bypass graft surgery. (msdmanuals.com)
  • Acute MI includes both non-ST-segment-elevation myocardial infarction (NSTEMI) and ST-segment-elevation myocardial infarction (STEMI). (msdmanuals.com)
  • Pathophysiology references Acute myocardial infarction is myocardial necrosis resulting from acute obstruction of a coronary artery. (msdmanuals.com)
  • ABSTRACT This cross-sectional study aimed to assess interpretation of symptoms as a cause of delays in patients with acute myocardial infarction (AMI). (who.int)
  • Myocardial infarction (MI) due to coronary artery disease is a leading cause of death in the United States, where more than 1 million people have acute myocardial infarctions (AMIs) each year. (medscape.com)
  • Apical 4-chamber views show a breach in the interventricular septum and free communication between ventricles through a large apical septum ventricular septal defect in a patient who recently had an anterior myocardial infarction. (medscape.com)
  • For other discussions on myocardial infarction, see Myocardial Infarction, Right Ventricular Infarction, Imaging of Acute Myocardial Infarcts, and Use of Cardiac Markers in the Emergency Department. (medscape.com)
  • About 90% of patients who have an acute myocardial infarction (AMI) develop some form of cardiac arrhythmia during or immediately after the event. (medscape.com)
  • The incidence of arrhythmia is higher with an ST-elevation myocardial infarction (STEMI) and lower with a non-ST-elevation myocardial infarction (NSTEMI). (medscape.com)
  • Patient delay' is the time from symptom onset to first medical contact (FMC), and 'system delay' the time from FMC until reperfusion therapy (primary percutaneous coronary intervention (PCI) or fibrinolysis). (ox.ac.uk)
  • It is unknown whether myocardial perfusion is decreased in diabetic compared with nondiabetic patients after primary percutaneous coronary intervention (PCI), which may contribute to their worse prognosis. (elsevierpure.com)
  • Thus, acidified NaNO2 exerts a significant protective action during ischemia and reperfusion injury, which suggests that endothelium-derived relaxing factor has a cardioprotective effect in MI. (aspetjournals.org)
  • Wild‐type C57BL/6J mice (male, 8-10 weeks old) were used and murine myocardial ischemia and reperfusion injury (IRI) model was conducted, cardiac function was evaluated by echocardiography. (edu.iq)
  • Since PCI can be administered only at PCI-capable hospitals, geographic factors may affect the choice of reperfusion therapy for STEMI patients. (cdc.gov)
  • PCI access site bleeding was the reperfusion strategy for STEMI patients. (cdc.gov)
  • Conclusions Our findings showed that compared with AT alone, combined AT and intracoronary GPI treatment resulted in improved myocardial reperfusion, better cardiac function, and MACE-free survival benefits at the long-term follow-up for patients with STEMI undergoing PPCI. (jgc301.com)
  • Manipulation of myocardial fatty acid metabolism may prove beneficial in the treatment of myocardial ischemia, particularly during situations of controlled ischemia and reperfusion, such as percutaneous transluminal coronary angioplasty and coronary artery bypass grafting. (elsevierpure.com)
  • The advent of coronary care units and early reperfusion therapy (lytic or percutaneous coronary intervention) has substantially decreased in-hospital mortality rates and has improved the outcome in survivors of the acute phase of MI. (medscape.com)
  • This coupled comorbidity of pathological ischemia and therapeutic reinjury of infarcted myocardium, namely, myocardial ischemia-reperfusion injury (MIRI), is particularly refractory to treatment [ 4 , 5 ]. (hindawi.com)
  • However, whether GRh2 has a protective effect on ischaemia/reperfusion (I/R) in the myocardium has yet to be elucidated. (spandidos-publications.com)
  • Reperfusion has the potential to salvage ischemic myocardium but paradoxically can cause injury, a phenomenon called as 'reperfusion injury' (IR). (aku.edu)
  • In rats and pigs, BSPC@HM NCs remarkably downregulates Sav1 in IR-injured myocardium, promotes myocardium regeneration, suppresses myocardial apoptosis, and recovers cardiac functions. (scimage.cn)
  • Ventricular dysrhythmias induced by coronary occlusion alone (without reperfusion) were attenuated markedly by alpha-receptor blockade under conditions in which perfusion (measured with radiolabeled microspheres) within ischemic zones was not affected. (jci.org)
  • Imaging tests such as stress radionuclide myocardial perfusion imaging or stress echocardiography can confirm a diagnosis when a person's history, physical exam, ECG and cardiac biomarkers suggest the likelihood of a problem. (wikipedia.org)
  • Diabetic patients had impaired myocardial perfusion after PCI as measured by myocardial blush grade 0/1 (34% vs 16%, p = 0.002) and lower rates of complete 30-minute STR (45% vs 65%, p = 0.005). (elsevierpure.com)
  • The pathophysiological nature of MIRI is the short-term disturbance of myocardial energy and metabolism caused by reflow after ischemia and hypoxia in the coronary artery and the dynamic changes in apoptosis and the prosurvival signaling pathways in response to related injury factors. (hindawi.com)
  • Dexmedetomidine pretreatment can obviously relieve myocardial ischemia-reperfusion injury and cardiomyocyte apoptosis in rats probably by activating the Janus kinase 2/signal transducers and activators of transcription 3 signaling pathway. (ijpsonline.com)
  • Myocardial I/R injury may induce cell apoptosis and autophagy by activating oxidative stress and upregulating inflammatory mediators, ultimately resulting in irreversible fibrotic damage ( 3 ). (spandidos-publications.com)
  • In conclusion, myocardial damage in MI is mainly due to ischemic necrosis and inflammatory mechanisms while apoptosis is the main mechanism of cell death in IR in addition to limited ischemic necrosis. (aku.edu)
  • H(2) saline treatment attenuated I/R-induced cardiac cell apoptosis, presenting as significant improvement of heart function parameters 24h after reperfusion, including left ventricular systolic pressure (LVSP), left ventricular diastolic pressure (LVEDP), +(dP/dt)max and -(dP/dt)max. (molecularhydrogenstudies.com)
  • Also, curcumin reduces cell apoptosis induced by myocardial IRI, curcumin reduces cell apoptosis induced by myocardial IRI and activates the Nrf-2/HO-1 signaling pathway during myocardial. (edu.iq)
  • Oral dosing of rats with SCN-, before acute ischemia-reperfusion injury (30 min occlusion, 24 h or 4 week recovery), significantly reduced the infarct size as a percentage of the total reperfused area (54% versus 74%), and increased the salvageable area (46% versus 26%) as determined by MRI imaging. (ku.dk)
  • We show that Bbeta(15-42) robustly and reproducibly reduced infarct size in all models of ischemia-reperfusion. (bris.ac.uk)
  • End points included final myocardial blush grade, complete ST-segment resolution (STR) 30 minutes after PCI, and final infarct size as determined by technetium-99m single proton emission computed tomography measured between days 5 and 14. (elsevierpure.com)
  • Modelling myocardial ischaemia and reperfusion. (ox.ac.uk)
  • The model is sufficiently complete to simulate calcium-overload arrhythmias during ischaemia and reperfusion-induced arrhythmias. (ox.ac.uk)
  • In summary, we have developed a biochemically and biophysically detailed model that provides a novel approach to studying myocardial ischaemia and reperfusion. (ox.ac.uk)
  • British Library EThOS: Aspects of ischaemia and reperfusion injury in the isolated rat heart. (bl.uk)
  • We performed a meta-analysis to evaluate the role of aspiration thrombectomy (AT) combined with intracoronary administration of glycoprotein IIb/IIIa inhibitors (GPI) in the improvement of myocardial reperfusion and clinical outcomes. (jgc301.com)
  • abstract = "Many compounds have been shown to prevent reperfusion injury in various animal models, although to date, translation into clinic has revealed several obstacles. (bris.ac.uk)
  • Klier M, Ayhan A, Dannenberg L, Gorressen S, Polzin A, Elvers M. Role of Platelets in Processes of Myocardial Healing After Myocardial Ischemia and Reperfusion in Mice [abstract]. (isth.org)
  • siRNA-mediated management of myocardial ischemia reperfusion (IR) injury is greatly hampered by the inefficient myocardial enrichment and cardiomyocyte transfection. (scimage.cn)
  • This case shows that potentially lethal arrhythmias can arise during reperfusion and that ventricular fibrillation during reperfusion may be self-terminating. (bmj.com)
  • We previously demonstrated that chronic pretreatment with a thiazolidinedione peroxisome proliferator-activated receptor (PPAR)-γ activator, troglitazone, improves recovery of left ventricular (LV) function and substrate metabolism after ischemia and reperfusion, without causing arrhythmias. (diabetesjournals.org)
  • The clinician must be aware of these arrhythmias, in addition to reperfusion strategies, and must treat those that require intervention to avoid exacerbation of ischemia and subsequent hemodynamic compromise. (medscape.com)
  • However, those that result in hypotension, increase myocardial oxygen requirements, and/or predispose the patient to develop additional malignant ventricular arrhythmias should be aggressively monitored and treated. (medscape.com)
  • citation needed] The 12 lead ECG is used to classify patients into one of three groups: those with ST segment elevation or new bundle branch block (suspicious for acute injury and a possible candidate for acute reperfusion therapy with thrombolytics or primary PCI), those with ST segment depression or T wave inversion (suspicious for ischemia), and those with a so-called non-diagnostic or normal ECG. (wikipedia.org)
  • METHODS: In 2015-17, 3,857 patients who received acute reperfusion therapy were captured in the All New Zealand Acute Coronary Syndrome Quality Improvement (ANZACS-QI) registry. (ox.ac.uk)
  • In conclusion, the present study confirmed that GRh2 could reduce oxidative stress and inflammation in cardiomyocytes after reperfusion, and its mechanism of action may be related to its regulation of the Nrf2/HO‑1/NLRP3 signalling pathway. (spandidos-publications.com)
  • Meng X, Zhang L, Han B and Zhang Z: PHLDA3 inhibition protects against myocardial ischemia/reperfusion injury by alleviating oxidative stress and inflammatory response via the Akt/Nrf2 axis. (spandidos-publications.com)
  • The findings of the present study indicated that inhibition of miR‑132 may ameliorate myocardial I/R injury by inhibiting oxidative stress and pyroptosis through activation of PGC‑1α/Nrf2 signalling by targeting SIRT1. (spandidos-publications.com)
  • It has been reported that SIRT1/peroxisome proliferator-activated receptor gamma coactivator (PGC)-1α/nuclear factor erythroid-2-related factor 2 (Nrf2) signalling can mediate oxidative stress, which plays an important role in myocardial I/R injury ( 14 , 15 ). (spandidos-publications.com)
  • The proposed mechanisms of the detrimental effects of free fatty acids include: (1) accumulation of toxic intermediates of fatty acid metabolism, such as long chain acyl-CoA thioesters and long chain acylcarnitines, (2) inhibition of glucose utilization, particularly glycolysis, during ischemia and/or reperfusion, and (3) uncoupling of oxidative metabolism from electron transfer. (elsevierpure.com)
  • The resulted data showed that curcumin alleviates myocardial inflammatory responses and oxidative stress during myocardial IRI. (edu.iq)
  • Alpha receptor blockade with either phentolamine or prazosin significantly reduced the number of premature ventricular complexes during coronary reperfusion (321 +/- 62-14 +/- 10 premature ventricular complexes, P less than 0.001), abolished early ventricular fibrillation (from 25% in controls to 0%), and prevented the increase in idioventricular rate seen with coronary reperfusion. (jci.org)
  • A patient in whom self-terminating ventricular fibrillation was a manifestation of myocardial reperfusion. (bmj.com)
  • Reperfusion was thought to be responsible for the ventricular fibrillation because the arrhythmia started while the ST segment was returning to the baseline during an episode of silent ischaemia that was probably caused by coronary spasm. (bmj.com)
  • Acute treatment with troglitazone increases susceptibility to ventricular fibrillation during myocardial ischemia and reperfusion. (diabetesjournals.org)
  • The aim of the study is to investigate the effects of curcumin in attenuates myocardial ischemia and reperfusion-induced proinflammatory response through activation of the Nrf-2/HO-1 signaling pathway. (edu.iq)
  • Inconclusion, this study demonstrates that curcumin attenuates myocardial IRI by inhibiting proinflammatory cytokines through a mechanism that may be related to activation of the Nrf-2/HO-1 signaling pathway. (edu.iq)
  • To evaluate the effects of dexmedetomidine on myocardial ischemia-reperfusion injury in rats and its anti-apoptotic role, as well as the mechanism by which it regulates Janus kinase 2/signal transducers and activators of transcription 3 signal. (ijpsonline.com)
  • Hypercholesterolemia causes endothelial and myocardial dysfunction, as well as aggravates ischemia/reperfusion (I/R)-induced myocardial injury. (nih.gov)
  • This study sought to determine the prevalence of spontaneous reperfusion of an infarct-related artery (IRA) and associated myocardial salvage in the absence of thrombolysis or angioplasty. (elsevierpure.com)
  • however, myocardial salvage (9% ± 9% vs -2% ± 7% left ventricle, p = 0.01), and salvage index (0.62 ± 0.37 vs 0.19 ± 0.33, p = 0.01) were greater in patients with spontaneous reperfusion. (elsevierpure.com)
  • In conclusion, increased FG and previously diagnosed DM were associated with less spontaneous reperfusion and less myocardial reperfusion after PPCI, resulting in worse clinical outcomes. (wustl.edu)
  • While effective early reperfusion of the criminal coronary artery after a confirmed AMI is the typical treatment at present, collateral myocardial ischemia-reperfusion injury (MIRI) and pertinent cardioprotection are still challenging to address and have inadequately understood mechanisms. (hindawi.com)
  • Heusch G: Myocardial ischaemia-reperfusion injury and cardioprotection in perspective. (spandidos-publications.com)
  • Cardioprotective effects of acidified sodium nitrite in myocardial ischemia with reperfusion. (aspetjournals.org)
  • In rodents, Bbeta(15-42) inhibits proinflammatory cytokine release and is cardioprotective during ischemia-reperfusion injury. (bris.ac.uk)
  • To study the potential of myocardial contrast echocardiography (MCE) to assess serial changes of microvascular flow during ischemia-reperfusion. (uniroma1.it)
  • Sun W, Wang Z, Sun M, Huang W and Wang Y and Wang Y: Aloin antagonizes stimulated ischemia/reperfusion-induced damage and inflammatory response in cardiomyocytes by activating the Nrf2/HO-1 defense pathway. (spandidos-publications.com)
  • Abouzaki NA, Christopher S, Trankle C, Van Tassell BW, Carbone S, Mauro AG, Buckley L, Toldo S and Abbate A: Inhibiting the inflammatory injury after myocardial ischemia reperfusion with plasma-derived Alpha-1 Antitrypsin: A post hoc analysis of the VCU-α1RT study. (spandidos-publications.com)
  • Commercial kits were used to measure the levels of serum myocardial enzymes and inflammatory factors. (spandidos-publications.com)
  • Apparent histologic injury and elevated levels of serum myocardial enzymes and inflammatory factors were observed in the myocardial I/R model. (spandidos-publications.com)
  • The aim of this study was to study the possible anti-inflammatory effect of hydrogen-rich saline (H(2) saline) on rat hearts with regional myocardial ischemia and reperfusion (I/R). Sixty-six rats were equally randomized to three groups: sham-operated group, I/R group (control group) and I/R plus H(2) saline treatment group. (molecularhydrogenstudies.com)
  • H(2) saline has an anti-inflammatory effect on rat hearts with regional myocardial I/R. (molecularhydrogenstudies.com)
  • Zhang Y, Sun Q, He B, Xiao J, Wang Z, Sun X. Anti-inflammatory effect of hydrogen-rich saline in a rat model of regional myocardial ischemia and reperfusion. (molecularhydrogenstudies.com)
  • For a study, researchers sought to determine the effect of shift work on reperfusion damage, which is a significant driver of clinical outcomes in AMI. (physiciansweekly.com)
  • 125 mg/dl or previously diagnosed diabetes mellitus (DM) and studied for electrocardiographic signs of myocardial reperfusion (both spontaneous and after PPCI) and clinical outcomes. (wustl.edu)
  • However, while myocardial reperfusion is well established, the process itself can trigger myocardial reperfusion injury by causing further cardiomyocyte death through multiple pathophysiological mechanisms [ 3 - 5 ]. (hindawi.com)
  • Conceptual diagram of the development and unknown mechanisms of myocardial ischemia-reperfusion injury. (hindawi.com)
  • The present study aimed to investigate the roles of miR‑132 in myocardial ischaemia/reperfusion (I/R) injury and the underlying mechanisms. (spandidos-publications.com)
  • However, despite numerous studies on myocardial I/R injury, deeper insight into the underlying mechanisms of myocardial I/R injury is needed. (spandidos-publications.com)
  • However, few studies have focused on the role of miR-132 in myocardial I/R injury and the underlying mechanisms. (spandidos-publications.com)
  • For patients outside the recommended time frame for PCI, reperfusion strategy includes pharmacoinvasive therapy with fibrinolysis, followed by either rescue PCI or routine early PCI. (cdc.gov)
  • Serum levels of free fatty acids frequently are elevated in patients with myocardial ischemia. (elsevierpure.com)
  • Results: Patients with a QRS score more than 4 had significantly worse EF, longer time to admission, fewer patients without ST-segment resolution, higher WMSI, fewer patients with myocardial blush grade (MBG) 3, more patients with MBG 1, and more patients with three-vessel disease than patients with a QRS score less than 4. (ekb.eg)
  • In the US, about 1.0 million myocardial infarctions occur annually. (msdmanuals.com)
  • Supplementation also decreased antibody recognition of HOCl-damaged myocardial proteins. (ku.dk)
  • Cardiac markers or cardiac enzymes are proteins that leak out of injured myocardial cells through their damaged cell membranes into the bloodstream. (wikipedia.org)
  • This approach has potential application in the evaluation and management of postischemic reperfusion in humans. (uniroma1.it)
  • This study reports a bioinspired strategy to overcome the multiple systemic barriers against myocardial siRNA delivery, and holds profound potential for gene therapy against cardiac injuries. (scimage.cn)
  • The left anterior descending coronary artery was ligated to construct the model of myocardial ischemia-reperfusion. (ijpsonline.com)
  • The effects of acidified sodium nitrite (NaNO2) which releases nitric oxide, a substance which is thought to be indistinguishable from endothelium-derived relaxing factor, were investigated in a 6-h model of myocardial ischemia (MI) with reperfusion in open-chest, anesthetized cats. (aspetjournals.org)
  • A rat model of myocardial I/R injury was constructed by ligating the left anterior descending coronary artery, which was subsequently treated with GRh2. (spandidos-publications.com)
  • Intracoronary methoxamine (0.1 microM) in animals depleted of myocardial catecholamines by 6-hydroxydopamine pretreatment did not affect idioventricular rate before coronary occlusion. (jci.org)
  • It also decreased neutrophil infiltration, 3-nitrotyrosine level, expression of intercellular adhesion molecule 1(ICAM-1) and myeloperoxidase (MPO) activity in the area at risk zones (AAR) of rat hearts subjected to regional myocardial I/R, and attenuated the increase of I/R induced proinflammatory cytokine tumor necrosis factor-α (TNF-a) and interleukin-1β (IL-1b) levels in the AAR. (molecularhydrogenstudies.com)
  • Alternative sympatholytic interventions including pretreatment with 6-hydroxydopamine to deplete myocardial norepinephrine from 8.8 +/- 1.4 to 0.83 +/- 0.2 ng/mg protein and render the heart unresponsive to tyramine (120 microgram/kg) attenuated dysrhythmias induced by both coronary occlusion and reperfusion in a fashion identical to that seen with alpha-receptor blockade. (jci.org)

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