Brain Ischemia: 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.Ischemia: 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.Myocardial Ischemia: 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).Reperfusion: 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.Ischemic Attack, Transient: 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)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.Gerbillinae: A subfamily of the Muridae consisting of several genera including Gerbillus, Rhombomys, Tatera, Meriones, and Psammomys.Brain: The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.Neuroprotective Agents: 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.Infarction, Middle Cerebral Artery: 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.Brain Chemistry: Changes in the amounts of various chemicals (neurotransmitters, receptors, enzymes, and other metabolites) specific to the area of the central nervous system contained within the head. These are monitored over time, during sensory stimulation, or under different disease states.Brain Infarction: Tissue NECROSIS in any area of the brain, including the CEREBRAL HEMISPHERES, the CEREBELLUM, and the BRAIN STEM. Brain infarction is the result of a cascade of events initiated by inadequate blood flow through the brain that is followed by HYPOXIA and HYPOGLYCEMIA in brain tissue. Damage may be temporary, permanent, selective or pan-necrosis.Brain Injuries: Acute and chronic (see also BRAIN INJURIES, CHRONIC) injuries to the brain, including the cerebral hemispheres, CEREBELLUM, and BRAIN STEM. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with DIFFUSE AXONAL INJURY or COMA, POST-TRAUMATIC. Localized injuries may be associated with NEUROBEHAVIORAL MANIFESTATIONS; HEMIPARESIS, or other focal neurologic deficits.Brain Edema: Increased intracellular or extracellular fluid in brain tissue. Cytotoxic brain edema (swelling due to increased intracellular fluid) is indicative of a disturbance in cell metabolism, and is commonly associated with hypoxic or ischemic injuries (see HYPOXIA, BRAIN). An increase in extracellular fluid may be caused by increased brain capillary permeability (vasogenic edema), an osmotic gradient, local blockages in interstitial fluid pathways, or by obstruction of CSF flow (e.g., obstructive HYDROCEPHALUS). (From Childs Nerv Syst 1992 Sep; 8(6):301-6)Rats, Sprague-Dawley: 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.Ischemic Preconditioning: 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)Disease Models, Animal: 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.Cerebrovascular Circulation: The circulation of blood through the BLOOD VESSELS of the BRAIN.Rats, Wistar: A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.Cerebral Infarction: 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).Cerebral Cortex: The thin layer of GRAY MATTER on the surface of the CEREBRAL HEMISPHERES that develops from the TELENCEPHALON and folds into gyri and sulchi. It reaches its highest development in humans and is responsible for intellectual faculties and higher mental functions.Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Brain Neoplasms: Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain.Hippocampus: A curved elevation of GRAY MATTER extending the entire length of the floor of the TEMPORAL HORN of the LATERAL VENTRICLE (see also TEMPORAL LOBE). The hippocampus proper, subiculum, and DENTATE GYRUS constitute the hippocampal formation. Sometimes authors include the ENTORHINAL CORTEX in the hippocampal formation.Hypoxia-Ischemia, Brain: A disorder characterized by a reduction of oxygen in the blood combined with reduced blood flow (ISCHEMIA) to the brain from a localized obstruction of a cerebral artery or from systemic hypoperfusion. Prolonged hypoxia-ischemia is associated with ISCHEMIC ATTACK, TRANSIENT; BRAIN INFARCTION; BRAIN EDEMA; COMA; and other conditions.Middle Cerebral Artery: The largest of the cerebral arteries. It trifurcates into temporal, frontal, and parietal branches supplying blood to most of the parenchyma of these lobes in the CEREBRAL CORTEX. These are the areas involved in motor, sensory, and speech activities.Menispermum: A plant genus of the family MENISPERMACEAE. Members contain dauricine and other ALKALOIDS.Brain Mapping: Imaging techniques used to colocalize sites of brain functions or physiological activity with brain structures.Hypoxia, Brain: A reduction in brain oxygen supply due to ANOXEMIA (a reduced amount of oxygen being carried in the blood by HEMOGLOBIN), or to a restriction of the blood supply to the brain, or both. Severe hypoxia is referred to as anoxia, and is a relatively common cause of injury to the central nervous system. Prolonged brain anoxia may lead to BRAIN DEATH or a PERSISTENT VEGETATIVE STATE. Histologically, this condition is characterized by neuronal loss which is most prominent in the HIPPOCAMPUS; GLOBUS PALLIDUS; CEREBELLUM; and inferior olives.Hypothermia, Induced: 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.Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.Blood-Brain Barrier: Specialized non-fenestrated tightly-joined ENDOTHELIAL CELLS with TIGHT JUNCTIONS that form a transport barrier for certain substances between the cerebral capillaries and the BRAIN tissue.Magnetic Resonance Imaging: Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques.Stroke: A group of pathological conditions characterized by sudden, non-convulsive loss of neurological function due to BRAIN ISCHEMIA or INTRACRANIAL HEMORRHAGES. Stroke is classified by the type of tissue NECROSIS, such as the anatomic location, vasculature involved, etiology, age of the affected individual, and hemorrhagic vs. non-hemorrhagic nature. (From Adams et al., Principles of Neurology, 6th ed, pp777-810)Myocardial Reperfusion Injury: Damage to the MYOCARDIUM resulting from MYOCARDIAL REPERFUSION (restoration of blood flow to ischemic areas of the HEART.) Reperfusion takes place when there is spontaneous thrombolysis, THROMBOLYTIC THERAPY, collateral flow from other coronary vascular beds, or reversal of vasospasm.Mongolia: The country is bordered by RUSSIA on the north and CHINA on the west, south, and east. The capita is Ulaanbaatar.Recovery of Function: A partial or complete return to the normal or proper physiologic activity of an organ or part following disease or trauma.Warm Ischemia: 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.Arterial Occlusive Diseases: Pathological processes which result in the partial or complete obstruction of ARTERIES. They are characterized by greatly reduced or absence of blood flow through these vessels. They are also known as arterial insufficiency.Astrocytes: A class of large neuroglial (macroglial) cells in the central nervous system - the largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the BLOOD-BRAIN BARRIER. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with MICROGLIA) respond to injury.Mice, Inbred C57BLPhenazocine: An opioid analgesic with actions and uses similar to MORPHINE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1095)Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid is the most common excitatory neurotransmitter in the CENTRAL NERVOUS SYSTEM.Cerebral Arteries: The arterial blood vessels supplying the CEREBRUM.Cerebrovascular Disorders: A spectrum of pathological conditions of impaired blood flow in the brain. They can involve vessels (ARTERIES or VEINS) in the CEREBRUM, the CEREBELLUM, and the BRAIN STEM. Major categories include INTRACRANIAL ARTERIOVENOUS MALFORMATIONS; BRAIN ISCHEMIA; CEREBRAL HEMORRHAGE; and others.Oxygen: 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.Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.Rats, Inbred Strains: Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.Brain Stem: The part of the brain that connects the CEREBRAL HEMISPHERES with the SPINAL CORD. It consists of the MESENCEPHALON; PONS; and MEDULLA OBLONGATA.Nerve Tissue ProteinsCorpus Striatum: Striped GRAY MATTER and WHITE MATTER consisting of the NEOSTRIATUM and paleostriatum (GLOBUS PALLIDUS). It is located in front of and lateral to the THALAMUS in each cerebral hemisphere. The gray substance is made up of the CAUDATE NUCLEUS and the lentiform nucleus (the latter consisting of the GLOBUS PALLIDUS and PUTAMEN). The WHITE MATTER is the INTERNAL CAPSULE.Rats, Inbred SHR: A strain of Rattus norvegicus with elevated blood pressure used as a model for studying hypertension and stroke.Phosphotungstic Acid: Tungsten hydroxide oxide phosphate. A white or slightly yellowish-green, slightly efflorescent crystal or crystalline powder. It is used as a reagent for alkaloids and many other nitrogen bases, for phenols, albumin, peptone, amino acids, uric acid, urea, blood, and carbohydrates. (From Merck Index, 11th ed)Analysis of Variance: A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.Cold Ischemia: 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.Necrosis: 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.Thiocarbamates: Carbamates in which the -CO- group has been replaced by a -CS- group.Cell Hypoxia: A condition of decreased oxygen content at the cellular level.Nerve Degeneration: Loss of functional activity and trophic degeneration of nerve axons and their terminal arborizations following the destruction of their cells of origin or interruption of their continuity with these cells. The pathology is characteristic of neurodegenerative diseases. Often the process of nerve degeneration is studied in research on neuroanatomical localization and correlation of the neurophysiology of neural pathways.Glial Fibrillary Acidic Protein: An intermediate filament protein found only in glial cells or cells of glial origin. MW 51,000.Body Temperature: The measure of the level of heat of a human or animal.Thiopental: A barbiturate that is administered intravenously for the induction of general anesthesia or for the production of complete anesthesia of short duration.Cells, Cultured: Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.Blotting, Western: Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.Spinal Cord Ischemia: Reduced blood flow to the spinal cord which is supplied by the anterior spinal artery and the paired posterior spinal arteries. This condition may be associated with ARTERIOSCLEROSIS, trauma, emboli, diseases of the aorta, and other disorders. Prolonged ischemia may lead to INFARCTION of spinal cord tissue.Mice, Knockout: Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.Myocardium: 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.Neurologic Examination: Assessment of sensory and motor responses and reflexes that is used to determine impairment of the nervous system.Sus scrofa: A species of SWINE, in the family Suidae, comprising a number of subspecies including the domestic pig Sus scrofa domestica.Glucose: A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement.Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.RNA, Messenger: RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.Animals, Newborn: Refers to animals in the period of time just after birth.Acute Disease: Disease having a short and relatively severe course.Encephalitis: Inflammation of the BRAIN due to infection, autoimmune processes, toxins, and other conditions. Viral infections (see ENCEPHALITIS, VIRAL) are a relatively frequent cause of this condition.Apoptosis: 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.Electroencephalography: Recording of electric currents developed in the brain by means of electrodes applied to the scalp, to the surface of the brain, or placed within the substance of the brain.Microglia: The third type of glial cell, along with astrocytes and oligodendrocytes (which together form the macroglia). Microglia vary in appearance depending on developmental stage, functional state, and anatomical location; subtype terms include ramified, perivascular, ameboid, resting, and activated. Microglia clearly are capable of phagocytosis and play an important role in a wide spectrum of neuropathologies. They have also been suggested to act in several other roles including in secretion (e.g., of cytokines and neural growth factors), in immunological processing (e.g., antigen presentation), and in central nervous system development and remodeling.Behavior, Animal: The observable response an animal makes to any situation.Lactates: Salts or esters of LACTIC ACID containing the general formula CH3CHOHCOOR.Ischemic Preconditioning, Myocardial: 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.CA1 Region, Hippocampal: One of four subsections of the hippocampus described by Lorente de No, located furthest from the DENTATE GYRUS.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Brain Abscess: A circumscribed collection of purulent exudate in the brain, due to bacterial and other infections. The majority are caused by spread of infected material from a focus of suppuration elsewhere in the body, notably the PARANASAL SINUSES, middle ear (see EAR, MIDDLE); HEART (see also ENDOCARDITIS, BACTERIAL), and LUNG. Penetrating CRANIOCEREBRAL TRAUMA and NEUROSURGICAL PROCEDURES may also be associated with this condition. Clinical manifestations include HEADACHE; SEIZURES; focal neurologic deficits; and alterations of consciousness. (Adams et al., Principles of Neurology, 6th ed, pp712-6)Intracranial Embolism and Thrombosis: Embolism or thrombosis involving blood vessels which supply intracranial structures. Emboli may originate from extracranial or intracranial sources. Thrombosis may occur in arterial or venous structures.Receptors, N-Methyl-D-Aspartate: A class of ionotropic glutamate receptors characterized by affinity for N-methyl-D-aspartate. NMDA receptors have an allosteric binding site for glycine which must be occupied for the channel to open efficiently and a site within the channel itself to which magnesium ions bind in a voltage-dependent manner. The positive voltage dependence of channel conductance and the high permeability of the conducting channel to calcium ions (as well as to monovalent cations) are important in excitotoxicity and neuronal plasticity.Rats, Long-Evans: An outbred strain of rats developed in 1915 by crossing several Wistar Institute white females with a wild gray male. Inbred strains have been derived from this original outbred strain, including Long-Evans cinnamon rats (RATS, INBRED LEC) and Otsuka-Long-Evans-Tokushima Fatty rats (RATS, INBRED OLETF), which are models for Wilson's disease and non-insulin dependent diabetes mellitus, respectively.Acid Sensing Ion Channels: A family of proton-gated sodium channels that are primarily expressed in neuronal tissue. They are AMILORIDE-sensitive and are implicated in the signaling of a variety of neurological stimuli, most notably that of pain in response to acidic conditions.In Situ Nick-End Labeling: An in situ method for detecting areas of DNA which are nicked during APOPTOSIS. Terminal deoxynucleotidyl transferase is used to add labeled dUTP, in a template-independent manner, to the 3 prime OH ends of either single- or double-stranded DNA. The terminal deoxynucleotidyl transferase nick end labeling, or TUNEL, assay labels apoptosis on a single-cell level, making it more sensitive than agarose gel electrophoresis for analysis of DNA FRAGMENTATION.Random Allocation: 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.Antioxidants: 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.Nervous System Diseases: Diseases of the central and peripheral nervous system. This includes disorders of the brain, spinal cord, cranial nerves, peripheral nerves, nerve roots, autonomic nervous system, neuromuscular junction, and muscle.Heart Arrest: Cessation of heart beat or MYOCARDIAL CONTRACTION. If it is treated within a few minutes, heart arrest can be reversed in most cases to normal cardiac rhythm and effective circulation.Myocardial Reperfusion: 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.Ultrasonography, Doppler, Transcranial: A non-invasive technique using ultrasound for the measurement of cerebrovascular hemodynamics, particularly cerebral blood flow velocity and cerebral collateral flow. With a high-intensity, low-frequency pulse probe, the intracranial arteries may be studied transtemporally, transorbitally, or from below the foramen magnum.Isoflurane: A stable, non-explosive inhalation anesthetic, relatively free from significant side effects.Cell Survival: The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.Oxidative Stress: 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).Cell Count: The number of CELLS of a specific kind, usually measured per unit volume or area of sample.Intracranial Embolism: Blocking of a blood vessel in the SKULL by an EMBOLUS which can be a blood clot (THROMBUS) or other undissolved material in the blood stream. Most emboli are of cardiac origin and are associated with HEART DISEASES. Other non-cardiac sources of emboli are usually associated with VASCULAR DISEASES.Diffusion Magnetic Resonance Imaging: A diagnostic technique that incorporates the measurement of molecular diffusion (such as water or metabolites) for tissue assessment by MRI. The degree of molecular movement can be measured by changes of apparent diffusion coefficient (ADC) with time, as reflected by tissue microstructure. Diffusion MRI has been used to study BRAIN ISCHEMIA and tumor response to treatment.Gene Expression Regulation: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.Tissue Plasminogen Activator: 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.Brain Damage, Chronic: A condition characterized by long-standing brain dysfunction or damage, usually of three months duration or longer. Potential etiologies include BRAIN INFARCTION; certain NEURODEGENERATIVE DISORDERS; CRANIOCEREBRAL TRAUMA; ANOXIA, BRAIN; ENCEPHALITIS; certain NEUROTOXICITY SYNDROMES; metabolic disorders (see BRAIN DISEASES, METABOLIC); and other conditions.Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.Oxygen Consumption: The rate at which oxygen is used by a tissue; microliters of oxygen STPD used per milligram of tissue per hour; the rate at which oxygen enters the blood from alveolar gas, equal in the steady state to the consumption of oxygen by tissue metabolism throughout the body. (Stedman, 25th ed, p346)Seizures: Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as EPILEPSY or "seizure disorder."Galectin 1: A galectin found abundantly in smooth muscle (MUSCLE, SMOOTH) and SKELETAL MUSCLE and many other tissues. It occurs as a homodimer with two 14-kDa subunits.Mice, Transgenic: Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.Coronary Circulation: The circulation of blood through the CORONARY VESSELS of the HEART.Up-Regulation: A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.Mitochondria: Semiautonomous, self-reproducing organelles that occur in the cytoplasm of all cells of most, but not all, eukaryotes. Each mitochondrion is surrounded by a double limiting membrane. The inner membrane is highly invaginated, and its projections are called cristae. Mitochondria are the sites of the reactions of oxidative phosphorylation, which result in the formation of ATP. They contain distinctive RIBOSOMES, transfer RNAs (RNA, TRANSFER); AMINO ACYL T RNA SYNTHETASES; and elongation and termination factors. Mitochondria depend upon genes within the nucleus of the cells in which they reside for many essential messenger RNAs (RNA, MESSENGER). Mitochondria are believed to have arisen from aerobic bacteria that established a symbiotic relationship with primitive protoeukaryotes. (King & Stansfield, A Dictionary of Genetics, 4th ed)Hindlimb: Either of two extremities of four-footed non-primate land animals. It usually consists of a FEMUR; TIBIA; and FIBULA; tarsals; METATARSALS; and TOES. (From Storer et al., General Zoology, 6th ed, p73)Signal Transduction: The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.Fibrinolytic Agents: Fibrinolysin or agents that convert plasminogen to FIBRINOLYSIN.Heart: The hollow, muscular organ that maintains the circulation of the blood.Gene Expression: The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.Perfusion: Treatment process involving the injection of fluid into an organ or tissue.Thrombolytic Therapy: Use of infusions of FIBRINOLYTIC AGENTS to destroy or dissolve thrombi in blood vessels or bypass grafts.Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.Dogs: 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)Carotid Arteries: Either of the two principal arteries on both sides of the neck that supply blood to the head and neck; each divides into two branches, the internal carotid artery and the external carotid artery.Hyperglycemia: Abnormally high BLOOD GLUCOSE level.Pyramidal Cells: Projection neurons in the CEREBRAL CORTEX and the HIPPOCAMPUS. Pyramidal cells have a pyramid-shaped soma with the apex and an apical dendrite pointed toward the pial surface and other dendrites and an axon emerging from the base. The axons may have local collaterals but also project outside their cortical region.Hemodynamics: The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.Prosencephalon: The anterior of the three primitive cerebral vesicles of the embryonic brain arising from the NEURAL TUBE. It subdivides to form DIENCEPHALON and TELENCEPHALON. (Stedmans Medical Dictionary, 27th ed)Myocardial Infarction: NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).Hydrogen-Ion Concentration: The normality of a solution with respect to HYDROGEN ions; H+. It is related to acidity measurements in most cases by pH = log 1/2[1/(H+)], where (H+) is the hydrogen ion concentration in gram equivalents per liter of solution. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.Motor Activity: The physical activity of a human or an animal as a behavioral phenomenon.Coronary Disease: 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.Image Processing, Computer-Assisted: A technique of inputting two-dimensional images into a computer and then enhancing or analyzing the imagery into a form that is more useful to the human observer.Constriction: The act of constricting.Subcellular Fractions: Components of a cell produced by various separation techniques which, though they disrupt the delicate anatomy of a cell, preserve the structure and physiology of its functioning constituents for biochemical and ultrastructural analysis. (From Alberts et al., Molecular Biology of the Cell, 2d ed, p163)Cardiotonic Agents: 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).Rabbits: 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.Regional Blood Flow: The flow of BLOOD through or around an organ or region of the body.Mesenteric Vascular Occlusion: Obstruction of the flow in the SPLANCHNIC CIRCULATION by ATHEROSCLEROSIS; EMBOLISM; THROMBOSIS; STENOSIS; TRAUMA; and compression or intrinsic pressure from adjacent tumors. Rare causes are drugs, intestinal parasites, and vascular immunoinflammatory diseases such as PERIARTERITIS NODOSA and THROMBOANGIITIS OBLITERANS. (From Juergens et al., Peripheral Vascular Diseases, 5th ed, pp295-6)Tissue Distribution: Accumulation of a drug or chemical substance in various organs (including those not relevant to its pharmacologic or therapeutic action). This distribution depends on the blood flow or perfusion rate of the organ, the ability of the drug to penetrate organ membranes, tissue specificity, protein binding. The distribution is usually expressed as tissue to plasma ratios.Enzyme Activation: Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.Electrocardiography: 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.Myocardial Contraction: Contractile activity of the MYOCARDIUM.Deep Brain Stimulation: Therapy for MOVEMENT DISORDERS, especially PARKINSON DISEASE, that applies electricity via stereotactic implantation of ELECTRODES in specific areas of the BRAIN such as the THALAMUS. The electrodes are attached to a neurostimulator placed subcutaneously.Leg: The inferior part of the lower extremity between the KNEE and the ANKLE.Treatment Outcome: 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.Exercise Test: Controlled physical activity which is performed in order to allow assessment of physiological functions, particularly cardiovascular and pulmonary, but also aerobic capacity. Maximal (most intense) exercise is usually required but submaximal exercise is also used.Lower Extremity: The region of the lower limb in animals, extending from the gluteal region to the FOOT, and including the BUTTOCKS; HIP; and LEG.Lactic Acid: A normal intermediate in the fermentation (oxidation, metabolism) of sugar. The concentrated form is used internally to prevent gastrointestinal fermentation. (From Stedman, 26th ed)Phosphocreatine: An endogenous substance found mainly in skeletal muscle of vertebrates. It has been tried in the treatment of cardiac disorders and has been added to cardioplegic solutions. (Reynolds JEF(Ed): Martindale: The Extra Pharmacopoeia (electronic version). Micromedex, Inc, Englewood, CO, 1996)Ischemic Postconditioning: 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.Microcirculation: The circulation of the BLOOD through the MICROVASCULAR NETWORK.Recombinant Proteins: Proteins prepared by recombinant DNA technology.Adenosine Triphosphate: An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter.Adenosine: 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.Laser-Doppler Flowmetry: A method of non-invasive, continuous measurement of MICROCIRCULATION. The technique is based on the values of the DOPPLER EFFECT of low-power laser light scattered randomly by static structures and moving tissue particulates.Myocardial Stunning: Prolonged dysfunction of the myocardium after a brief episode of severe ischemia, with gradual return of contractile activity.Swine: 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).Kidney: Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.Tomography, Emission-Computed, Single-Photon: A method of computed tomography that uses radionuclides which emit a single photon of a given energy. The camera is rotated 180 or 360 degrees around the patient to capture images at multiple positions along the arc. The computer is then used to reconstruct the transaxial, sagittal, and coronal images from the 3-dimensional distribution of radionuclides in the organ. The advantages of SPECT are that it can be used to observe biochemical and physiological processes as well as size and volume of the organ. The disadvantage is that, unlike positron-emission tomography where the positron-electron annihilation results in the emission of 2 photons at 180 degrees from each other, SPECT requires physical collimation to line up the photons, which results in the loss of many available photons and hence degrades the image.Aging: The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.Amputation: The removal of a limb or other appendage or outgrowth of the body. (Dorland, 28th ed)Creatine Kinase: 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.Neovascularization, Physiologic: The development of new BLOOD VESSELS during the restoration of BLOOD CIRCULATION during the healing process.Anoxia: Relatively complete absence of oxygen in one or more tissues.Mitochondria, Heart: The mitochondria of the myocardium.Cerebellum: The part of brain that lies behind the BRAIN STEM in the posterior base of skull (CRANIAL FOSSA, POSTERIOR). It is also known as the "little brain" with convolutions similar to those of CEREBRAL CORTEX, inner white matter, and deep cerebellar nuclei. Its function is to coordinate voluntary movements, maintain balance, and learn motor skills.Heart Rate: The number of times the HEART VENTRICLES contract per unit of time, usually per minute.Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.Alzheimer Disease: A degenerative disease of the BRAIN characterized by the insidious onset of DEMENTIA. Impairment of MEMORY, judgment, attention span, and problem solving skills are followed by severe APRAXIAS and a global loss of cognitive abilities. The condition primarily occurs after age 60, and is marked pathologically by severe cortical atrophy and the triad of SENILE PLAQUES; NEUROFIBRILLARY TANGLES; and NEUROPIL THREADS. (From Adams et al., Principles of Neurology, 6th ed, pp1049-57)Autoradiography: The making of a radiograph of an object or tissue by recording on a photographic plate the radiation emitted by radioactive material within the object. (Dorland, 27th ed)Angina Pectoris: The symptom of paroxysmal pain consequent to MYOCARDIAL ISCHEMIA usually of distinctive character, location and radiation. It is thought to be provoked by a transient stressful situation during which the oxygen requirements of the MYOCARDIUM exceed that supplied by the CORONARY CIRCULATION.Magnetic Resonance Spectroscopy: Spectroscopic method of measuring the magnetic moment of elementary particles such as atomic nuclei, protons or electrons. It is employed in clinical applications such as NMR Tomography (MAGNETIC RESONANCE IMAGING).Models, Animal: Non-human animals, selected because of specific characteristics, for use in experimental research, teaching, or testing.Brain Injury, Chronic: Conditions characterized by persistent brain damage or dysfunction as sequelae of cranial trauma. This disorder may result from DIFFUSE AXONAL INJURY; INTRACRANIAL HEMORRHAGES; BRAIN EDEMA; and other conditions. Clinical features may include DEMENTIA; focal neurologic deficits; PERSISTENT VEGETATIVE STATE; AKINETIC MUTISM; or COMA.L-Lactate Dehydrogenase: 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.Brain Waves: Wave-like oscillations of electric potential between parts of the brain recorded by EEG.Energy Metabolism: The chemical reactions involved in the production and utilization of various forms of energy in cells.Peroxidase: 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.Collateral Circulation: Maintenance of blood flow to an organ despite obstruction of a principal vessel. Blood flow is maintained through small vessels.Neuroglia: The non-neuronal cells of the nervous system. They not only provide physical support, but also respond to injury, regulate the ionic and chemical composition of the extracellular milieu, participate in the BLOOD-BRAIN BARRIER and BLOOD-RETINAL BARRIER, form the myelin insulation of nervous pathways, guide neuronal migration during development, and exchange metabolites with neurons. Neuroglia have high-affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitters, but their role in signaling (as in many other functions) is unclear.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.Biological Markers: Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Microdialysis: A technique for measuring extracellular concentrations of substances in tissues, usually in vivo, by means of a small probe equipped with a semipermeable membrane. Substances may also be introduced into the extracellular space through the membrane.Nitric Oxide: 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.Arrhythmias, Cardiac: Any disturbances of the normal rhythmic beating of the heart or MYOCARDIAL CONTRACTION. Cardiac arrhythmias can be classified by the abnormalities in HEART RATE, disorders of electrical impulse generation, or impulse conduction.Coronary Vessels: The veins and arteries of the HEART.Cats: The domestic cat, Felis catus, of the carnivore family FELIDAE, comprising over 30 different breeds. The domestic cat is descended primarily from the wild cat of Africa and extreme southwestern Asia. Though probably present in towns in Palestine as long ago as 7000 years, actual domestication occurred in Egypt about 4000 years ago. (From Walker's Mammals of the World, 6th ed, p801)Ventricular Function, Left: 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.Prospective Studies: 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.Cytoprotection: The process by which chemical compounds provide protection to cells against harmful agents.Tomography, X-Ray Computed: Tomography using x-ray transmission and a computer algorithm to reconstruct the image.Neural Pathways: Neural tracts connecting one part of the nervous system with another.Limb Salvage: An alternative to amputation in patients with neoplasms, ischemia, fractures, and other limb-threatening conditions. Generally, sophisticated surgical procedures such as vascular surgery and reconstruction are used to salvage diseased limbs.Electrocardiography, Ambulatory: Method in which prolonged electrocardiographic recordings are made on a portable tape recorder (Holter-type system) or solid-state device ("real-time" system), while the patient undergoes normal daily activities. It is useful in the diagnosis and management of intermittent cardiac arrhythmias and transient myocardial ischemia.Ligation: Application of a ligature to tie a vessel or strangulate a part.Myocytes, Cardiac: Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).Functional Laterality: Behavioral manifestations of cerebral dominance in which there is preferential use and superior functioning of either the left or the right side, as in the preferred use of the right hand or right foot.Mesenteric Artery, Superior: A large vessel supplying the whole length of the small intestine except the superior part of the duodenum. It also supplies the cecum and the ascending part of the colon and about half the transverse part of the colon. It arises from the anterior surface of the aorta below the celiac artery at the level of the first lumbar vertebra.Organ Specificity: Characteristic restricted to a particular organ of the body, such as a cell type, metabolic response or expression of a particular protein or antigen.

Genetic and gender influences on sensitivity to focal cerebral ischemia in the stroke-prone spontaneously hypertensive rat. (1/7625)

We have investigated genetic transmission of increased sensitivity to focal cerebral ischemia and the influence of gender in the stroke-prone spontaneously hypertensive rat (SHRSP). Halothane-anesthetized, 3- to 5-month-old male and female Wistar-Kyoto rats (WKY), SHRSP, and the first filial generation rats (F1 crosses 1 and 2) underwent distal (2 mm) permanent middle cerebral artery occlusion (MCAO) by electrocoagulation. Infarct volume was measured by using hematoxylin-eosin-stained sections and image analysis 24 hours after ischemia and expressed as a percentage of the volume of the ipsilateral hemisphere. Infarct volume in males and females grouped together were significantly larger in SHRSP, F1 cross 1 (SHRSP father), and F1 cross 2 (WKY father), at 36.6+/-2.3% (mean+/-SEM, P<0.001, n=15), 25.4+/-2.4% (P<0.01, n=14), and 33. 9+/-1.6% (P<0.001, n=18), respectively, compared with WKY (14+/-2%, n=17). Male F1 cross 1 (18.9+/-2.4%, n=6) developed significantly smaller infarcts than male F1 cross 2 (32.8+/-2%, n=8, P<0.005). Females, which underwent ischemia during metestrus, developed larger infarcts than respective males. A group of females in which the cycle was not controlled for developed significantly smaller infarcts than females in metestrus. Thus, the increased sensitivity to MCAO in SHRSP is retained in both F1 cross 1 and cross 2 hybrids, suggesting a dominant or codominant trait; response to cerebral ischemia appears to be affected by gender and stage in the estrous cycle. In addition, the male progenitor of the cross (ie, SHRSP versus WKY) influences stroke sensitivity in male F1 cohorts.  (+info)

Ischemic tolerance in murine cortical cell culture: critical role for NMDA receptors. (2/7625)

Murine cortical cultures containing both neurons and glia (days in vitro 13-15) were exposed to periods of oxygen-glucose deprivation (5-30 min) too brief to induce neuronal death. Cultures "preconditioned" by sublethal oxygen-glucose deprivation exhibited 30-50% less neuronal death than controls when exposed to a 45-55 min period of oxygen-glucose deprivation 24 hr later. This preconditioning-induced neuroprotection was specific in that neuronal death induced by exposure to excitotoxins or to staurosporine was not attenuated. Neuroprotection was lost if the time between the preconditioning and severe insult were decreased to 7 hr or increased to 72 hr and was blocked if the NMDA antagonist 100 microM 3-((D)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid was applied during the preconditioning insult. This was true even if the duration of preconditioning was increased as far as possible (while still remaining sublethal). A similar preconditioning effect was also produced by sublethal exposure to high K+, glutamate, or NMDA but not to kainate or trans-1-aminocyclopentane-1, 3-dicarboxylic acid.  (+info)

Disease pattern in cranial and large-vessel giant cell arteritis. (3/7625)

OBJECTIVE: To identify variables that distinguish large-vessel giant cell arteritis (GCA) with subclavian/axillary/brachial artery involvement from cranial GCA. METHODS: Seventy-four case patients with subclavian/axillary GCA diagnosed by angiography and 74 control patients with temporal artery biopsy-proven GCA without large vessel involvement matched for the date of first diagnosis were identified. Pertinent initial symptoms, time delay until diagnosis, and clinical symptoms, as well as clinical and laboratory findings at the time of diagnosis, were recorded by retrospective chart review. Expression of cytokine messenger RNA in temporal artery tissue from patients with large-vessel and cranial GCA was determined by semiquantitative polymerase chain reaction analysis. Distribution of disease-associated HLA-DRB1 alleles in patients with aortic arch syndrome and cranial GCA was assessed. RESULTS: The clinical presentation distinguished patients with large-vessel GCA from those with classic cranial GCA. Upper extremity vascular insufficiency dominated the clinical presentation of patients with large-vessel GCA, whereas symptoms related to impaired cranial blood flow were infrequent. Temporal artery biopsy findings were negative in 42% of patients with large-vessel GCA. Polymyalgia rheumatica occurred with similar frequency in both patient groups. Large-vessel GCA was associated with higher concentrations of interleukin-2 gene transcripts in arterial tissue and overrepresentation of the HLA-DRB1*0404 allele, indicating differences in pathogenetic mechanisms. CONCLUSION: GCA is not a single entity but includes several variants of disease. Large-vessel GCA produces a distinct spectrum of clinical manifestations and often occurs without involvement of the cranial arteries. Large-vessel GCA requires a different approach to the diagnosis and probably also to treatment.  (+info)

N-Acetylaspartate distribution in rat brain striatum during acute brain ischemia. (4/7625)

Brain N-acetylaspartate (NAA) can be quantified by in vivo proton magnetic resonance spectroscopy (1H-MRS) and is used in clinical settings as a marker of neuronal density. It is, however, uncertain whether the change in brain NAA content in acute stroke is reliably measured by 1H-MRS and how NAA is distributed within the ischemic area. Rats were exposed to middle cerebral artery occlusion. Preischemic values of [NAA] in striatum were 11 mmol/L by 1H-MRS and 8 mmol/kg by HPLC. The methods showed a comparable reduction during the 8 hours of ischemia. The interstitial level of [NAA] ([NAA]e) was determined by microdialysis using [3H]NAA to assess in vivo recovery. After induction of ischemia, [NAA]e increased linearly from 70 micromol/L to a peak level of 2 mmol/L after 2 to 3 hours before declining to 0.7 mmol/L at 7 hours. For comparison, [NAA]e was measured in striatum during global ischemia, revealing that [NAA]e increased linearly to 4 mmol/L after 3 hours and this level was maintained for the next 4 h. From the change in in vivo recovery of the interstitial space volume marker [14C]mannitol, the relative amount of NAA distributed in the interstitial space was calculated to be 0.2% of the total brain NAA during normal conditions and only 2 to 6% during ischemia. It was concluded that the majority of brain NAA is intracellularly located during ischemia despite large increases of interstitial [NAA]. Thus, MR quantification of NAA during acute ischemia reflects primarily changes in intracellular levels of NAA.  (+info)

Delayed increase in infarct volume after cerebral ischemia: correlations with thrombolytic treatment and clinical outcome. (5/7625)

BACKGROUND AND PURPOSE: Growing experimental evidence indicates that the development of cerebral ischemic damage is slower than previously believed. The aims of this work were (1) to study the evolution of CT hypoattenuation between 24 to 36 hours and 7 days in ischemic stroke patients; (2) to evaluate whether thrombolytic treatment given within 6 hours of stroke affects delayed infarction evolution; and (3) to investigate possible correlations between lesion volume changes over time and clinical outcome. METHODS: Of 620 patients included in the European Cooperative Acute Stroke Study 1 (ECASS1), we selected 450 patients whose control CT scans at day 1 (CT1) and day 7 (CT7) were available. They had been randomly divided into 2 groups: 206 patients had been treated with rtPA and 244 with placebo. CT1 and CT7 were classified according to the location of the infarct. The volume of CT hypoattenuation was measured using the formula AxBxC/2 for irregular volumes. The 95% confidence interval of inter- and intrarater variability was used to determine whether significant changes in lesion volume had occurred between CT1 and CT7. Clinical severity was evaluated by means of the Scandinavian Stroke Scale (SSS) at entry (SSS0) and at day 30 (SSS30). RESULTS: Mean lesion volumes were significantly (P<0.0001) higher at day 7 than at day 1 in all the subgroups of patients and particularly in patients with a subcortical lesion. Of the 450 patients studied, 287 (64%) did not show any significant change in lesion volume between CT1 and CT7, 143 (32%) showed a significant increase and the remaining 20 (4%) a significant decrease. No significant correlation was observed between treatment and lesion evolution between CT1 and CT7. Both clinical scores (SSS0 and SSS30) and degree of neurological recovery were significantly (P<0.05) lower in the subgroup of patients with a significant lesion volume increase than in the other 2 groups. CONCLUSIONS: In approximately two thirds of patients, infarct size is established 24 to 36 hours after stroke onset, whereas in the remaining one third, changes in lesion volume may occur later than the first 24 to 36 hours. Many factors may be responsible for delayed infarct enlargement and for a lower degree of clinical recovery, both of which may occur despite early recombinant tissue plasminogen activator treatment.  (+info)

Dose escalation study of the NMDA glycine-site antagonist licostinel in acute ischemic stroke. (6/7625)

BACKGROUND AND PURPOSE: Licostinel (ACEA 1021; 5-nitro-6, 7-dichloro-2,3-quinoxalinedione), a competitive antagonist of glycine at the N-methyl-D-aspartate (NMDA) receptor, is an effective neuroprotective agent in animal models of cerebral ischemia. The purpose of this study was to assess the safety, tolerability, and pharmacokinetics of licostinel in patients with acute stroke. METHODS: In this 5-center dose escalation trial, patients were enrolled within 48 hours of an ischemic stroke and treated with ascending doses of a short infusion of licostinel or a placebo. Adverse effects were assessed with clinical and laboratory measurements, and patient outcome was determined with the National Institutes of Health Stroke Scale. RESULTS: Sixty-four patients (44 treated with escalating doses of licostinel and 20 who received placebo) were treated. Lower doses of licostinel (0.03 to 0.60 mg/kg) were not associated with any significant adverse effects. Higher doses of licostinel (1.2 to 3.0 mg/kg) were associated with a variety of mild-to-moderate adverse effects including neurological and gastrointestinal complaints. No major psychotomimetic effects or significant safety concerns occurred. At the higher dose levels, peak plasma concentrations of licostinel were substantially higher than those required for neuroprotection in animal stroke models. A similar improvement in National Institutes of Health Stroke Scale scores over time was seen in both the placebo group and the licostinel-treated patients. CONCLUSIONS: A short infusion of licostinel in doses up to 3.0 mg/kg is safe and tolerable in acute stroke patients. Licostinel may be a safer and better tolerated neuroprotective agent than many of the previously evaluated NMDA antagonists.  (+info)

Anger expression and incident stroke: prospective evidence from the Kuopio ischemic heart disease study. (7/7625)

BACKGROUND AND PURPOSE: High levels of anger are associated with an increased risk of coronary heart disease and hypertension, but little is known about the role of anger in stroke risk. METHODS: Anger expression style and risk of incident stroke were examined in 2074 men (mean age, 53.0+/-5.2 years) from a population-based, longitudinal study of risk factors for ischemic heart disease and related outcomes in eastern Finland. Self-reported style of anger expression was assessed by questionnaire at baseline. Linkage to the FINMONICA stroke and national hospital discharge registers identified 64 first strokes (50 ischemic) through 1996. Average follow-up time was 8.3+/-0.9 (mean+/-SD) years. RESULTS: Men who reported the highest level of expressed anger were at twice the risk of stroke (relative hazard, 2.03; 95% CI, 1.05 to 3.94) of men who reported the lowest level of anger, after adjustments for age, resting blood pressure, smoking, alcohol consumption, body mass index, low-density and high-density lipoprotein cholesterol, fibrinogen, socioeconomic status, history of diabetes, and use of antihypertensive medications. Additional analysis showed that these associations were evident only in men with a history of ischemic heart disease (n=481), among whom high levels of outwardly expressed anger (high anger-out) predicted >6-fold increased risk of stroke after risk factor adjustment (relative hazard, 6.87; 95% CI, 1.50 to 31.4). Suppressed anger (anger-in) and controlled anger (anger-control) were not consistently related to stroke risk. CONCLUSIONS: This is the first population-based study to show a significant relationship between high levels of expressed anger and incident stroke. Additional research is necessary to explore the mechanisms that underlie this association.  (+info)

Increased platelet activation in the chronic phase after cerebral ischemia and intracerebral hemorrhage. (8/7625)

BACKGROUND AND PURPOSE: Enhanced thromboxane (TX) biosynthesis has previously been reported in the acute phase after ischemic stroke. We investigated whether enhanced urinary excretion of 11-dehydro-TXB2, a noninvasive index of platelet activation, was present in the chronic phase after a transient ischemic attack (TIA) or stroke, including intracerebral hemorrhage. METHODS: We obtained a single urinary sample from 92 patients between 3 and 9 months after onset of stroke or TIA. The urinary excretion of the major enzymatic metabolite of TXA2, 11-dehydro-TXB2, was measured by a previously validated radioimmunoassay. The excretion rates were compared with those of 20 control patients with nonvascular neurological diseases. RESULTS: Urinary 11-dehydro-TXB2 averaged 294+/-139, 413+/-419, and 557+/-432 pmol/mmol creatinine for patients with TIA, ischemic stroke, and intracerebral hemorrhage, respectively; the values were higher in all subgroups (P<0.01) than that in control patients (119+/-66 pmol/mmol). Increased 11-dehydro-TXB2 excretion was present in 59% of all patients, in 60% (P<0.001) of patients with TIA, in 56% (P<0.001) of patients with ischemic stroke, and in 73% (P<0.001) of patients with intracerebral hemorrhage. Atrial fibrillation, no aspirin use, and severity of symptoms at follow-up contributed independently to the level of 11-dehydro-TXB2 excretion in a multiple linear regression analysis. CONCLUSIONS: Platelet activation is often present in patients in the chronic phase after stroke, including those with intracerebral hemorrhage. Persistent platelet activation, which is associated with atrial fibrillation and poor stroke outcome, can be substantially suppressed by aspirin treatment.  (+info)

We investigated the effects of the angiotensin-converting enzyme inhibitor captopril on neurologic outcome in a rat model of incomplete cerebral ischemia. Twenty male Sprague-Dawley rats were anesthetized with 70% nitrous oxide in oxygen and fentanyl (10 micrograms x kg-1 i.v. bolus, 25 micrograms x kg-1 x hr-1 i.v. continuous infusion). Animals in group 1 (n = 10) received no angiotensin-converting enzyme inhibitor while animals in group 2 (n = 10) were given 10 mg x kg-1 i.v. captopril 30 minutes prior to the ischemic period. Ischemia was produced by unilateral carotid artery ligation and hemorrhagic hypotension to 35 mm Hg for 30 minutes. Body temperature, arterial blood gases, and arterial pH were maintained constant. Neurologic outcome was evaluated every 24 hours for 3 days using a graded deficit score (0, normal; 18, stroke-related death). On the third day after ischemia, captopril significantly improved neurologic outcome (median deficit score = 4) compared with controls (median deficit ...
TY - JOUR. T1 - Treatment of acute focal cerebral ischemia with dimethyl sulfoxide. AU - Little, J. R.. AU - Cook, A.. AU - Lesser, Ronald P. PY - 1981. Y1 - 1981. N2 - The object of this investigation was to study the effects of dimethyl sulfoxide (DMSO) upon the evolution of cerebral infarction. Twenty adult cats anesthetized lightly with ketamine hydrochloride underwent right middle cerebral artery occlusion for 6 hours. Ten cats were not treated and 10 cats received DMSO (2.5 g/kg i.v.) immediately after occlusion. Regional cerebral blood flow (rCBF) changes in the right sylvian region were similar in the untreated and treated groups. The mean rCBF before occlusion was 46 ± 10 ml/100 g/minute in the untreated group and 45 ± 10 ml/100 g/minute in the treated group. Eight cats in both groups had rCBF measurements consistently below 18 ml/100 g/minute during the 6-hour period after occlusion. An index of erythrocyte flow was determined by measuring the transit of technetium-99 (99Tc)-labeled ...
The effects of isosmolar loads of glucose and saline after onset of focal cerebral ischaemia (middle cerebral artery occlusion) were compared in cats. In cats given saline cerebral blood flow (CBF) fell and then rose slightly on the marginal gyrus (infarct penumbra). There was a sustained fall in CBF on the suprasylvian and ectosylvian gyri (infarct core). Reperfusion restored blood flow to preocclusion levels with no overall postischaemic hypoperfusion. Below ischaemic flows of 14 ml/100 g/min brain specific gravity was reduced in a smaller proportion of gyri by contrast with non reperfused cortex, suggesting that in some gyri resolution of cerebral oedema had taken place. GABA uptake was normal in the infarct core, but was reduced within the ischaemic penumbra. In animals given glucose after occlusion, CBF fell on the marginal gyrus during reperfusion. The degree of resolution of cerebral oedema was less than in saline infused cats. GABA uptake showed a pattern of abnormality similar to that ...
Interleukin-1 (IL-1) is a key regulator of inflammation and ischaemic brain injury, but the contribution of central and peripheral sources of IL-1 to brain injury is not well understood. Here we show that haematopoietic-derived IL-1 is a key driver of ischaemic brain injury. Wild type (WT) mice transplanted with IL-1αβ-deficient bone marrow displayed a significant (40%) reduction in brain injury induced by focal cerebral ischaemia compared to WT mice transplanted with WT bone marrow. This was paralleled by improved neurological outcome and the almost complete absence of splenic-derived, but not liver-derived, IL-1α after stroke in WT mice lacking haematopoietic-derived IL-1. IL-1αβ knockout (KO) mice transplanted with IL-1αβ-deficient bone marrow showed a 60% reduction in brain injury compared to WT mice receiving WT bone marrow. Transplantation of WT bone marrow in IL-1αβ KO mice resulted in a similar level of blood-brain-barrier injury to that observed in WT mice receiving ...
OBJECTIVES: Prolonged global cerebral ischaemia leads to irreversible injury, often with lethal outcome. Brain injuries are partly caused by the uncontrolled reperfusion that occurs once the circulation is re-established. Recent animal experiments suggest that controlled reperfusion following lengthy ischaemia might prevent severe brain injury. This study aimed at further exploring cerebral alterations and outcome following prolonged global cerebral ischaemia and mechanically manipulated reperfusion.. METHODS: Three groups of pigs were included; one sham operated (n = 3) and two that underwent 30-min global cerebral ischaemia. All vessels that supply the brain were isolated intrathoracically, after which they were occluded for 30 min in the ischaemic groups. In one of the ischaemic groups uncontrolled reperfusion was applied (URep, n = 6), i.e. normal circulation was restored 30 min after arrested cerebral circulation. The second ischaemic group received mechanical reperfusion (MRep, n = 6) with ...
TY - JOUR. T1 - Intraluminal suture occlusion of the middle cerebral artery in spontaneously hypertensive rats. AU - Dogan, Aclan. AU - Başkaya, Mustafa K.. AU - Rao, V. L Raghavendra. AU - Rao, A. Muralikrishna. AU - Dempsey, Robert J.. PY - 1998/4. Y1 - 1998/4. N2 - In models of middle cerebral artery occlusion using intraluminal suture, the size and the distribution of ischemic injury vary considerably among laboratories. In transcranial models of cerebral ischemia, a more consistent cerebral ischemic lesion is seen in Spontaneously Hypertensive rats (SHR). In the present study, we performed intraluminal suture occlusion of the MCA in SHR and compared its reproducibility with those in Sprague-Dawley (SD) rats. Male SHR and SD rats were anesthetized with halothane and subjected to 2 h of temporary middle cerebral artery occlusion by an intraluminal suture. Comparisons of regional cerebral blood flow figures taken throughout the experiment and lesion volume figures taken at 24 h after ...
Hypoxic-ischaemic brain injury at birth is associated with 1-3/1000 cases of moderate to severe encephalopathy. Previously, we have shown that connexin 43 hemichannel blockade, with a specific mimetic peptide, reduced the occurrence of seizures, improved recovery of EEG power and sleep state cycling, and improved cell survival following global cerebral ischaemia. In the present study, we examined the dose response for intracerebroventricular mimetic peptide infusion (50 µmol/kg/h for 1 h, followed by 50 µmol/kg/24 h (low dose) or 50 µmol/kg/h for 25 h (high dose) or vehicle only (control group), starting 90 min after the end of ischaemia), following global cerebral ischaemia, induced by 30 min bilateral carotid artery occlusion, in near-term fetal sheep (128 ± 1 days gestation). Both peptide infusion groups were associated with a transient significant increase in EEG power between 2-12 h after ischaemia. The ischaemia-low dose group showed a significant recovery of EEG power from day five compared
The present study shows that PC-SOD, the lecithinized form of SOD, decreased infarct volume and improved neurological outcomes at different time points after focal cerebral ischemic injury. PC-SOD decreased oxidative stress and provided neuronal protection through antiapoptotic mechanisms.. Previous studies have highlighted that unmodified SOD plays an important role in attenuating different forms of brain injury, including cerebral ischemia.1,2,3 However, its short in vivo half-life and low tissue affinity have hampered the practical use of unmodified SOD formulations.4 The enzymatic activity of PC-SOD is comparable to that of unmodified SOD. The in vitro activity of unmodified SOD by the xanthine-xanthine oxidase method was 3467 U/mg, whereas that of PC-SOD was 2876 U/mg. Therefore, the activity of PC-SOD was equivalent to 83% of unmodified SOD.15 PC-SOD, however, has many advantages, such as longer in vivo half-life, greater tissue affinity, and better drug delivery, resulting in ...
Brain ischemia (a.k.a. cerebral ischemia, cerebrovascular ischemia) is a condition in which there is insufficient blood flow to the brain to meet metabolic demand. This leads to poor oxygen supply or cerebral hypoxia and thus to the death of brain tissue or cerebral infarction / ischemic stroke. It is a sub-type of stroke along with subarachnoid hemorrhage and intracerebral hemorrhage. Ischemia leads to alterations in brain metabolism, reduction in metabolic rates, and energy crisis. There are two types of ischemia: focal ischemia, which is confined to a specific region of the brain; and global ischemia, which encompasses wide areas of brain tissue. The main symptoms involve impairments in vision, body movement, and speaking. The causes of brain ischemia vary from sickle cell anemia to congenital heart defects. Symptoms of brain ischemia can include unconsciousness, blindness, problems with coordination, and weakness in the body. Other effects that may result from brain ischemia are stroke, ...
TY - JOUR. T1 - Postischemic gene transfer of midkine, a neurotrophic factor, protects against focal brain ischemia. AU - Takada, J.. AU - Ooboshi, H.. AU - Ago, T.. AU - Kitazono, T.. AU - Yao, H.. AU - Kadomatsu, K.. AU - Muramatsu, T.. AU - Ibayashi, S.. AU - Iida, M.. PY - 2005/3/1. Y1 - 2005/3/1. N2 - Gene therapy may be a promising approach for treatment of brain ischemia. In this study, we examined the effect of postischemic gene transfer of midkine, a heparin-binding neurotrophic factor, using a focal brain ischemia model with the photothrombotic occlusion method. At 90 min after induction of brain ischemia in spontaneously hypertensive rats, a replication-deficient recombinant adenovirus encoding mouse midkine (AdMK, n = 7) or a control vector encoding β-galactosidase (Adβgal, n = 7) was injected into the lateral ventricle ipsilateral to ischemia. At 2 days after ischemia, we determined infarct volume by 2,3,5-triphenyltetrazolium chloride staining. There were no significant ...
Introduction: The aim of the study was to evaluate the endothelioprotective activity of 4-hydroxy-3,5-di-tret-butylcinnamic acid in conditions of experimental cerebral ischemia. Materials and methods: The brain ischemia was reproduced by the method of irreversible right-sided thermocoagulation of the middle cerebral artery. As comparative drugs, mexidol (30 mg/kg) and sulodexide (30 U/kg) were used. The vasodilating function of the vascular endothelium was assessed by the change in the rate of cerebral blood flow when the synthesis of nitric oxide was modified. Antithrombotic function was assessed by changes in the concentration of thromboxane A2, fibrinogen, von Willebrand factor activity and platelet aggregation activity. Serum concentration of C-reactive protein served as a marker of the state of anti-inflammatory endothelial function. To determine the potential mechanism of endothelioprotective activity of 4-4-hydroxy-3,5-di-tret-butylcinnamic acid, the anti-radical activity of
אינדוקציה כירורגי של נזק מוחי איסכמי בחולדה הוא מודל בשימוש נרחב עבור מחקר שבץ. כאן אנו מדגימים את האינדוקציה של איסכמיה מוחית המוקד על ...
Aging is a risk factor for stroke. Animal models of stroke have been widely used to study the pathophysiology of ischemic stroke, which in turn helped to develop numerous therapeutic strategies. Despite the considerable success of therapeutic strategies in animal models of ischemic stroke, almost all of them have been proved to be unsuccessful in the clinical trials. One of explanation is that data obtained from young animals may not fully resemble the effects of ischemic stroke in aged animals or elder patients, causing the discrepancy between animal experiments and clinical trials. To investigate these differences with regard to age, pathway specific gene arrays were used to identify and isolate differentially expressed genes in periinfarct following focal cerebral ischemia. The results from this study showed a persistent up-regulation of pro-apoptotic and inflammatory-related genes up to 14 days post stroke, a 50% reduction in the number of transcriptionally active stem cell-related genes and ...
TY - JOUR. T1 - Ablation of Neurogenesis Attenuates Recovery of Motor Function after Focal Cerebral Ischemia in Middle-Aged Mice. AU - Sun, Fen. AU - Wang, Xiaomei. AU - Mao, Xiao Ou. AU - Xie, Lin. AU - Jin, Kunlin. PY - 2012/10/26. Y1 - 2012/10/26. N2 - Depletion of neurogenesis worsens functional outcome in young-adult mice after focal cerebral ischemia, but whether a similar effect occurs in older mice is unknown. Using middle-aged (12-month-old) transgenic (DCX-TK(+)) mice that express herpes simplex virus thymidine kinase (HSV-TK) under control of the doublecortin (DCX) promoter, we conditionally depleted DCX-positive cells in the subventricular zone (SVZ) and hippocampus by treatment with ganciclovir (GCV) for 14 days. Focal cerebral ischemia was induced by permanent occlusion of the middle cerebral artery (MCAO) or occlusion of the distal segment of middle cerebral artery (dMCAO) on day 14 of vehicle or GCV treatment and mice were killed 24 hr or 12 weeks later. Increased infarct volume ...
ABSTRACT MECHANISMS OF PERSISTENT TRANSLATION ARREST FOLLOWING GLOBAL BRAIN ISCHEMIA and REPERFUSION by JILL T. JAMISON December 2011 Advisor: Donald J. DeGracia, Ph.D. Major: Physiology Degree: Doctor of Philosophy The information presented here studies the mechanisms that underlie persistent translation arrest (TA) following global brain ischemia and reperfusion (I/R). To summarize the main findings I have discovered a new mechanism for prolonged post-ischemic TA that correlated exactly with in vivo translation rates and correlated precisely with cell outcome. Through the extensive colocalization studies, my results indicate that the mRNA granules are ribonomic structures involved with mRNA regulation. This finding is significant because it shifts the focus onto mRNA metabolism and away from ribosomal molecular biology. I have identified new pathways to investigate for understanding why there is selective delayed death in post-ischemic neurons, however my work also gives insight into why resistant
It is crucial to establish an MCAO/R animal model according to the clinical characteristics of a human cerebral natural infarct. The model characteristics are as follows: i) single damage mechanism that is easy to study; ii) simple method, small wound, easy to control condition, stable infarct site, and distinct symptomatic reaction and high achievement ratio; iii) uniformity of cerebral infarction and good reproducibility; and iv) necrotic brain tissue following injury, with a similar pathophysiological process to clinical cerebral ischemia. In this study, a rat cerebral ischemia-reperfusion injury model was established according to the Zea-Longa method (4). Following cerebral ischemia for 1 h, the rats developed severe nervous and behavioral functional impairment symptoms, indicating the establishment of a successful model.. The Bederson (5) score method was employed for qualitative and semiquantitative evaluation, with particular emphasis on motor function evaluation. The balance beam walking ...
1. Li PA, He Q. Mechanisms of hyperglycemia-enhanced ischemic brain damage. Transl Med Res. 2013;3:1-11 2. Capes SE, Hunt D, Malmberg K, Pathak P, Gerstein HC. Stress hyperglycemia and prognosis of stroke in nondiabetic and diabetic patients: a systematic overview. Stroke. 2001;32:2426-2432 3. Rajesh G, Ajay C, Frederick M, Paresh D. Hyperglycemia, insulin, and acute ischemic stroke: A mechanistic justification for a trial of insulin infusion therapy. Stroke. 2006;37:267-273 4. Balan IS, Fiskum G, Hazelton J, Cotto-Cumba C, Rosenthal RE. Oximetry-guided reoxygenation improves neurological outcome after experimental cardiac arrest. Stroke. 2006;37:3008-3013 5. Cipolla MJ, Godfrey JA. Effect of hyperglycemia on brain penetrating arterioles and cerebral blood flow before and after ischemia/reperfusion. Transl Stroke Res. 2010;1:127-134 6. Stead LG, Gilmore RM, Bellolio MF, Mishra S, Bhagra A, Vaidyanathan L, Decker WW, Brown RD Jr. Hyperglycemia as an independent predictor of worse outcome in ...
Increasing evidence suggests that toll-like receptors (TLRs) play an important role in cerebral ischemia-reperfusion injury. The endogenous ligands released from ischemic neurons activate the TLR signaling pathway, resulting in the production of a large number of inflammatory cytokines, thereby causing secondary inflammation damage following cerebral ischemia. However, the preconditioning for minor cerebral ischemia or the preconditioning with TLR ligands can reduce cerebral ischemic injury by regulating the TLR signaling pathway following ischemia in brain tissue (mainly, the inhibition of the TLR4/NF-κB signaling pathway and the enhancement of the interferon regulatory factor-dependent signaling), resulting in TLR ischemic tolerance. Additionally, recent studies found that postconditioning with TLR ligands after cerebral ischemia can also reduce ischemic damage through the regulation of the TLR signaling pathway, showing a significant therapeutic effect against cerebral ischemia. These studies
Cerebral ischemia is a life-threatening condition associated with a substantial morbidity and mortality. Hyperglycemia, a common coexisting phenomenon in both stroke and cardiac arrest (CA), may further aggravate ischemic brain injury. To date, the therapeutic possibilities are lim-ited and the search for new treatment modalities is warranted. One aspect of such a research could be to better understand the cerebral pathogenesis induced by hyperglycemic ischemia-reperfusion.. We investigated the combination of ischemia and hyperglycemia in two experimental models of stroke and CA. The aims were to test the neuroprotective potential of the sulfonated nitrone 2-sulfophenyl-N-tert-butylnitrone (S-PBN) in focal hyperglycemic cerebral ischemia (1), to outline the short-terms effects of hyperglycemia in prolonged (2) and short CA (3) and to performed a global transcriptome analysis of brain from hyperglycemic and normoglycemic CA (4).. In a stroke model rats were made hyperglycemic prior to transient ...
phdthesis{e6a24cb9-3a1a-4b11-91f1-3152114bb8fb, abstract = {Enriched environment (EE) housing significantly ameliorates neurological deficits induced by cortical brain ischemia without changing infarction size, suggesting that EE-related functional benefits are associated with neuronal plasticity events in the remaining tissue. Brain-derived neurotrophic factor (BDNF), nerve growth factor-induced gene A (NGFI-A) and corticosteroid receptors (mineralocorticoid receptor, MR; glucocorticoid receptor, GR) have been demonstrated to be involved in brain plasticity. The purpose of this thesis was to determine if post-ischemic housing conditions had a significant effect on transcription and/or translation of BDNF, NGFI-A and corticosteroid receptors. We found that BDNF gene was down regulated in EE-housed rats when compared to the rats housed in standard cages at 2~12 days after cortical brain ischemia in peri-infarct cortex, contralateral cortex and bilateral hippocampus. The protein level of BDNF in ...
Female gender, which is abolished following ovariectomy and reproductive senescence, is associated with improved outcome following cerebral stroke. Estrogen replacement partially restores this benefit of the female gender but the effect of progesterone in hormone-deficient animals is currently unknown. We evaluated various outcomes following middle cerebral artery occlusion (MCAO) in ovariectomised female mice, with a physiologically relevant restoration of progesterone levels. Ovariectomised female mice had significantly elevated plasma (P=,0.05) and brain progesterone levels (P=,0.01) following implantation of a 21-day release pellet (50mg) compared with mice that received placebo implants 7 days prior to undergoing 60 min MCAO. Assessment of well-being (body weight recovery) and neurological score at 24h and 48h post-MCAO indicated that MCAO significantly worsened outcome compared with sham-operated mice but progesterone had no effect. MCAO resulted in a substantial lesion formation and a ...
Bilateral carotid occlusion coupled with systemic hypotension produces global brain ischemia in the rat, resulting in damage to the...
Older research outputs will score higher simply because theyve had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 222,049 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 1st percentile - i.e., 1% of its contemporaries scored the same or lower than it ...
Reversible protein phosphorylation is under the control of opposing activities of protein kinases and protein phosphatases, and has a crucial role in the regulation of cellular signal transduction in a plethora of neural cell functions, including neurogenesis, differentiation, gene transcription and cell death signalling (Klumpp & Krieglstein, 2002b). During the symposium, expert reviews of research on reversible protein phosphorylation, examples from screening approaches for kinase functions in neurons and studies on particular signalling pathways highlighted the importance of this fast‐emerging topic for the understanding of neuronal cell death, and the development of novel neuroprotective strategies.. Protein kinases have been established as key regulators in many important cellular processes, such as proliferation, maintenance of cell shape, survival signalling and apoptosis. Approximately 500 genes encode members of the kinase family in the human genome, and the predicted human kinome ...
Diabetes is a major risk factor for ischemic stroke and is associated with increased mortality. Additionally, hyperglycemia, a common complication in acute stroke, is associated with poor outcome.In order to identify the correlation between blood glucose and early mortality, multiple logistic regression analyses were used and odds ratios calculated in a retrospective study of 447 stroke patients. Eighty-one patients (18%) had diabetes. The odds ratios for 30-day case-fatality and blood glucose were 1.9 and 1.6 in diabetic and non-diabetic patients respectively. Optimal blood glucose concentrations in respective group were 10.3 and 6.3 mmol/L, as determined by receiver operator characteristic (ROC) curves.Cerebral ischemia triggers different signaling pathways including mitogen-activated protein kinases (MAPK) which regulate fundamental cell functions. In an experimental rat model of combined hyperglycemia and transient middle cerebral artery occlusion (MCAO), the activation pattern of one such ...
Several experimental studies have indicated that nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox) exert detrimental effects on ischemic brain tissue; Nox-knockout mice generally exhibit resistance to damage due to experimental stroke following middle cerebral artery occlusion (MCAO). Furthermore, our previous MCAO study indicated that infarct size and blood-brain barrier breakdown are enhanced in mice with pericyte-specific overexpression of Nox4, relative to levels observed in controls. However, it remains unclear whether Nox affects the stroke outcome directly by increasing oxidative stress at the site of ischemia, or indirectly by modifying physiological variables such as blood pressure or cerebral blood flow (CBF ...
Cerebral hyperperfusion, or reperfusion syndrome, is a rare, but serious, complication following revascularization. Hyperperfusion is defined as a major increase in ipsilateral cerebral blood flow (CBF) that is well above the metabolic demands of the brain tissue.
TY - CHAP. T1 - Histopathology of Cerebral Ischemia and Stroke. AU - Dalton Dietrich, W.. PY - 2017/3/7. Y1 - 2017/3/7. N2 - Ischemic stroke is a serious neurological problem and one of the leading causes of death and disability worldwide. The histopathological consequences of stroke are complex and may result in a variety of deficits including severe motor and cognitive disturbances. The histopathological consequences of severe focal ischemia are well described with characteristic structural changes occurring in both gray and white brain regions depending on the severity, location, and duration of the ischemic insult. Following focal ischemic injury, neuronal, astrocytic, vascular endothelial, and inflammatory cell changes occur. In white mater tracts, axonal injury with oligodendrocyte damage and subsequent demyelination are also commonly observed. In contrast, less severe or more transient ischemic insults can lead to patterns of selective neuronal injury whereby vulnerable neuronal ...
In our previous study, β-hydroxybutyrate (BHB) was found to prolong survival time and to inhibit cerebral edema by improving energy metabolism in the hypoxia, anoxia and global cerebral ischemia models. In this study, the cerebroprotective effect of BHB was examined in rats with permanent (p)-occlusion and transient (t)-occlusion of middle cerebral artery (MCA). BHB (30 mg · kg,sup,−,/sup,,sup,1,/sup, · h,sup,−,/sup,,sup,1,/sup,) was continuously administered through the femoral vein. In rats with p-MCA occlusion, BHB significantly reduced infarct area at 24 h after the occlusion, but not at 72 h after the occlusion. In rats with 2-h t-MCA occlusion followed by 22-h reperfusion, BHB significantly reduced cerebral infarct area, edema formation, lipid peroxidation and neurological deficits. Moreover, in the t-MCA occlusion model, delayed administration of BHB started at 1 h after the initiation of the MCA occlusion also significantly reduced cerebral infarct area. Taking together the ...
1. Stub D, Bernard S, Duffy SJ, Kaye DM. Post cardiac arrest syndrome: a review of therapeutic strategies. Circulation. 2011;123:1428-35 2. Harukuni I, Bhardwaj A. Mechanisms of brain injury after global cerebral ischemia. Neurol Clin. 2006;24:1-21 3. Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, Gutteridge G. et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med. 2002;346:557-63 4. Camara AK, Bienengraeber M, Stowe DF. Mitochondrial approaches to protect against cardiac ischemia and reperfusion injury. Front Physiol. 2011;2:13 5. Honda HM, Korge P, Weiss JN. Mitochondria and ischemia/reperfusion injury. Ann N Y Acad Sci. 2005;1047:248-58 6. Perez-Pinzon MA, Stetler RA, Fiskum G. Novel mitochondrial targets for neuroprotection. J Cereb Blood Flow Metab. 2012;32:1362-76 7. Cour M, Loufouat J, Paillard M, Augeul L, Goudable J, Ovize M. et al. Inhibition of mitochondrial permeability transition to prevent the post-cardiac arrest ...
If the entire ischemic region supplied by the occluded artery evolved into infarction within minutes or even 1 to 2 hours after onset, there would be little if any opportunity to successfully intervene to improve functional and neurologic outcome. Abundant experimental data suggest that brain injury, secondary to an arterial occlusion, is a dynamic process involving varying degrees of early ischemic injury related primarily to the severity of local cerebral blood flow (CBF) impairment. Ischemic regions with very low CBF (,10 mL/100 g/min) rapidly become irreversibly damaged and are referred to as the ischemic core. [14] In stroke models, surrounding or intermixed zones of less severely impaired CBF (approximately 15 to 40 mL/100 g/min) occur and likely also exist in many ischemic stroke patients. This zone of mild to moderately reduced CBF relates to the concept of the ischemic penumbra originally suggested by Astrup et al. [15] As initially defined, the ischemic penumbra encompasses that ...
The present study aimed to investigate the anti-inflammatory effect of 4-methylcyclopentadecanone (4-MCPC) in rats suffering from a cerebral ischemia/ reperfusion (I/R) injury. In this study, the focal cerebral ischemia in rats was induced by middle cerebral artery occlusion (MCAO) for 2 h, and the rats were treated with 4-MCPC (8 mg/kg) just 0.5 h before reperfusion. The ischemic infarct volume was recorded 24 h after the MCAO. In addition, myeloperoxidase (MPO) activity and TNF-α and IL-1β levels in the ischemic cerebral cortex were determined by ELISA, while nuclear translocation of NF-κB p65 subunit and expression of p-IκBα were investigated by western blotting ...
This article examines the pathophysiology of lesions caused by focal cerebral ischemia. Ischemia due to middle cerebral artery occlusion encompasses a densely ischemic focus and a less densely ischemic penumbral zone. Cells in the focus are usually doomed unless reperfusion is quickly instituted. In …
The animal model of stroke that is most frequently used is a rat model of focal brain ischemia caused by middle cerebral artery occlusion (MCAO). Several studies have reported a link between levels of cell-free DNA (CFD) and neurologic outcome in human stroke. The purpose of this study was to assess brain injury and measure CFD levels in 2 models of MCAO in rats, and to determine whether brain injury correlates with CFD. A total of 60 rats were used for this study. Twenty rats underwent a sham procedure, 20 rats had MCAO using a monofilament, and 20 rats had MCAO with a silicon-coated filament. Groups were further divided into 2 subgroups. In 1 subgroup of 10 rats, neurologic performance [measured as a neurologic severity score, (NSS)] was measured at 1 and 24 hours after the procedure, and brain edema and infarct volume were determined at 24 hours. In the second subgroup of 10 rats, CFD was measured at 0, 1, 2, 4, 8, 12, and 24 hours and at 2, 3, 4, and 5 days. Neurologic performance (measured ...
The histologic description of cerebral ischemia is complex, and within most lesions there are regional variations in degrees of neuronal cell injury, edema, and neuropil disruption. These parameters of tissue injury were analyzed histopathologically in transient and permanent experimental cerebral ischemia in 15 rabbits and the results were spatially correlated with MR images of pre- and postmortem (formalin-fixed) brains. MR was performed at 1.5 T (eight animals) and at 0.38 T (seven animals). Areas of high signal on T2-weighted MR images were closely correlated with histologic signs of cytotoxic glial edema and with disruption of the neuropil (widening of the interstitial spaces in the background matrix of glial and neuronal cellular processes), but MR tended to underestimate the extent of ischemic neuronal injury, especially low-grade histologic changes (mild neuronal shrinkage and nuclear basophilia). Low-grade ischemic neuronal changes were often found in the penumbra zone of ischemic ...
Intense efforts are being undertaken to understand the pathophysiological mechanisms triggered after brain ischemia and to develop effective pharmacological treatments. However, the underlying molecular mechanisms are complex and not completely understood. One of the main problems is the fact that the ischemic damage is time-dependent and ranges from negligible to massive, involving different cell types such as neurons, astrocytes, microglia, endothelial cells, and some blood-derived cells (neutrophils, lymphocytes, etc.). Thus, approaching such a complicated cellular response generates a more complex combination of molecular mechanisms, in which cell death, cellular damage, stress and repair are intermixed. For this reason, animal and cellular model systems are needed in order to dissect and clarify which molecular mechanisms have to be promoted and/or blocked.Brain ischemia may be analyzed from two different perspectives: that of oxygen deprivation (hypoxic damage per se) and that of deprivation of
DESCRIPTION (provided by applicant): There is growing evidence that estrogen (E2) and SERMs may have beneficial effects upon the CNS in neurodegenerative diseases. This application would study the potential mechanisms of E2/SERM neuroprotection in cerebral ischemia, and would follow up on exciting preliminary work by our lab which suggests that E2/SERMs enhance neurogenesis following cerebral ischemia. With regards to neuroprotection, our preliminary studies suggest that E2 and the SERM, tamoxifen (TMX) inhibit activation of putative prodeath factors (ROS, ERKs, INK, c-Jun), with an increase in activation of the prosurvival factor, Akt. To confirm these preliminary findings and clarify the underlying mechanisms, Aim 1 would determine the temporal pattern and cell type of ERK/JNK/Akt activation following cerebral ischemia in female animals (which is currently lacking), establish the onset and duration of E2/SERM regulatory effects upon these key kinases, and determine the role of estrogen ...
During recent years neurotransmitters and neuromodulators have been recognized as important extracellular modulators of ischemic and hypoglycemic brain damage. Several investigations have...
Synonyms for Cerebral ischaemia in Free Thesaurus. Antonyms for Cerebral ischaemia. 54 synonyms for stroke: caress, rub, fondle, pat, pet, apoplexy, fit, seizure, attack, shock, collapse, mark, line, slash, movement, action, motion, chime.... What are synonyms for Cerebral ischaemia?
Looking for Cerebral ischemia? Find out information about Cerebral ischemia. Localized tissue anemia as a result of obstruction of the blood supply or to vasoconstriction. a local deficiency of blood; insufficient blood in an organ... Explanation of Cerebral ischemia
Intravenous Administration of Cilostazol Nanoparticles Ameliorates Acute Ischemic Stroke in a Cerebral Ischemia-Reperfusion-Induced Injury Model. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
Intensive attention was recently payed to brain impairment due to acute cerebral ischemia and reperfusion, this paper reports on cortex somatosensory evoked potentials (SEPs), light microscope and electron microscope have been used to study the effect of calcium channel blocker I -65 on the brain impairment due to acute cerebral ischemia and reperfusion. The results suggest that 1-65 can protect electric activily of cerebral cortex neurons and ultrastructure of mitochondria and RER of neurons during acute cerebral ischemia and reperfusion. The mechanism may be blocking Ca2+ channel selectively so that preventing the increase of concentrations of Ca2+ within neurons.
Background Traumatic brain injury is a major medical problem globally and is one of the leading causes of death and disability. There is no known treatment for stroke or ischaemic brain injury. A stroke is a medical emergency and can cause permanent brain damage and death. Risk factors for stroke include old age, high blood pressure, previous stroke or transient ischemic attack (TIA), diabetes, high cholesterol, smoking and heart attack. Stroke is the second leading cause of death worldwide. The Technology This invention has arisen from our discovery of a novel isoform of the TRPC3 ...
This stock medical exhibit compares three coronal views of the head and brain to describe the Progression of Brain Ischemia. The following views are illustrated: 1- Initial infarct in the region of the left cerebral artery. 2- Generalized spread of hypoxia and swelling from the left to right side. 3- Involvement of the right cerebral artery with further brain damage.
What is Cerebral Ischemia? What are its causes? And how can Ischemia be treated effectively? ► Learn more about Cerebral Ischemia now
Interview with Shelagh B. Coutts, MD, FRCPC, author of Rate and Prognosis of Brain Ischemia in Patients With Lower-Risk Transient or Persistent Minor Neurologic
Ferrer Therapeutics has made available CerAxon Oral Solution, a medical food containing citicoline, for the dietary management of brain ischemia due to stroke or traumatic brain injury in patients who have difficulty swallowing.
Atif F, Yousuf S, Agrawal SK. S-allyl L-cysteine diminishes cerebral ischemia-induced mitochondrial dysfunctions in hippocampus ...
Dr. Eatons current research focuses on how dysfunction of astrocytic potassium channels provides a link between diabetes and epilepsy and ischemia-induced brain damage. Diabetics (particularly those with poorly controlled blood glucose) are likely to suffer a stroke and the brain damage that occurs may be more severe or extensive if blood glucose levels are high when a stroke happens. In addition, uncontrolled hyperglycemia (diabetes) increases the susceptibility to epileptiform activity and seizures but the mechanism is still unknown.. ...
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A composition and method for the treatment of cerebral ischemia is disclosed, the composition is a mixture of caffeine and alcohol and is used to treat cerebral ischemia by administering to a subject in need thereof a dose of an effective amount of caffeine and at least a effective amount of an alcohol or mixtures thereof.
Patients who present with symptoms of stroke and who demonstrate hypodensity on CT within first six hours were proven to have larger infarct volumes, more severe symptoms, less favorable clinical courses and they even have a higher risk of hemorrhage ...
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Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day ...
An 8-vessel-occlusion (8VO) method was developed to compare with the conventional 4-vessel-occlusion (4VO) in hippocampal ischemic damage and progenitor cell induction 10 days following ischemia in female rats. Eight posture-relevant tests were perfo
Principal Investigator:ISHII Nagao, Project Period (FY):2002 - 2004, Research Category:Grant-in-Aid for Scientific Research (B), Section:一般, Research Field:Anesthesiology/Resuscitation studies
Brain, Transient, Gelatinase, Ischemia, Mice, Concentration, Brain Ischemia, Cerebral Ischemia, Gelatin, Inhibition, Growth, Hippocampus, Neuroprotective Effects, Tea, Tunel, Oxygen, Artery, Brain Infarction, Infarction, Neuroprotective Effect
There has been much evidence suggesting that reactive oxygen species (ROS) generated in mitochondria during cerebral ischemia play a major role in pro..
Page AB، Owen CR، Kumar R، Miller JM، Rafols JA، White BC، DeGracia DJ، Krause GS (Jul 2003). "Persistent eIF2alpha(P) is colocalized with cytoplasmic cytochrome c in vulnerable hippocampal neurons after 4 hours of reperfusion following 10-minute complete brain ischemia". Acta Neuropathologica. 106 (1): 8-16. PMID 12687390. doi:10.1007/s00401-003-0693-2. الوسيط ...
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by freeoxbio-admin , Mar 15, 2019 , News. FreeOx Biotech has taken on AEC Partners as a strategic partner in the company to accelerate development and marketing of its drug to treat brain ischemia. The priority drug is Ox-01, which is about to begin phase-III clinical trials. AEC Partners analysed the brand ...
Shares of healthcare company Penumbra, Inc. (PEN) gained 5.32% on Tuesday before closing at $168.89. The stock has been trading in a range of $12.40- $185.70 in the past one year and rose nearly 130% in the past three years.
TY - JOUR. T1 - Isovolemic hemodilution in experimental focal cerebral ischemia. Part 1. T2 - Effects on hemodynamics, hemorheology, and intracranial pressure. AU - Tu, Y. K.. AU - Heros, R. C.. AU - Candia, G.. AU - Hyodo, A.. AU - Lagree, K.. AU - Callahan, R.. AU - Zervas, N. T.. AU - Karacostas, D.. PY - 1988/1/1. Y1 - 1988/1/1. N2 - A total of 76 splenectomized dogs were entered in a study of the value and effects of isovolemic hemodilution. Of these, seven were not included in the analysis because of technical errors. Of the remaining 69 dogs, 35 were treated with hemodilution; 28 were subjected to a 6-hour period of temporary occlusion of the distal internal carotid artery and the proximal middle cerebral artery, and seven underwent a sham operation only, with arterial manipulation but no occlusion. The other 34 dogs were not subjected to hemodilution; 26 of these underwent temporary arterial occlusion and eight had a sham operation only. In each group the animals were about equally ...
In this experimental study, the neuroprotective effect of the xanthine oxidase inhibitor allopurinol on focal cerebral ischaemia created by permanent middle cerebral artery occlusion (MCAO) was investigated. Using high performance liquid chromatography (HPLC), we measured hypoxanthine, xanthine, and uric acid (UA) levels in rabbit brains following focal cerebral ischaemia. Rabbits were randomly and blindly assigned into four groups of eight animals each. The control groups received 2% carboxymethylcellulose solution, while 10% allopurinol 150 mg/kg was given to the treatment group 1 h before ischaemia. Each group was subdivided into two groups which were sacrificed 4 h or 24 h after ischaemia, respectively. UA and xanthine values of the rabbits in the control groups were quite high at both times and highest after 24 h, particularly in the centre of the ischaemia. A significant decrease in UA and xanthine values was observed in rabbits that were given allopurinol ( ...
Experimental focal cerebral ischemia was produced in monkeys (Macaca radiata) by occlusion of the right middle cerebral artery (MCA). The release of the lysosomal glycosidases, β-D-hexosaminidase, α-L-fucosidase and α-D-mannosidase into the soluble fraction in the right basal ganglia of the experimental animals was measured at different periods from 30 min to 12 hr after occlusion and compared with the corresponding sham operated control animals. There was a significant increase in the released lysosomal enzymes in the MCA occluded animals at all periods and particularly at 4 hr after occlusion. The CSF from the experimental animals also showed elevated levels of hexosaminidase and fucosidase. The free fatty acids (FFA) measured in the basal ganglia at 30 min and 2 hr after occlusion showed a 100 fold increase in the experimental animals. The predominant fatty acid released was linoleic acid (18:2) followed by arachidonic acid (20:4). Lipid peroxidation in the basal ganglia measured by the ...
TY - JOUR. T1 - Characteristics of Transient Cerebral Ischemia-Induced Deficits on Various Learning and Memory Tasks in Male Mongolian Gerbils. AU - Amano, Manabu. AU - Hasegawa, Masaya. AU - Hasegawa, Takaaki. AU - Nabeshima, Toshitaka. PY - 1993/1/1. Y1 - 1993/1/1. N2 - We examined the characteristics of 5-min cerebral ischemia-induced behavioral deficits in spontaneous locomotor activity and their effects on the performance of habituation (HAB), passive avoidance (PA) and 8-arm radial maze (RM) tasks in Mongolian gerbils. Performances in HAB, PA and RM were impaired within 2 days after occlusion, and gerbils showed hyperlocomotion during this period. Ten days after ischemia, the hyperlocomotion disappeared and performance in the HAB and PA was the same as that in the sham-operated group. Retention in the RM was impaired at that period, but this impairment was overcome, and retention recovered easily to the sham-operated level with a few additional trials. When the acquisition trial in the RM ...
TY - JOUR. T1 - Activation of protein kinase c delta following cerebral ischemia leads to release of cytochrome c from the mitochondria via bad pathway. AU - Dave, Kunjan R.. AU - Bhattacharya, Sanjoy K.. AU - Saul, Isabel. AU - DeFazio, R. Anthony. AU - Dezfulian, Cameron. AU - Lin, Hung Wen. AU - Raval, Ami P.. AU - Perez-Pinzon, Miguel A.. PY - 2011/7/19. Y1 - 2011/7/19. N2 - Background: The release of cytochrome c from the mitochondria following cerebral ischemia is a key event leading to cell death. The goal of the present study was to determine the mechanisms involved in post-ischemic activation of protein kinase c delta (δPKC) that lead to cytochrome c release. Methods/Findings: We used a rat model of cardiac arrest as an in vivo model, and an in vitro analog, oxygen glucose deprivation (OGD) in rat hippocampal synaptosomes. Cardiac arrest triggered translocation of δPKC to the mitochondrial fraction at 1 h reperfusion. In synaptosomes, the peptide inhibitor of δPKC blocked OGD-induced ...
Platelet-Oriented Inhibition in New TIA and minor ischemic stroke (POINT) Trial, is a prospective, randomized, double-blind, multicenter trial with the primary null hypothesis that, in patients with TIA or minor ischemic stroke treated with aspirin 50-325 mg/day, there is no difference in the event-free survival at 90 days in those treated with clopidogrel (600 mg loading dose then 75 mg/day) compared to placebo when subjects are randomized within 12 hours of time last known free of new ischemic symptoms.. Its primary objective is to determine whether clopidogrel 75 mg/day by mouth after a loading dose of 600 mg of clopidogrel is effective in preventing major ischemic vascular events (ischemic stroke, myocardial infarction, and ischemic vascular death) at 90 days when initiated within 12 hours of TIA or minor ischemic stroke onset in patients receiving aspirin 50-325 mg/day (with a dose of 150-200 mg daily for 5 days followed by 75-100 mg daily strongly recommended).. Patients over 18 years of ...
Platelet-Oriented Inhibition in New TIA and minor ischemic stroke (POINT) Trial, is a prospective, randomized, double-blind, multicenter trial with the primary null hypothesis that, in patients with TIA or minor ischemic stroke treated with aspirin 50-325 mg/day, there is no difference in the event-free survival at 90 days in those treated with clopidogrel (600 mg loading dose then 75 mg/day) compared to placebo when subjects are randomized within 12 hours of time last known free of new ischemic symptoms.. Its primary objective is to determine whether clopidogrel 75 mg/day by mouth after a loading dose of 600 mg of clopidogrel is effective in preventing major ischemic vascular events (ischemic stroke, myocardial infarction, and ischemic vascular death) at 90 days when initiated within 12 hours of TIA or minor ischemic stroke onset in patients receiving aspirin 50-325 mg/day (with a dose of 150-200 mg daily for 5 days followed by 75-100 mg daily strongly recommended).. Patients over 18 years of ...
Sekhon, Ainslie and Griesdale identify Cerebral Oedema as one of the factors relevant to secondary brain injury after Hypoxic Ischaemic Brain Injury (HIBI). The authors note that Cerebral Oedema leads to intracranial hypertension which leads to Decreasing Cerebral Perfusion Pressure which leads to Decreasing Cerebral Blood Flow which leads to Reduced regional oxygen saturation…
Background: Given the limited time window available for treatment with tPA in acute ischemic stroke patients, guidelines recommend door-to-imaging time within 25 minutes of hospital arrival and a door-to-needle time (DTN) within 60 minutes. Despite temporal improvements in door-to-image and DTN, tPA treatment times remain suboptimal.. Objectives: To examine the contributions of door-to-image and imaging-to-needle times to delays in timely delivery of tPA to ischemic stroke patients, and to examine between-hospital variation in DTN.. Methods: A cohort analysis of 1,193 ischemic stroke patients treated with intravenous tPA from 2009-2012 at 25 Michigan hospitals participating in the Paul Coverdell National Acute Stroke Registry. The primary outcome was DTN (time in minutes from emergency department arrival to tPA delivery). Multi-level linear regression models included hospital-specific random effects.. Results: Mean patient age was 68 years, median NIHSS score was 11 (IQR 6-17), 51% were female, ...
Ischemic stroke causes neuronal cell death and triggers a cascade of inflammatory signals that contribute to secondary brain damage. Microglia, the brain-resident macrophages that remove dead neurons, play a critical role in the brains response to ischemic injury. Our previous studies showed that IRF2BP2 regulates peripheral macrophage polarization, limits their inflammatory response and reduces susceptibility to atherosclerosis. Here, we show that loss of IRF2BP2 in microglia leads to increased inflammatory cytokine expression in response to lipopolysaccharide challenge and impaired activation of anti-inflammatory markers in response to interleukin-4 (IL4) stimulation. Focal ischemic brain injury of the sensorimotor cortex induced by photothrombosis caused more severe functional deficits in mice with IRF2BP2 ablated in macrophages/microglia, associated with elevated expression of inflammatory cytokines in the brain. These mutant mice had larger infarctions 4 days after stroke associated with fewer
The effect of the free radical spin-trap alpha-phenyl-butyl-tert-nitrone (alpha-PBN) in permanent focal cerebral ischemia in rats was examined in two series of experiments. In the first, rats were subjected to permanent occlusion of the middle cerebral artery (MCAO) and treated 1 h after occlusion with a single dose of alpha-PBN (100 mg/kg) or saline. Body temperature was measured and controlled for the first 24 h to obtain identical temperature curves in the two groups. Cortical infarct volumes were determined on histological sections 7 days later. alpha-PBN did not significantly reduce infarct volume (control: 28.3+/-16.3 mm3 vs. alpha-PBN 23.7+/-7.4 mm3). In the second series of experiments, periinfarct depolarizations (PIDs) were recorded with an extracellular DC electrode at two locations in the ischemic penumbra for the initial 3 h following MCAO. alpha-PBN (100 mg/kg, single dose in conjunction with occlusion) significantly reduced the total number (median value of 3 PIDs in the control ...
article{3f0ddea8-dd33-4fdd-a777-97a29bef9f47, abstract = {Stroke outcome is determined by a complex interplay, where age and stroke severity are predominant predictors. Studies on hemorrhagic stroke indicate that APOE genotype is a predictor of poststroke outcomes,1,2 but results from studies on ischemic stroke are more conflicting.1,3 There is 1 study suggesting an influence of APOE genotype on age at ischemic stroke onset,4 and sex-specific effects on outcome have been reported.5 Taken together, there is a need for larger studies on APOE and ischemic stroke outcomes with integrated information on age, severity, and sex.,br/,,br/,The 3 common APOE alleles ε2, ε3, and ε4 can be separated by a combination of 2 single nucleotide polymorphisms (SNPs), rs429358 and rs7412. Thus, associations with APOE alleles are not directly captured in a regular genome-wide association study (GWAS), where each SNP is investigated separately. We derived the 3 common APOE alleles and investigated the interplay ...
... Cochrane Database Syst Rev. 2008;(3):CD000029. Authors: Sandercock PA, Counsell C, Gubitz GJ, Tseng MC. BACKGROUND: In patients with acute ischaemic stroke, platelets become activated. Antiplatelet therapy might reduce the volume of brain damaged by ischaemia and reduce the risk of early recurrent ischaemic stroke. This might reduce the risk of early death and improve long-term outcome in survivors. However, antiplatelet therapy might also increase the risk of fatal or disabling intracranial haemorrhage. OBJECTIVES: To assess the efficacy and safety of antiplatelet therapy in acute ischaemic stroke. SEARCH STRATEGY: We searched the Cochrane Stroke Group Trials Register (last searched June 2007), the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library Issue 2, 2007), MEDLINE (June 1998 to May 2007), and EMBASE (June 1998 to May 2007). In 1998, for a previous version of this review, we searched the register of the ...
Object. A critical review of the literature indicates that the effects of nitric oxide synthase (NOS) inhibitors on focal cerebral ischemia are contradictory. In this experiment the authors methodically examined the dose-dependent effects of two NOS inhibitors and two NO donors on cortical infarction volume in an animal model of temporary focal cerebral ischemia simulating potential ischemia during neurovascular interventions.. Methods. Ninety-two Wistar rats underwent 3 hours of combined left middle cerebral artery and bilateral common carotid artery occlusion after having been anesthetized with 1% halothane. A nonselective NOS inhibitor, NG-nitro-l-arginine-methyl-ester (l-NAME), and two NO donors, 3-morpholinosydnonimine hydrochloride and NOC-18, DETA/NO, (Z)-1-[2(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate, were administered intravenously 30 minutes before ischemia was induced. A selective neuronal NOS inhibitor, 7-nitroindazole (7-NI), was administered intraperitoneally ...
Evidence suggests that brain infiltration of lymphocytes contributes to acute neural injury after cerebral ischemia. However, the spatio-temporal dynamics of brain-infiltrating lymphocytes during the late stage after cerebral ischemia remains unclear. C57BL/6 (B6) mice were subjected to sham, photothrombosis, or 60-min transient middle cerebral artery occlusion (MCAO) procedures. Infarct volume, neurodeficits, production of reactive oxygen species (ROS) and inflammatory factors, brain-infiltrating lymphocytes, and their activation as well as pro-inflammatory cytokine IFN-γ production were assessed. Brain-infiltrating lymphocytes were also measured in tissue sections from post-mortem patients after ischemic stroke by immunostaining. In mice subjected to transient MCAO or photothrombotic stroke, we found that lymphocyte infiltration persists in the ischemic brain until at least day 14 after surgery, during which brain infarct volume significantly diminished. These brain-infiltrating lymphocytes express
BACKGROUND AND PURPOSE: The purpose of this study was to determine whether neuroprotection is feasible without cerebral blood flow augmentation in experimental permanent middle cerebral artery occlusion. METHODS: Rats were subjected to permanent middle cerebral artery occlusion by the suture occlusion method and were treated 1 hour thereafter with a single 5-minute intravenous infusion of the postsynaptic density-95 protein inhibitor Tat-NR2B9c (7.5 mg/kg) or saline (n=8/group). Arterial spin-labeled perfusion-weighted MRI and diffusion weighted MRI were obtained with a 4.7-T Bruker system at 30, 45, 70, 90, 120, 150, and 180 minutes postmiddle cerebral artery occlusion to determine cerebral blood flow and apparent diffusion coefficient maps, respectively. At 24 hours, animals were neurologically scored (0 to 5), euthanized, and the brains stained with 2-3-5-triphenyl tetrazolium chloride to ascertain infarct volumes corrected for edema. Additionally, the effects of Tat-NR2B9c on adenosine 5
BRAIN ischemia stroke is a devastating disease, with more than 10% stroke patients either severely disabled or dead. Although rodent fil- ament middle cerebral artery occlusion (MCAO) model can mimic human brain ischemic stroke well, its wide use was
MECHANISMS OF TRANSLATION ARREST FOLLOWING FOCAL BRAIN ISCHEMIA by MONIQUE K. LEWIS August 2011 Advisor: Dr. Donald DeGracia Major: Physiology Degree: Doctor of Philosophy The loss of blood flow to the brain is termed ischemia and the subsequent resumption of blood flow is termed reperfusion. Brain ischemia and reperfusion (I/R) occurs primarily following resuscitation from cardiac arrest and stroke and presents one of the most significant clinical challenges. At present, there are no clinically effective pharmacologic interventions to halt brain damage following I/R. The major Aim of this dissertation will be to investigate possible mechanisms involved in neuron death following brain I/R, which may potentially lead to the development of effective therapies. A second major facet of this dissertation will be to address the issue of stroke and diabetes. It is very well established clinically that stroke outcome in diabetic patients is significantly worse than in non-diabetic patients. Diabetes has
33 New Zealand white rabbits were taken and randomly divided into a control group, a hyperbaric air group, and a hyperbaric oxyengation (HBO) group. All were reirrigated types following the creation of acute, incomplete cerebral ischemia. Respective measurements were taken of the overall carotid artery and interior jugular vein blood gases as well as cortical brain tissue homogenate amounts of 6-Keto-PGF1 and TXB2 contained. In conjunction with this, pathological investigations were made. The results were that: the amounts of 6-Keto-PGF1 contained for the HBO group were clearly greatly increased (P< 0.01). TXB2 clearly dropped (P< 0.05). Blood P02 in the HB0 group clearly went up (P < 0.0l). Pathological investigations showed that the HBO groups brain tissue damage was relatively light. Conclusion: there were clear effects on PGI2 and TXA2 with HBO when there was reirrigation after acute cerebral ischemia in the domestic rabbits. This is possibly one mechanism of HBO
Although post-ischemic inflammation induced by the innate immune response is considered an essential step in the progression of cerebral ischemia injury, the role of triggering receptor expressed on myeloid cells 2 (TREM2) in the pathogenesis of ischemic stroke remains to be elucidated. Here, we found that the transcriptional and post-transcriptional levels of TREM2 were increased in cultured primary microglia after oxygen-glucose deprivation and reoxygenation and in the ischemic penumbra of the cerebral cortex after middle cerebral artery occlusion (MCAO) and reperfusion in mice. TREM2 was mainly expressed in microglia, but not in astrocytes, neurons, or oligodendrocytes in mice subjected to MCAO. Manipulating TREM2 expression levels in vitro and in vivo significantly regulated the production of pro- and anti-inflammatory mediators after ischemic stroke. TREM2 overexpression markedly suppressed the inflammatory response and neuronal apoptosis. By contrast, TREM2 gene silencing intensified the ...
TY - JOUR. T1 - Post-ischaemic thyroid hormone treatment in a rat model of acute stroke. AU - Genovese, Tiziana. AU - Impellizzeri, Daniela. AU - Ahmad, Akbar. AU - Cornelius, Carolin. AU - Campolo, Michela. AU - Cuzzocrea, Salvatore. AU - Esposito, Emanuela. PY - 2013/6/4. Y1 - 2013/6/4. N2 - Stroke is a devastating brain injury that is a leading cause of adult disability with limited treatment options. We examined the effects of prohormone thyroxine (T4) and the underlying mechanisms in the post-ischaemic rat brain after transient focal cerebral ischemia-induced brain injury. Ischaemic injury was induced for 2 h by middle cerebral artery occlusion (MCAo) followed by 24-h reperfusion. T4 (1.1 μg/100 g BW) was administered by intraperitoneally injection twice, at 1 after the onset of ischemia and 6 h after reperfusion. Cerebral infarct area and infarct volume were measured 24 h after MCAo. Furthermore, the mechanism of neuroprotective effect of T4 was investigated with a focus on inflammatory ...
Antagonism of the adenosine A2A receptor (A2AR) has been shown to elicit substantial neuroprotective properties when given immediately after cerebral ischemia. We asked whether the continuous application of a selective A2AR antagonist within a clinically relevant time window will be a feasible and effective approach to treat focal cerebral ischemia. To answer this question, we subjected 20 male spontaneously hypertensive rats to permanent middle cerebral artery occlusion and randomized them equally to a verum and a control group. Two hours after stroke onset, the animals received a subcutaneous implantation of an osmotic minipump filled with 5 mg kg−1 day−1 8-(3-chlorostyryl) caffeine (CSC) or vehicle solution. The serum level of CSC was measured twice a day for three consecutive days. The infarct volume was determined at days 1 and 3 using magnetic resonance imaging. We found the serum level of CSC showing a bell-shaped curve with its maximum at 36 h. The infarct volume was not affected by ...
Lipoic acid (LA) is a naturally occurring compound and dietary supplement with powerful antioxidant properties. Although LA is neuroprotective in models of stroke, little is known about the cellular mechanisms by which it confers protection during the early stages of ischemia. Here, using a rat model of permanent middle cerebral artery occlusion (MCAO), we demonstrated that administration of LA 30 min prior to stroke, reduces infarct volume in a dose dependent manner. Whole-cell patch clamp Show moreLipoic acid (LA) is a naturally occurring compound and dietary supplement with powerful antioxidant properties. Although LA is neuroprotective in models of stroke, little is known about the cellular mechanisms by which it confers protection during the early stages of ischemia. Here, using a rat model of permanent middle cerebral artery occlusion (MCAO), we demonstrated that administration of LA 30 min prior to stroke, reduces infarct volume in a dose dependent manner. Whole-cell patch clamp ...
Our results for diabetes duration are consistent with prior research conducted within a general population of patients, which found an increased rate of ischemic stroke as duration increased compared with nondiabetic patients (9,10). However, our results for HbA1c in diabetic patients with AF are not consistent with prior research conducted in diabetic patients in general. In our study, increased HbA1c did not have a substantial effect on the rate of ischemic stroke, whereas elevated HbA1c was significantly associated with ischemic stroke in predominantly non-AF populations (11-13). A possible reason for HbA1c having no association with ischemic stroke in diabetic patients with AF is the difference in the primary mechanism for stroke in diabetic patients with and without AF. Among patients with diabetes without AF, stroke is often due to underlying atherosclerosis (22,23). This mechanism may not be as important among diabetic patients with AF, because the primary mechanism for ischemic stroke is ...
Recurrent strokes make up almost 25% of the nearly 800,000 strokes that occur annually in the United States. Risk factors for ischemic stroke include hypertension, diabetes mellitus, hyperlipidemia, sleep apnea, and obesity. Lifestyle modifications, including tobacco cessation, decreased alcohol use, and increased physical activity, are also important in the management of patients with a history of stroke or transient ischemic attack. Antiplatelet therapy is recommended to reduce the risk of recurrent ischemic stroke. The selection of antiplatelet therapy should be based on timing, safety, effectiveness, cost, patient characteristics, and patient preference. Aspirin is recommended as initial treatment to prevent recurrent ischemic stroke. Clopidogrel is recommended as an alternative monotherapy and in patients allergic to aspirin. The combination of clopidogrel and aspirin is not recommended for long-term use (more than two to three years) because of increased bleeding risk. Aspirin/dipyridamole is at
Oxidative stress induced cell injury is reported to contribute to the pathogenesis of cerebral ischemia. Reactive oxygen species such as hydrogen peroxide (H2O2) and superoxide radical along with nitric oxide and peroxynitrite generated during ischemia-reperfusion injury, causes the overactivation of poly (ADP-ribose) polymerase (PARP) leading to neuronal cell death. In the present study we have evaluated the effects of PARP inhibitor, 8-hydroxy-2 methyl-quinazolin-4-[3H]one (NU1025) in H2O2 and 3-morphilinosyndonimine (SIN-1) induced cytotoxicity in PC12 cells as well as in middle cerebral artery occlusion (MCAO) induced focal cerebral ischemia in rats. Exposure of PC12 cells to H2O2 (0.4 mM) and SIN-1 (0.8 mM) resulted in a significant decrease in cell viability after 6 h. Pretreatment with NU1025 (0.2 mM) restored cell viability to approximately 73 and 82% in H2O2 and SIN-1 injured cells, respectively. In MCAO studies, NU1025 was administered at different time points (1 h before reperfusion, ...
Carbamylerythropoietin (CEPO) does not bind to the classical erythropoietin (EPO) receptor. Nevertheless, similarly to EPO, CEPO promotes neuroprotection on the histologic level in short-term stroke models. In the present study, we investigated whether CEPO and other nonerythropoietic EPO analogs could enhance functional recovery and promote long-term histologic protection after experimental focal cerebral ischemia. Rats were treated with the compounds after focal cerebral ischemia. Animals survived 1, 7, or 60 days and underwent behavioral testing (sensorimotor and foot-fault tests). Brain sections were stained and analyzed for Iba-1, myeloperoxidase, Tau-1, CD68 (ED1), glial fibrillary acidic protein (GFAP), Fluoro-Jade B staining, and overall infarct volumes. Treatment with CEPO reduced perifocal microglial activation (P, 0.05), polymorphomonuclear cell infiltration (P, 0.05), and white matter damage (P , 0.01) at 1 day after occlusion. Carbamylerythropoietin- treated rats showed better ...
Nitroxyl (HNO) donor compounds function as potent vasorelaxants, improve myocardial contractility and reduce ischemia-reperfusion injury in the cardiovascular system. With respect to the nervous system, HNO donors have been shown to attenuate NMDA receptor activity and neuronal injury, suggesting that its production may be protective against cerebral ischemic damage. Hence, we studied the effect of the classical HNO-donor, Angelis salt (AS), on a cerebral ischemia/reperfusion injury in a mouse model of experimental stroke and on related in vitro paradigms of neurotoxicity. I.p. injection of AS (40 mumol/kg) in mice prior to middle cerebral artery occlusion exacerbated cortical infarct size and worsened the persistent neurological deficit. AS not only decreased systolic blood pressure, but also induced systemic oxidative stress in vivo indicated by increased isoprostane levels in urine and serum. In vitro, neuronal damage induced by oxygen-glucose-deprivation of mature neuronal cultures was exacerbated
Polyamines are ubiquitous components of all eukaryotic cells and are found in brain tissue. A number of studies have shown that changes in the levels of polyamines occur following cerebral ischaemia. However, whether polyamines are neurotoxic or neuroprotective in ischaemia still remains unclear, although most of the evidence points to a toxic effect. The polyamine/NMDA antagonist N1-dansyl-spermine has been shown to be neuroprotective in a global ischaemia model. However, at the onset of the present study, the neuroprotective potential of this compound was not known in using focal ischaemia models, which are of more clinical relevance. Very recently, more novel polyamine analogues (BU31b, BU37b, BU33b, BU36b and BU43b) have been synthesized. These compounds, with the exception of BU37b, have shown some polyamine antagonist potential in vivo. Therefore these polyamine analogues are candidate neuroprotective agents. The pre-ischaemic effect of all these compounds mentioned above was investigated ...
Looking for online definition of ischemic penumbra in the Medical Dictionary? ischemic penumbra explanation free. What is ischemic penumbra? Meaning of ischemic penumbra medical term. What does ischemic penumbra mean?
Latest industry research report on Acute Ischemic Stroke Diagnosis and Treatment Market. Ischemic stroke is caused by a dysfunction in the supply of blood to the brain due to emboli, thrombus or atherosclerosis occurring in cerebral arteries. According to a World Health Organization (WHO) estimate, around 17 million people die every year due to cardiovascular diseases.. Heart attacks and strokes respectively account for the highest number of deaths due to cardiovascular diseases, globally. The statistics of the Centres for Disease Control and Prevention suggest that about 87% of all strokes are ischemic strokes. Stroke is one of the leading causes of long term disability, occurring at a higher rate in the old age population.. Get Free Sample Report Of Acute Ischemic Stroke Diagnosis and Treatment Market @ http://www.marketresearchstore.com/report/world-acute-ischemic-stroke-diagnosis-and-treatment-market-71669#RequestSample. Moreover, stroke leads to 1 out of every 20 deaths, costing around $34 ...
TY - JOUR. T1 - Neuroprotection of selenite against ischemic brain injury through negatively regulating early activation of ASK1/JNK cascade via activation of PI3K/AKT pathway. AU - Wang, Qing. AU - Zhang, Quan Guang. AU - Wu, Dong Na. AU - Yin, Xiao Hui. AU - Zhang, Guang Yi. PY - 2007/1. Y1 - 2007/1. N2 - Aim: To investigate whether selenite, a known antioxidant, could decrease the activation of apoptosis signal regulating kinase 1/c-jun N-terminal kinase (ASK1/ JNK) signaling cascade in cerebral ischemia/reperfusion (I/R) by activating the phosphatidylinositol 3-kinase (PI3K)/AKT pathway in rat hippocampi, and the neuroprotective effect of selenite against ischemic injury after 15 min of transient brain ischemia. Methods: Transient global brain ischemia was induced by 4-vessel occlusion into adult male Sprague-Dawley rats weighing 250-300 g. The rats were pretreated only with selenite (0.3 mg/kg dissolved in 0.9% saline) every 24 h for 7 d by means of intravenous injection of the tail or ...
Background: Most ischaemic strokes are caused by blood clots blocking an artery in the brain. Clot prevention with anticoagulants might improve outcome if bleeding risks were low. This is an update of a Cochrane review first published in 1995, and previously updated in 2004. Objectives:To assess the effect of anticoagulant therapy versus control in the early treatment (less than 14 days) of Patients with acute ischaemic stroke. Search strategy: We searched the Cochrane Stroke Group Trials Register (last searched 2 October 2007), and two Internet clinical trials registries for relevant ongoing studies (last searched October 2007). Selection criteria: Randomised trials comparing early anticoagulant therapy (started within two weeks of stroke onset) with control in Patients with acute presumed or confirmed ischaemic stroke. Data collection and analysis: Two review authors independently selected trials for inclusion, assessed trial quality, and extracted the data. Main results: Twenty-four trials involving
Zanzmera P, Srivastava P, Garg A, Bhatia R, Singh M, Tripathi M, Prasad K. Prediction of stroke outcome in relation to alberta stroke program early CT score (ASPECTS) at admission in acute ischemic stroke: A prospective study from tertiary care hospital in north india. Neurology Asia 2012;17(2):101-7.. ...
Ischemic stroke is major cause of disability and mortality worldwide, and aging is strong risk factor for poor post-stroke outcome. Neutrophils traffic rapidly to the brain following ischemic stroke, and recent evidence has suggested that aging may alter neutrophil function after tissue injury. In this study, we hypothesize that aging enhances the pro-inflammatory function of neutrophils, directly contributing to the poorer outcomes seen in aging patients. We utilized demographic data and biological specimens from ischemic stroke patients and an experimental mouse model to determine the correlation between age, neutrophil function and stroke outcomes. In ischemic stroke patients, age was associated with increased mortality and morbidity and higher levels of neutrophil-activating cytokines. In mice, aged animals had higher stroke mortality and morbidity, higher levels of neutrophil-activating cytokines and enhanced generation of neutrophil reactive oxygen species compared to young mice. Finally,
BACKGROUND: Early risk of stroke after a transient ischaemic attack (TIA) can be reliably predicted with risk scores based on clinical features of the patient and the event, but it is unclear how these features correlate with findings on brain imaging and few studies have investigated this in the subacute phase. METHODS: Two hundred consecutive patients attending a specialist clinic underwent diffusion-weighted brain imaging (DWI) on the day of the clinic (| or =3 days after a TIA) and the presence of recent lesions (positive DWI) was related to the presence of clinical features associated with a high stroke risk and to 2 validated risk scores (ABCD and California). RESULTS: Thirty-one patients (16%) had positive DWI. Increasing ABCD and California scores were associated with positive DWI (p = 0.02 for both) independent of the delay from TIA to scan. CONCLUSION: Presence of recent ischaemic lesions on DWI correlates with validated clinical scores for risk of stroke after TIA in patients scanned
Recent trials of antithrombotic therapy in patients with coronary artery disease (CAD) have demonstrated substantial reductions in ischemic stroke. Our aim was to examine ischemic stroke risk in patients with CAD and to identify those at highest risk. We examined ischemic stroke risk in patients without atrial fibrillation who underwent coronary angiography between 2004 and 2012. Patients were stratified according to presence or absence of CAD and further stratified by extent of CAD (0 vessel disease [VD], 1 VD, 2 VD, 3 VD, and diffuse VD). End points were composites of ischemic stroke, transient ischemic attack (TIA), and systemic embolism, as well as major adverse cardiovascular and cerebrovascular events (MACCE) defined as cardiac death, myocardial infarction, plus ischemic stroke, TIA, and systemic embolism. Adjusted incidence rate ratios (IRRs) were estimated. A total of 68,829 patients were included, 25,032 had 0 VD, 4,736 had diffuse VD, 18,471 had 1 VD, 10,588 had 2 VD, and 10,002 had 3 ...
36-. ISBN 978-0-306-48644-9. Eugene I. Gusev; Veronika I. Skvortsova (30 April 2003). Brain Ischemia. Springer Science & ... It was under investigation by Acea Pharmaceuticals as a neuroprotective agent for the treatment of cerebral ischemia associated ...
Nonthrombolytic approach to acute brain ischemia". Critical Care Clinics. 15 (4): 755-776. doi:10.1016/s0749-0704(05)70086-5. ... In the early 1990s he coined the phrase Time is Brain!, as an argument for the need to expedite the treatment of stroke victims ... additional History Gomez CR: Time is Brain! J Stroke and Cerebrovasc Dis 3:1-2. 1993, additional Time Gomez CR, Malkoff MD, ... He has written in his specialty and is credited with having coined the phrase Time is Brain! to denote the urgency required in ...
"Hippo/YAP signaling pathway mitigates blood-brain barrier disruption after cerebral ischemia/reperfusion injury". Behavioural ... signaling pathway may exert neuroprotective effects through mitigating blood-brain barrier disruption after cerebral ischemia/ ... Brain Research. 356: 8-17. doi:10.1016/j.bbr.2018.08.003. PMC 6193462. PMID 30092249.. ...
The deletion of p66SHC also protects from ischemia/reperfusion brain injuries through blunted production of free radicals.[14] ...
... brain, and lung injury; injury due to ischemia in the heart, brain, kidney, and gut; and stress-induced central nervous system ... Based on these and other studies, the overproduction of cyclopentenone prostaglandins by the brain has been suggested to ... 14-PGJ2 appears to cause the dilation of coronary arteries and thereby protect against cardiac ischemia and heart attack in a ...
... d-Deprenyl attenuates apoptosis in experimental brain ischaemia". European Journal of Pharmacology. 430 (2-3): 235-241. doi: ... Molecular Brain Research. 49 (1-2): 127-136. doi:10.1016/S0169-328X(97)00135-6. PMID 9387872. Srinivasan ThyagaRajan; Kelley S ...
On 7 October 2017, Mele died, aged 60, of a brain ischemia. "Morto l'ex parlamentare Udc Cosimo Mele". La Stampa (in Italian). ...
"Matrix Metalloproteinases in Ischemia - Reperfusion Injury in Brain: Anti-oxidants as Rescuer". Role of Proteases in Cellular ... "Matrix Metalloproteinases in Ischemia - Reperfusion Injury in Brain: Anti-oxidants as Rescuer". Role of Proteases in Cellular ... brain, oral, breast, pancreatic, blood and cervical cancers. He led a team of scientists who worked on the therapeutic ...
"Endocannabinoids mediate neuroprotection after transient focal cerebral ischemia". Brain Research. 1240: 213-220. doi:10.1016/j ... Proposed role in the diseased brain". Experimental Neurology. 224 (1): 48-55. doi:10.1016/j.expneurol.2010.03.022. PMID ... Brain, Behavior, and Immunity. 25 (6): 1099-1112. doi:10.1016/j.bbi.2011.02.006. PMID 21354467. Scuderi, C.; Esposito, G.; ... "Palmitoylethanolamide Reduces Early Renal Dysfunction and Injury Caused by Experimental Ischemia and Reperfusion in Mice". ...
"Honokiol protects rat brain from focal cerebral ischemia-reperfusion injury by inhibiting neutrophil infiltration and reactive ... Because of its physical properties, honokiol can readily cross the blood brain barrier and the blood-cerebrospinal fluid ... Studies examining honokiol as a protective therapy against focal cerebral ischemia-reperfusion injury have identified a number ... "Honokiol inhibits the inflammatory reaction during cerebral ischemia reperfusion by suppressing NF-κB activation and cytokine ...
"Neuroprotective role of a brain-enriched tyrosine phosphatase, STEP, in focal cerebral ischemia". The Journal of Neuroscience. ... a subfamily of brain-enriched protein tyrosine phosphatases". Brain Research. Molecular Brain Research. 32 (1): 87-93. doi: ... Thus, STEP levels or activity is decreased in Huntington's disease, cerebral ischemia, alcohol abuse, and stress disorders. The ... was the first brain-specific PTP discovered. The human STEP locus maps to chromosome 11p15.2-p15.1 and the murine STEP gene to ...
These symptoms can be indicative of insufficient blood flow to the brain (ischemia) as well as compression of arterioles. In ... Compression then results in diminished blood supply to the brain, a condition known as cerebral ischemia. alpha-1 adrenergic ... 2005). "Value of Cushing Reflex as warning sign for brain ischemia during neuroendoscopy". Br J Anaes. 94 (6): 791-9. doi: ... Brain plateau wave changes are also associated with the Cushing reflex. These waves are characterized by acute rises of the ICP ...
"MiR-497 regulates neuronal death in mouse brain after transient focal cerebral ischemia". Neurobiology of Disease. 38 (1): 17- ... "MicroRNAs Show Mutually Exclusive Expression Patterns in the Brain of Adult Male Rats". PLoS ONE. 4 (10): e7225. doi:10.1371/ ...
"Neuroprotective role of a brain-enriched tyrosine phosphatase, STEP, in focal cerebral ischemia". The Journal of Neuroscience. ... The expression of PTPN5 is restricted to the brain. Differential expression of PTPN5 is found in many brain regions, with no ... Decreased levels of PTPN5 has been implicated in Huntington's disease, cerebral ischemia alcohol abuse, and stress disorders. ... Brain, and Behavior. 11 (5): 586-600. doi:10.1111/j.1601-183X.2012.00781.x. PMC 3922131 . PMID 22405502. Kurup P, Zhang Y, Xu J ...
"Neuroprotection against hypoxia-ischemia in neonatal rat brain by novel superoxide dismutase mimetics". Neuroscience Letters ... M40401 was also found to protect against hypoxic-ischemic brain injury. Mn (III) Salen complexes are found to be more stable ... causing a one hundredfold increase in catalytic activity in treatment of ischemia-reperfusion injuries. ...
Prevention of brain ischemia: The prevention of brain ischemia is aided by decreasing the amount of CSF in the limited space ... Clearing waste: CSF allows for the removal of waste products from the brain,[1] and is critical in the brain's lymphatic system ... Buoyancy: The actual mass of the human brain is about 1400-1500 grams; however, the net weight of the brain suspended in CSF is ... CSF acts as a cushion or buffer for the brain, providing basic mechanical and immunological protection to the brain inside the ...
Potential mechanism for brain ischemia reperfusion injury". Journal of Cerebral Blood Flow and Metabolism. 37 (12): 3649-3658. ... Recent studies have examined other roles of complex I activity in the brain. Andreazza et al. (2010) found that the level of ... Defects in this enzyme are responsible for the development of several pathological processes such as ischemia/reperfusion ... This can take place during tissue ischaemia, when oxygen delivery is blocked.[48] ...
This is especially important after an ischemia, when arachidonic acid levels are elevated. The brain prefers to use choline to ... "Does CDP-choline modulate phospholipase activities after transient forebrain ischemia?". Brain Research. 893 (1-2): 268-72. doi ... "Neuroprotection afforded by prior citicoline administration in experimental brain ischemia: effects on glutamate transport". ... Once these cross the blood-brain barrier it is reformed into citicoline by the rate-limiting enzyme in phosphatidylcholine ...
Effects of ischemia and electroconvulsive shock on free fatty acid pool in the brain. Biochim Biophys Acta 218:1-10, 1970 Bazan ... Implications in cerebral ischemia. Prog in Brain Res 96:247-257, 1993 Giusto NM, Bazan NG: Phosphatidic acid of retinal ... Bazan demonstrated that brain ischemia triggers the release of free essential fatty acids (arachidonic and docosahexaenoic acid ... J Lipid Res 24:628-638, 1983 Aveldano MI, Bazan NG: Differential lipid deacylation during brain ischemia in a homeotherm and a ...
"Blood-brain barrier taurine transport during osmotic stress and in focal cerebral ischemia". Journal of Cerebral Blood Flow and ... Taurine crosses the blood-brain barrier and has been implicated in a wide array of physiological phenomena including inhibitory ... Tsuji, A; Tamai, I (1996). "Sodium- and chloride-dependent transport of taurine at the blood-brain barrier". Advances in ... Urquhart, N; Perry, TL; Hansen, S; Kennedy, J (1974). "Passage of taurine into adult mammalian brain". Journal of ...
Functional changes include evidence of ischemia in vessels of the brain (ICA, ACA, MCA, specifically). It is important to also ... The arteries are either sewn directly into the brain circulation, or placed on the surface of the brain to reestablish new ... brain reaching out to grasp and develop new and more efficient means of bringing blood to the brain and bypassing the areas of ... The artery is then sutured to a branch of the middle cerebral artery on the surface of the brain and the bone is replaced. In ...
Bobu died in 2014 in a Bucharest hospital, as the result of a brain ischemia. He married Maria Cristian in 1957; she served as ...
... causes an altered mental status due to ischemia in the brain.[1] ... Reduced breathing effort (drug effects, brain stem lesion, extreme obesity). *A decrease in the area of the lung available for ...
"Beneficial Effect of Agmatine on Brain Apoptosis, Astrogliosis, and Edema after Rat Transient Cerebral Ischemia." BMC ... Also, agmatine is a neurotransmitter, which means it is a chemical substance inside the brain that allows communication between ... Halaris A, Plietz J (2007). "Agmatine : metabolic pathway and spectrum of activity in brain". CNS Drugs. 21 (11): 885-900. doi: ... It is synthesized in the brain, stored in synaptic vesicles, accumulated by uptake, released by membrane depolarization, and ...
Elevated MMP9 levels can be found in the cases of rheumatoid arthritis and focal brain ischemia. One of MMP9's most widely ... activities in human brain after focal ischemia". Neuroscience Letters. 238 (1-2): 53-6. doi:10.1016/s0304-3940(97)00859-8. PMID ... Brain. 128 (Pt 7): 1622-33. doi:10.1093/brain/awh489. PMID 15800021. Vandooren J, Van den Steen PE, Opdenakker G (2013). " ... "Time course of upregulation of inflammatory mediators in the hemorrhagic brain in rats: correlation with brain edema". ...
... an endogenous clonidine-displacing substance in the brain. Science. 1994 Feb 18;263(5149):966-9. PMID 7906055 ... Neuroprotective effect of agmatine in rats with transient cerebral ischemia using MR imaging and histopathologic evaluation. ...
... and ethical grounds that a person dies when brain death occurs.1Yet, the brain is highly vulnerable to a... ... The singular importance of the brain to life is exemplified by agreement on medical, legal, ... Brain Ischemia Global Ischemia Focal Ischemia Ischemic Brain Injury Global Brain Ischemia These keywords were added by machine ... Nemoto E.M. (1985) Brain Ischemia. In: Lajtha A. (eds) Alterations of Metabolites in the Nervous System. Springer, Boston, MA. ...
Focal brain ischemia occurs when a blood clot has occluded a cerebral vessel. Focal brain ischemia reduces blood flow to a ... During brain ischemia, the brain cannot perform aerobic metabolism due to the loss of oxygen and substrate. The brain is not ... The causes of brain ischemia vary from sickle cell anemia to congenital heart defects. Symptoms of brain ischemia can include ... Brain ischemia (a.k.a. cerebral ischemia, cerebrovascular ischemia) is a condition in which there is insufficient blood flow to ...
It is well-established that ischemia leads to very complex and heterogenous changes in microcirculation and metabolism of the ... Raichle, M. A., 1983, The pathophysiology of brain ischemia, Ann. Neurol., 13: 2.PubMedCrossRefGoogle Scholar ... Middle Cerebral Artery Brain Cortex Sham Control Ischemic Brain Damage Stroke Group These keywords were added by machine and ... Microcirculation and Mitochondrial Function in Focal Brain Ischemia. In: Longmuir I.S. (eds) Oxygen Transport to Tissue VIII. ...
This reduction in blood flow restricts oxygen to the brain and may result in dead brain tissue, cerebral infarction... ... Cerebral or brain ischemia occurs when there is not enough blood flow to the brain. ... Brain ischemia may be categorized as focal ischemia or global ischemia, and the cause for ischemia can range from congenital ... brain ischemia may result in irreversible brain damage, stroke or cardiac arrest. Treatments for brain ischemia include ...
The small-animal model of focal cerebral ischemia produced by occluding a middle cerebral (MCA) of the rat has already proved ... Specific Gravity Middle Cerebral Artery Occlusion Caudate Nucleus Brain Edema Focal Cerebral Ischemia These keywords were added ... Shigeno T., Teasdale G.M., McCulloch J., Mandelow D., Graham D.I. (1984) Brain Edema Following Focal Cerebral Ischemia in the ... Schuier FJ, Hossmann KA: Experimental brain infarcts in cats. II. Ischémie brain edema. Stroke 11: 593-601 (1980).CrossRef ...
Brain ischemia is an interruption of the supply of blood to the brain, which disrupts the flow of oxygen and nutrients that are ... Brain ischemia is an interruption of the supply of blood to the brain, disrupting the flow of oxygen and nutrients needed to ... Most commonly, brain ischemia involves not the carotid artery, but one of the smaller blood vessels in the brain. Blood vessels ... When brain ischemia involves the areas of the brain responsible for regulating functions such as breathing and heart rate, this ...
To clarify the underlying mechanism, the influence of acute ischemic insult to the brain on gastric hemodynamics and mucosal ... Brain ischemia is often accompanied by acute gastric lesions. ... brain ischemia gastric mucosal blood flow integrity of the ... One hour after brain ischemia, gastric mucosal blood flow decreased to 71% of the preischemic levels in the control rats but ... Brain ischemia is often accompanied by acute gastric lesions. To clarify the underlying mechanism, the influence of acute ...
Role of oxygen free radicals in carcinogenesis and brain ischemia.. Floyd RA1. ... may be a key event in stroke-induced brain injury. Oxygen free radicals may play a key role in carcinogenesis by mediating ... recent results show that oxidative damage plays a key role in brain injury that occurs in stroke. Subtle changes, such as ...
... Call for Papers. Brain injury of diverse ... Transient global ischemic brain injury may result from cardiac arrest where cerebral perfusion diminishes to the point that ... How different or similar the mechanisms of these two brain injuries and their management are and whether they can be grouped ... We invite our peers to submit original research and review articles that seek to define the mechanisms of brain injury after ...
This project is supported by the Canadian Institutes of Health Research (award #111062), Alberta Innovates - Health Solutions, and by The Metabolomics Innovation Centre (TMIC), a nationally-funded research and core facility that supports a wide range of cutting-edge metabolomic studies. TMIC is funded by Genome Alberta, Genome British Columbia, and Genome Canada, a not-for-profit organization that is leading Canadas national genomics strategy with funding from the federal government. Maintenance, support, and commercial licensing is provided by OMx Personal Health Analytics, Inc. Designed by Educe Design & Innovation Inc. ...
Brain Ischemia: Alzheimers Disease Mechanisms. Ryszard Pluta, MD, PhD (Editor). Head of Laboratory of Ischemic and ... Chapter 9. Dual Role of Autophagy in Ischemia-Reperfusion Brain Injury: Linking Ischemic Autophagy to Alzheimers Disease. ( ... Dual Role of Mitophagy Following Ischemia-Reperfusion Brain Injury: Ischemic Mitophagy Link to Alzheimers Disease. (Marzena ... Chapter 4. Alzheimers Disease-Related Proteins Following Ischemia-Reperfusion Brain Injury. (Ryszard Pluta, MD, PhD, Marzena ...
... Ling-Hua Tang, Zhong-Yuan Xia ... It has been confirmed that PCr is effective in preventing and treating cardiac and renal ischemia-reperfusion injury. In this ... indicated that PCr can decrease the morphological damage and the neuron apoptosis of the ischemia-reperfusion injury brain ... Compared with sham-operated group (sham group), TUNEL-positive cells, MDA, and level of CaM activity increased in ischemia- ...
Affiliations: Center of Excellence for Aging & Brain Repair, Department of Neurosurgery & Brain Repair, University of South ... Rather than the conventional cell replacement mechanism, we advance alternative pathways of graft-mediated brain repair ...
The brain can store so little energy reserves that it is highly sensitive to ischemia and hypoxia. Studies have shown that ... In ischemia-reperfusion injury brain, the apoptotic neurons extensively exist. The cytoplasm is light red with uneven ... Phosphocreatine Preconditioning Attenuates Apoptosis in Ischemia-Reperfusion Injury of Rat Brain. Ling-Hua Tang, Zhong-Yuan Xia ... ischemia-reperfusion group (I/R group, ), PCr preconditioning group (PCr group, ). The rats were anesthetized by 10% chloral ...
... brain disorder) abbreviated? H/I stands for Hypoxia-Ischemia (brain disorder). H/I is defined as Hypoxia-Ischemia (brain ... New trends in brain hypoxia ischemia research. Effects of the 21-amino steroid tirilazad mesylate (U-74006F) on brain damage ... and practitioners contribute nine chapters on recent and significant research on brain hypoxia-ischemia. ... S.v. "H/I." Retrieved March 21 2019 from https://www.acronymfinder.com/Hypoxia_Ischemia-(brain-disorder)-(H%2fI).html ...
Ischemia of the brain is a reduction of cerebral blood flow below a critical threshold necessary for maintaining normal ... Hossmann, K.-A.: Total ischemia of the brain. In: Brain and heart infarct. Zülch, K.J. et al. (eds.), pp. 107-122. Berlin, ... Kleihues, P., Hossmann, K.-A.: Protein synthesis in the cat brain after prolonged cerebral ischemia. Brain Res. 35, 409-418 ( ... 1979) Cerebral Dysfunction Related to Local and Global Ischemia of the Brain. In: Hoffmeister F., Müller C. (eds) Brain ...
Using an intranasal administration route in a rat model of focal cerebral ischemia, we demonstrate that nose-to-brain delivery ... surgery results in the delivery and retention of FBP in Fas-expressing ischemic areas of the brain. A single intranasal ... reduced neurologic deficit scores and recovery from cerebral ischemia. Intranasally delivered FBP might be a promising strategy ... that by obstructing Fas signaling in cerebral ischemia inhibits apoptosis. ...
Brain ischemia may be analyzed from two different perspectives: that of oxygen deprivation (hypoxic damage per se) and that of ... systems are needed in order to dissect and clarify which molecular mechanisms have to be promoted and/or blocked.Brain ischemia ... is one of the players deregulated after ischemia and OGD. In addition, neuroprotective intervention either by estradiol or by ... Intense efforts are being undertaken to understand the pathophysiological mechanisms triggered after brain ischemia and to ...
... studies have suggested both exercise and mitochondrial biogenesis contribute to improved post-ischemic recovery of brain ... In the ischemia-exercise group, only peroxisome proliferator activated receptor coactivator-1 (PGC-1) expression was increased ... On the other hand, the benefit of exercise-induced mitochondrial biogenesis in brain has been confirmed. In this study, we ... We subjected adult male rats to ischemia, followed by either treadmill exercise or non-exercise and analyzed the effect of ...
... in brain tissue in simulated ischemia in rats. The study seeks to cast light on NO as a signalling molecule in a modeled ... "The development of brain ischemia is often commonly referred to not only by physicians, but also other "specialists" as James ... In this new study, the team of scientists conducted experimental analysis of NO role in brain tissue in simulated ischemia in ... Nitric oxide: Experimental analysis of its role in brain tissue in simulated ischemia. Pensoft Publishers ...
Novel docosanoids inhibit brain ischemia-reperfusion-mediated leukocyte infiltration and pro-inflammatory gene expression.. ... Docosahexaenoic acid released from membrane phospholipids during brain ischemia is a major source of lipid peroxides. Leukocyte ... The newly discovered brain messenger 10,17S-docosatriene potently inhibited leukocyte infiltration, NFkappaB, and ... These results challenge the view that docosahexaenoate only participates in brain damage and demonstrate that this fatty acid ...
What to look for to determine whether you have a childbirth brain injury case and the settlement value of these medical ... Causes of Infant Brain Ischemia Infant brain ischemia can occur when blood and oxygen flood to the baby are cut off or ... Brain ischemia occurs when brain cells are permanently damaged due to a lack of adequate blood flow. The human brain requires a ... Types of Injuries Caused by Infant Brain Ischemia Brain ischemia is not an injury but rather the name of a medical condition ( ...
PGD(2) DP1 receptor protects brain from ischemia-reperfusion injury.. [Sofiyan Saleem, Hean Zhuang, Artur J de Brum-Fernandes, ... Development of drugs to stimulate the DP1 receptor in brain could provide a new therapeutic strategy against cerebral ischemia ... Ischemia-reperfusion injury was produced by a 90-min occlusion of the right middle cerebral artery followed by a 4-day ... Therefore, in this study, the effect of the DP1 receptor on the outcome of cerebral ischemia in wildtype (WT) and DP1 knockout ...
... a cerebral ischemia-reperfusion (I/R) group, and (iii) an I/R+bexarotene group. Brain water content was measured by the dry wet ... Results After 24 h, 48 h, and 72 h post-I/R, several effects were observed with bexarotene administration: (i) brain water ... in the ischemic brain. The retinoid X receptor agonist bexarotene suppresses MMP-9 expression in endothelial cells and displays ... over-expression disrupts the blood-brain barrier (BBB) ... Brain damage Is the Subject Area "Brain damage" applicable to ...
The neurologic implications of diabetic hyperglycemia during surgical procedures at increased risk for brain ischemia.. Sieber ... It is only in circumstances where temporary focal or global ischemia are used as part of the surgical procedure that aggressive ... implications of diabetic hyperglycemia for the vast majority of surgical procedures at increased risk for brain ischemia are ... Laboratory studies show that following permanent focal ischemia, a situation analogous to stroke, diabetic hyperglycemia is ...
  • Our aim was to test whether immediate treatment with cannabidiol and hypothermia act through complementary brain pathways in hypoxic-ischemic newborn piglets. (frontiersin.org)
  • The present study demonstrated that cannabidiol and hypothermia act complementarily and show additive effects on the main factors leading to hypoxic-ischemic brain damage if applied shortly after the insult. (frontiersin.org)
  • It therefore appears that hypothermia can prevent effectively mitochondrial dysfunction due to ischemia. (springer.com)
  • In in vivo studies, argon-hypothermia treatment decreased hypoxia/ischemia-induced brain infarct size (n = 10) and both caspase-3 and nuclear factor-κB activation in the cortex and hippocampus. (ovid.com)
  • We compared the effects of normothermia (38℃, group A), mild-hypothermia (33℃, group B), and severe-hypothermia (28℃, group C) on the central nervous functions after the global brain ischemia using 24 mongrel dogs (BW 13.5±3.4 kg). (nii.ac.jp)
  • Brain hypothermia, induced by cooling a baby to around 33 °C for three days after birth, is a treatment for hypoxic ischemic encephalopathy. (wikipedia.org)
  • There are both more potential side effects on the developing premature with lung disease, and there is more evident protection by hypothermia when a greater volume of complex brain is actively developing. (wikipedia.org)
  • Targeted temperature management (TTM) previously known as therapeutic hypothermia or protective hypothermia is an active treatment that tries to achieve and maintain a specific body temperature in a person for a specific duration of time in an effort to improve health outcomes during recovery after a period of stopped blood flow to the brain. (wikipedia.org)
  • Hypothermia therapy for neonatal encephalopathy has been proven to improve outcomes for newborn infants affected by perinatal hypoxia-ischemia, hypoxic ischemic encephalopathy or birth asphyxia. (wikipedia.org)
  • Accordingly, most early hypotheses suggested that hypothermia reduces the harmful effects of ischemia by decreasing the body's need for oxygen. (wikipedia.org)
  • Cerebral morphology, as well as vascular and physiological measures (before, during, and after ischemia) did not differ between A 2A receptor knock-out and wild-type littermates. (jneurosci.org)
  • He is one of the first 100 vascular neurologists certified by the American Board of Psychiatry and Neurology (ABPN), and one of the founders of the subspecialty of interventional neurology in the United States, He has written in his specialty and is credited with having coined the phrase Time is Brain! (wikipedia.org)
  • Chronic ischemia of the brain may result in a form of dementia called vascular dementia. (wikipedia.org)
  • Any of these diseases can result in vascular dementia due to ischemic damage to the brain. (wikipedia.org)
  • Designed by University of California, Los Angeles in 2001, MERCI was the first device approved in the U.S. to remove blood clots in patients suffering from acute brain ischemia. (wikipedia.org)
  • 4 Thus, brain damage is a major public health problem deserving every effort towards understanding its pathogenesis and treatment. (springer.com)
  • Although the severity of brain damage depends mainly on the degree and duration of the decrease of cerebral blood flow /CBF/, and hence the depletion of macroerg phosphates, mitochondria seem quite resistant to ischemia /Ikrényi et al. (springer.com)
  • Global ischemia is often the result of cardiac arrest, and if left untreated for too long, may result in severe brain damage, explains the Columbia University Medical Center. (reference.com)
  • Cerebral palsy is a term used for disorders that consist of difficulty controlling movement due to damage to the developing brain, according to WebMD. (reference.com)
  • Even brief interruptions can cause brain ischemia, and potentially result in a situation called an ischemic cascade , where brain cells with inadequate blood supply start dying and releasing toxins that damage neighboring cells, causing them to rupture and release toxins of their own, creating a ripple effect across the brain. (wisegeek.com)
  • Other patients may experience brain damage and could need therapy to relearn some skills. (wisegeek.com)
  • The brain stem cannot recover from severe damage. (wisegeek.com)
  • More mild brain stem damage may result in impairments requiring a patient to use a ventilator for respiration. (wisegeek.com)
  • An interruption of blood flow to the brain for more than 10 seconds causes unconsciousness, and an interruption in flow for more than a few minutes generally results in irreversible brain damage. (wikipedia.org)
  • Accordingly, this discovery raised the possibility of intervening after brain ischemia before the damage becomes irreversible. (wikipedia.org)
  • However, if a significant amount of time passes before restoration, brain damage may be permanent. (wikipedia.org)
  • Similar to cerebral hypoxia, severe or prolonged brain ischemia will result in unconsciousness, brain damage or death, mediated by the ischemic cascade. (wikipedia.org)
  • If cerebral blood flow is blocked for more than 5 min, permanent brain damage is inevitable [ 1 ]. (hindawi.com)
  • Brain ischemia may be analyzed from two different perspectives: that of oxygen deprivation (hypoxic damage per se ) and that of deprivation of glucose/serum factors. (frontiersin.org)
  • Once brain cells die they cannot be restored and the damage is permanent. (millerandzois.com)
  • The placental abruption caused brain ischemia which resulted in permanent brain damage. (millerandzois.com)
  • To overcome these pharmacological limitations, we explored the consequences of deleting the A 2A adenosine receptor on brain damage after transient focal ischemia. (jneurosci.org)
  • Hypoattenuation on CT is highly specific for irreversible ischemic brain damage if it is detected within first 6 hours (1). (radiologyassistant.nl)
  • Brain structural damage in spinocerebellar ataxia type 1. (ebscohost.com)
  • The conditions of coagulation the distal segment of middle cerebral artery were selected, which caused necrosis localized in the fronto-parietal and dorso-lateral regions of the brain cortex without any damage of subcortical structures. (nih.gov)
  • Writing All disadvantages like the download mechanisms of secondary brain damage in cerebral, but these 'm the ordnance slowly. (nooranch.com)
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  • Its download mechanisms of secondary brain damage in on both identifiable electronics and primary other leaves is that QPSO lysine with the EPS queer is an electromagnetic expression. (nooranch.com)
  • The blood-brain barrier (BBB) plays an important role in brain damage. (biomedcentral.com)
  • At present, there are no clinically effective pharmacologic interventions to halt brain damage following I/R. The major Aim of this dissertation will be to investigate possible mechanisms involved in neuron death following brain I/R, which may potentially lead to the development of effective therapies. (wayne.edu)
  • In the highly metabolically active tissues of the heart and brain, irreversible damage to tissues can occur in as little as 3-4 minutes at body temperature. (wikipedia.org)
  • Imbalances in some neurotransmitters can lead to excitotoxicity, damage to brain cells that results from overactivation of biochemical receptors for excitatory neurotransmitters (those that increase the likelihood that a neuron will fire). (wikipedia.org)
  • Ischemia is one of the leading causes of secondary brain damage after head trauma. (wikipedia.org)
  • It has recently been proven to be the only medical intervention which reduces brain damage, and improves an infant's chance of survival and reduced disability. (wikipedia.org)
  • Hypothermic neural rescue therapy is an evidence-based clinical treatment which increases a severely injured full term infant's chance of surviving without brain damage detectable at 18 months by about 50%, an effect which seems to be sustained into later childhood. (wikipedia.org)
  • Brain function is temporarily or permanently impaired and structural damage may or may not be detectable with current technology. (wikipedia.org)
  • Usually brain damage or later brain death results after longer intervals of clinical death even if the heart is restarted and blood circulation is successfully restored. (wikipedia.org)
  • In 1990, the laboratory of resuscitation pioneer Peter Safar discovered that reducing body temperature by three degrees Celsius after restarting blood circulation could double the time window of recovery from clinical death without brain damage from 5 minutes to 10 minutes. (wikipedia.org)
  • This reduction in carbon dioxide is caused by contraction of cranial arteries from damage caused by lesions in the brain stem. (wikipedia.org)
  • Certain individuals with alcohol-related dementia present with damage to the frontal lobes of their brain causing disinhibition, loss of planning and executive functions, and a disregard for the consequences of their behavior. (wikipedia.org)
  • This would allow them to target very specific areas of the brain with great accuracy and without inflicting damage to its surroundings. (wikipedia.org)
  • After 4 to 6 minutes of sustained cerebral anoxia, permanent brain damage will begin to occur, but the long-term effects of a controlled choke-out for less than 4 minutes (as most are applied for mere seconds and released when unconsciousness is achieved) are disputed. (wikipedia.org)
  • Is the Subject Area "Blood-brain barrier permeability assay" applicable to this article? (plos.org)
  • Gu Y, Dee CM, Shen J. Interaction of free radicals, matrix metalloproteinases and caveolin-1 impacts blood-brain barrier permeability. (springermedizin.de)
  • Sphingosine-1-phosphate protects against brain microvascular endothelial junctional protein disorganization and barrier dysfunction caused by alcohol. (bioportfolio.com)
  • Role of Proteases in Cellular Dysfunction (in en. (wikipedia.org)
  • The plasma concentrations of both BNP and NT-proBNP are also typically increased in patients with asymptomatic or symptomatic left ventricular dysfunction and is associated with coronary artery disease and myocardial ischemia. (wikipedia.org)
  • These findings suggested that the brain may generate neuronal protection by increasing the levels of Cx43 and amplifying the astrocytic gap junctional intercellular communication under hypoxic condition. (nih.gov)
  • They are differentially regulated in the brain as well as other organs under hypoxic and ischemic conditions. (eurekaselect.com)
  • Hypoxic ischemic encephalopathy has many causes and is essentially the reduction in the supply of blood or oxygen to a baby's brain before, during, or even after birth. (wikipedia.org)
  • Oftentimes, fetal hypoxic-ischemic brain injuries occur as a result of a pregnancy complications such as placental abruption, cord accident, or cardiovascular stress due to a difficult delivery. (wikipedia.org)