Myocardial reperfusion injury. Medical search

Damage to the MYOCARDIUM resulting from MYOCARDIAL REPERFUSION (restoration of blood flow to ischemic areas of the HEART.) Reperfusion takes place when there is spontaneous thrombolysis, THROMBOLYTIC THERAPY, collateral flow from other coronary vascular beds, or reversal of vasospasm.

Generally, restoration of blood supply to heart tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. Reperfusion can be induced to treat ischemia. Methods include chemical dissolution of an occluding thrombus, administration of vasodilator drugs, angioplasty, catheterization, and artery bypass graft surgery. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing MYOCARDIAL REPERFUSION INJURY.

Adverse functional, metabolic, or structural changes in ischemic tissues resulting from the restoration of blood flow to the tissue (REPERFUSION), including swelling; HEMORRHAGE; NECROSIS; and damage from FREE RADICALS. The most common instance is MYOCARDIAL REPERFUSION INJURY.

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.

NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).

The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.

A 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.

Solutions which, upon administration, will temporarily arrest cardiac activity. They are used in the performance of heart surgery.

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).

The circulation of blood through the CORONARY VESSELS of the HEART.

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.

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).

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.

Cell adhesion molecule and CD antigen that mediates the adhesion of neutrophils and monocytes to activated platelets and endothelial cells.

Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.

The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.

The hollow, muscular organ that maintains the circulation of the blood.

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.

A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.

A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.

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)

Contractile activity of the MYOCARDIUM.

Granular leukocytes having a nucleus with three to five lobes connected by slender threads of chromatin, and cytoplasm containing fine inconspicuous granules and stainable by neutral dyes.

Surgical removal of an obstructing clot or foreign material from a blood vessel at the point of its formation. Removal of a clot arising from a distant site is called EMBOLECTOMY.

Damage inflicted on the body as the direct or indirect result of an external force, with or without disruption of structural continuity.

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.

The removal of secretions, gas or fluid from hollow or tubular organs or cavities by means of a tube and a device that acts on negative pressure.

Elements of limited time intervals, contributing to particular results or situations.

Dilation of an occluded coronary artery (or arteries) by means of a balloon catheter to restore myocardial blood supply.

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.

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.

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)

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.

Treatment process involving the injection of fluid into an organ or tissue.

A procedure to stop the contraction of MYOCARDIUM during HEART SURGERY. It is usually achieved with the use of chemicals (CARDIOPLEGIC SOLUTIONS) or cold temperature (such as chilled perfusate).

Use of infusions of FIBRINOLYTIC AGENTS to destroy or dissolve thrombi in blood vessels or bypass grafts.

The veins and arteries of the HEART.

Radiography of the vascular system of the heart muscle after injection of a contrast medium.

The pathological process occurring in cells that are dying from irreparable injuries. It is caused by the progressive, uncontrolled action of degradative ENZYMES, leading to MITOCHONDRIAL SWELLING, nuclear flocculation, and cell lysis. It is distinct it from APOPTOSIS, which is a normal, regulated cellular process.

A 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.

An isoenzyme of creatine kinase found in the CARDIAC MUSCLE.

The mitochondria of the myocardium.

Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).

MYOCARDIAL INFARCTION in which the anterior wall of the heart is involved. Anterior wall myocardial infarction is often caused by occlusion of the left anterior descending coronary artery. It can be categorized as anteroseptal or anterolateral wall myocardial infarction.

Coagulation of blood in any of the CORONARY VESSELS. The presence of a blood clot (THROMBUS) often leads to MYOCARDIAL INFARCTION.

Proteins involved in the transport of specific substances across the membranes of the MITOCHONDRIA.

A family of percutaneous techniques that are used to manage CORONARY OCCLUSION, including standard balloon angioplasty (PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY), the placement of intracoronary STENTS, and atheroablative technologies (e.g., ATHERECTOMY; ENDARTERECTOMY; THROMBECTOMY; PERCUTANEOUS TRANSLUMINAL LASER ANGIOPLASTY). PTCA was the dominant form of PCI, before the widespread use of stenting.

Injuries incurred during participation in competitive or non-competitive sports.

Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.

The circulation of the BLOOD through the MICROVASCULAR NETWORK.

Penetrating and non-penetrating injuries to the spinal cord resulting from traumatic external forces (e.g., WOUNDS, GUNSHOT; WHIPLASH INJURIES; etc.).

The dialdehyde of malonic acid.

Abrupt reduction in kidney function. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; ACUTE KIDNEY TUBULAR NECROSIS; and other less severe conditions.

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.

Damage to any compartment of the lung caused by physical, chemical, or biological agents which characteristically elicit inflammatory reaction. These inflammatory reactions can either be acute and dominated by NEUTROPHILS, or chronic and dominated by LYMPHOCYTES and MACROPHAGES.

Synthetic or natural substances which are given to prevent a disease or disorder or are used in the process of treating a disease or injury due to a poisonous agent.

The 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.

Univalent antigen-binding fragments composed of one entire IMMUNOGLOBULIN LIGHT CHAIN and the amino terminal end of one of the IMMUNOGLOBULIN HEAVY CHAINS from the hinge region, linked to each other by disulfide bonds. Fab contains the IMMUNOGLOBULIN VARIABLE REGIONS, which are part of the antigen-binding site, and the first IMMUNOGLOBULIN CONSTANT REGIONS. This fragment can be obtained by digestion of immunoglobulins with the proteolytic enzyme PAPAIN.

Platelet membrane glycoprotein complex important for platelet adhesion and aggregation. It is an integrin complex containing INTEGRIN ALPHAIIB and INTEGRIN BETA3 which recognizes the arginine-glycine-aspartic acid (RGD) sequence present on several adhesive proteins. As such, it is a receptor for FIBRINOGEN; VON WILLEBRAND FACTOR; FIBRONECTIN; VITRONECTIN; and THROMBOSPONDINS. A deficiency of GPIIb-IIIa results in GLANZMANN THROMBASTHENIA.

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).

Ultrasonic recording of the size, motion, and composition of the heart and surrounding tissues. The standard approach is transthoracic.

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.

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.

Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.

An anatomic severity scale based on the Abbreviated Injury Scale (AIS) and developed specifically to score multiple traumatic injuries. It has been used as a predictor of mortality.

The diffusion or accumulation of neutrophils in tissues or cells in response to a wide variety of substances released at the sites of inflammatory reactions.

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).

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.

A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.

General or unspecified injuries involving the leg.

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.

The process by which organs are kept viable outside of the organism from which they were removed (i.e., kept from decay by means of a chemical agent, cooling, or a fluid substitute that mimics the natural state within the organism).

Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.

The process by which chemical compounds provide protection to cells against harmful agents.

Solutions used to store organs and minimize tissue damage, particularly while awaiting implantation.

A condition of lung damage that is characterized by bilateral pulmonary infiltrates (PULMONARY EDEMA) rich in NEUTROPHILS, and in the absence of clinical HEART FAILURE. This can represent a spectrum of pulmonary lesions, endothelial and epithelial, due to numerous factors (physical, chemical, or biological).

An oxidoreductase that catalyzes the reaction between superoxide anions and hydrogen to yield molecular oxygen and hydrogen peroxide. The enzyme protects the cell against dangerous levels of superoxide. EC 1.15.1.1.

An enzyme that catalyzes the conversion of L-alanine and 2-oxoglutarate to pyruvate and L-glutamate. (From Enzyme Nomenclature, 1992) EC 2.6.1.2.

Enzymes of the transferase class that catalyze the conversion of L-aspartate and 2-ketoglutarate to oxaloacetate and L-glutamate. EC 2.6.1.1.

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.

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.

Damage or trauma inflicted to the eye by external means. The concept includes both surface injuries and intraocular injuries.

Non-human animals, selected because of specific characteristics, for use in experimental research, teaching, or testing.

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.

Highly reactive molecules with an unsatisfied electron valence pair. Free radicals are produced in both normal and pathological processes. They are proven or suspected agents of tissue damage in a wide variety of circumstances including radiation, damage from environment chemicals, and aging. Natural and pharmacological prevention of free radical damage is being actively investigated.

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.

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.

General or unspecified injuries to the neck. It includes injuries to the skin, muscles, and other soft tissues of the neck.

A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.

Substances that influence the course of a chemical reaction by ready combination with free radicals. Among other effects, this combining activity protects pancreatic islets against damage by cytokines and prevents myocardial and pulmonary perfusion injuries.

Prolonged dysfunction of the myocardium after a brief episode of severe ischemia, with gradual return of contractile activity.

Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids.

The act of constricting.

Devices that provide support for tubular structures that are being anastomosed or for body cavities during skin grafting.

In screening and diagnostic tests, the probability that a person with a positive test is a true positive (i.e., has the disease), is referred to as the predictive value of a positive test; whereas, the predictive value of a negative test is the probability that the person with a negative test does not have the disease. Predictive value is related to the sensitivity and specificity of the test.

Differential regulation of Bcl-2, AP-1 and NF-kappaB on cardiomyocyte apoptosis during myocardial ischemic stress adaptation. (1/3052)

Acute ischemia followed by prolonged reperfusion has been shown to induce cardiomyocyte apoptosis. In this report, we demonstrate that myocardial adaptation to ischemia induced by repeated cyclic episodes of short-term ischemia each followed by another short duration of reperfusion reduced cardiomyocyte apoptosis and DNA fragmentation. This was associated with the induction of the expression of Bcl-2 mRNA and translocation and activation of NF-kappaB. Another transcription factor, AP-1, remained unaffected by repeated ischemia and reperfusion, but exhibited significant upregulation by a single episode of 30 min ischemia followed by 2 h of reperfusion. This activation of AP-1 was inhibited by a scavenger of oxygen free radicals, DMTU. Thirty minutes ischemia and 120 min reperfusion downregulated the induction of the expression of Bcl-2 mRNA, but moderately activated NF-kappaB binding activity. This was associated with an increased number of apoptotic cells and DNA fragmentation in cardiomyocytes which were attenuated by DMTU. The results of this study indicate that Bcl-2, AP-1 and NF-kappaB differentially regulate cardiomyocyte apoptosis mediated by acute ischemia and prolonged reperfusion. (+info)

Reactive oxygen species play an important role in the activation of heat shock factor 1 in ischemic-reperfused heart. (2/3052)

BACKGROUND: The myocardial protective role of heat shock protein (HSP) has been demonstrated. Recently, we reported that ischemia/reperfusion induced a significant activation of heat shock factor (HSF) 1 and an accumulation of mRNA for HSP70 and HSP90. We examined the role of reactive oxygen species (ROSs) in the induction of stress response in the ischemic-reperfused heart. METHODS AND RESULTS: Rat hearts were isolated and perfused with Krebs-Henseleit buffer by the Langendorff method. Whole-cell extracts were prepared for gel mobility shift assay using oligonucleotides containing the heat shock element. Induction of mRNA for HSP70 and HSP90 was examined by Northern blot analysis. Repetitive ischemia/reperfusion, which causes recurrent bursts of free radical generation, resulted in burst activation of HSF1, and this burst activation was significantly reduced with either allopurinol 1 mmol/L (an inhibitor of xanthine oxidase) or catalase 2x10(5) U/L (a scavenger of H2O2). Significant activation of HSF1 was observed on perfusion with buffer containing H2O2 150 micromol/L or xanthine 1 mmol/L plus xanthine oxidase 5 U/L. The accumulation of mRNA for HSP70 or HSP90 after repetitive ischemia/reperfusion was reduced with either allopurinol or catalase. CONCLUSIONS: Our findings demonstrate that ROSs play an important role in the activation of HSF1 and the accumulation of mRNA for HSP70 and HSP90 in the ischemic-reperfused heart. (+info)

Nonanticoagulant heparin prevents coronary endothelial dysfunction after brief ischemia-reperfusion injury in the dog. (3/3052)

BACKGROUND: Coronary endothelial dysfunction after brief ischemia-reperfusion (IR) remains a clinical problem. We investigated the role of heparin and N-acetylheparin, a nonanticoagulant heparin derivative, in modulating coronary endothelial function after IR injury, with an emphasis on defining the role of the nitric oxide (NO)-cGMP pathway in the heparin-mediated effect. METHODS AND RESULTS: Male mongrel dogs were surgically instrumented, and the effects of both bovine heparin and N-acetylheparin on coronary endothelial vasomotor function, expressed as percent change from baseline flow after acetylcholine challenge, were studied after 15 minutes of regional ischemia of the left anterior descending artery (LAD) followed by 120 minutes of reperfusion. In dogs treated with placebo (saline), coronary vasomotor function was significantly (P+info)

Tumor necrosis factor-alpha contributes to ischemia- and reperfusion-induced endothelial activation in isolated hearts. (4/3052)

-During myocardial reperfusion, polymorphonuclear neutrophil (PMN) adhesion involving the intercellular adhesion molecule-1 (ICAM-1) may lead to aggravation and prolongation of reperfusion injury. We studied the role of early tumor necrosis factor-alpha (TNF-alpha) cleavage and nuclear factor-kappaB (NF-kappaB) activation on ICAM-1 expression and venular adhesion of PMN in isolated hearts after ischemia (15 minutes) and reperfusion (30 to 480 minutes). NF-kappaB activation (electromobility shift assay) was found after 30 minutes of reperfusion and up to 240 minutes. ICAM-1 mRNA, assessed by Northern blot, increased during the same interval. Functional effect of newly synthesized adhesion molecules was found by quantification (in situ fluorescence microscopy) of PMN, given as bolus after ischemia, which became adherent to small coronary venules (10 to 50 microm in diameter). After 480 minutes of reperfusion, ICAM-1-dependent PMN adhesion increased 2.5-fold compared with PMN adhesion obtained during acute reperfusion. To study the influence of NF-kappaB on PMN adhesion, we inhibited NF-kappaB activation by transfection of NF-kappaB decoy oligonucleotides into isolated hearts using HJV-liposomes. Decoy NF-kappaB but not control oligonucleotides blocked ICAM-1 upregulation and inhibited the subacute increase in PMN adhesion. Similar effects were obtained using BB 1101 (10 microg), an inhibitor of TNF-alpha cleavage enzyme. These data suggest that ischemia and reperfusion in isolated hearts cause liberation of TNF-alpha, activation of NF-kappaB, and upregulation of ICAM-1, an adhesion molecule involved in inflammatory response after ischemia and reperfusion. (+info)

Effects of isoproterenol on myocardial structure and function in septic rats. (5/3052)

In this study we sought to determine the effect of sepsis on two sequelae of prolonged (24-h) beta-agonist administration, myocardial hypertrophy and catecholamine-induced cardiotoxicity. Sprague-Dawley rats were randomized to cecal ligation and perforation (CLP) or sham study groups and then further randomized to receive isoproterenol (2.4 mg. kg-1. day-1 iv) or placebo treatment. At 24 h, myocardial function was assessed by using the Langendorff isolated-heart technique or the heart processed for plain light microscopy. We found that 1) sepsis reduced contractile function, indicated by a rightward shift in the Starling curve (ANOVA with repeated measures, sepsis effect, P < 0.002); 2) sepsis-induced myocardial depression was reversed by isoproterenol treatment (isoproterenol effect, P < 0.0001); 3) sepsis reduced, but did not block, isoproterenol-induced myocardial hypertrophy (isoproterenol effect, P < 0.0001); 4) sepsis did not protect the heart from catecholamine-induced tissue injury; 5) the septic heart was protected against the effects of ischemiareperfusion (decreased postreperfusion resting tension, ANOVA with repeated measures, P < 0.01), an effect attenuated by isoproterenol treatment (P < 0.005); and 6) sepsis reduced the incidence of sustained asystole or ventricular fibrillation after ischemia-reperfusion (P < 0.05), an effect also attenuated by isoproterenol treatment (P < 0.01). We conclude that, in sepsis, beta-agonists induce changes in myocardial weight and function consistent with acute myocardial hypertrophy. These changes occur at the expense of significant tissue injury and increased sensitivity to ischemia-reperfusion-induced tissue injury. (+info)

Formation of 4-hydroxy-2-nonenal-modified proteins in ischemic rat heart. (6/3052)

4-Hydroxy-2-nonenal (HNE) is a major lipid peroxidation product formed during oxidative stress. Because of its reactivity with nucleophilic compounds, particularly metabolites and proteins containing thiol groups, HNE is cytotoxic. The aim of this study was to assess the extent and time course for the formation of HNE-modified proteins during ischemia and ischemia plus reperfusion in isolated rat hearts. With an antibody to HNE-Cys/His/Lys and densitometry of Western blots, we quantified the amount of HNE-protein adduct in the heart. By taking biopsies from single hearts (n = 5) at various times (0, 5, 10, 15, 20, 35, and 40 min) after onset of zero-flow global ischemia, we showed a progressive, time-dependent increase (which peaked after 30 min) in HNE-mediated modification of a discrete number of proteins. In studies with individual hearts (n = 4/group), control aerobic perfusion (70 min) resulted in a very low level (296 arbitrary units) of HNE-protein adduct formation; by contrast, after 30-min ischemia HNE-adduct content increased by >50-fold (15,356 units, P < 0.05). In other studies (n = 4/group), administration of N-(2-mercaptopropionyl)glycine (MPG, 1 mM) to the heart for 5 min immediately before 30-min ischemia reduced HNE-protein adduct formation during ischemia by approximately 75%. In studies (n = 4/group) that included reperfusion of hearts after 5, 10, 15, or 30 min of ischemia, there was no further increase in the extent of HNE-protein adduct formation over that seen with ischemia alone. Similarly, in experiments with MPG, reperfusion did not significantly influence the tissue content of HNE-protein adduct. Western immunoblot results were confirmed in studies using in situ immunofluorescent localization of HNE-protein in cryosections. In conclusion, ischemia causes a major increase in HNE-protein adduct that would be expected to reflect a toxic sequence of events that might act to compromise tissue survival during ischemia and recovery on reperfusion. (+info)

Metallothionein inhibits ischemia-reperfusion injury in mouse heart. (7/3052)

Oxidative stress is believed to play a major role in ischemia-reperfusion injury to the heart. Metallothionein (MT), a potential free radical scavenger, may function in cardiac protection against ischemia-reperfusion damage. To test this hypothesis, a specific cardiac MT-overexpressing transgenic mouse model was used. The hearts isolated from these animals were subjected to 50 min of warm (37 degrees C) zero-flow ischemia followed by 60- or 90-min reflow. Compared with the nontransgenic controls, the transgenic mouse hearts with MT concentrations approximately 10-fold higher than normal showed significantly improved recovery of contractile force postischemia (69.2 +/- 4.2 vs. 26.0 +/- 6.0% at the end of 60-min reperfusion, P < 0.01). Efflux of creatine kinase from these transgenic hearts was reduced by more than 50% (P < 0.01). In addition, the zone of infarction induced by ischemia-reperfusion at the end of 90-min reperfusion was suppressed by approximately 40% (P < 0.01) in the transgenic hearts. The results strongly indicate that MT provides protection against ischemia-reperfusion-induced heart injury. (+info)

Acute exercise can improve cardioprotection without increasing heat shock protein content. (8/3052)

The aim of this study was to determine the effects of acute bouts of exercise on myocardial recovery after ischemia and heat shock protein expression. Adult female Sprague-Dawley rats were divided into five groups: 1) 1-day run (1DR; n = 6) and 2) 3-day run (3DR; n = 7), in which rats ran for 100 min at a speed of 20 m/min up a 6 degrees grade for 1 or 3 consecutive days; 3) 1-day cold run (1CR), in which rats ran the same as 1DR but with wet fur at 8 degrees C, which prevented an elevation of core temperature (n = 8); 4) heat shock sedentary (HS), in which rats had their core temperatures raised to 42 degrees C one time for 15 min (n = 5); and 5) sedentary control (n=15). Cardiac function was analyzed 24 h after the last treatment using an isolated, working heart model. Nonpaced hearts were initially perfused under normoxic conditions, then underwent 17 min of global, normothermic (37 degrees C) ischemia, and, finally, were allowed to recover for 30 min under normoxic conditions. The concentration of the 72-kDa heat shock protein (HSP 72) was measured in each left ventricle. Compared with that in the sedentary group, recovery of cardiac output x systolic pressure (CO x SP) was enhanced (P < 0.05) in all treatment groups when the postischemic value was covaried with the preischemic value. No differences in CO x SP were found (P > 0.05) between the following groups: 1DR vs. 3DR, 1DR vs. HS, and 1DR vs. 1CR. Heat shock protein concentration was significantly greater (P < 0.05) than that in the sedentary controls in HS, 1DR, and 3DR groups, but not for 1CR. The concentration of HSP 72 was not significantly correlated with postischemic CO x SP (R2 = 0.197, P > 0.05). We conclude that acute bouts of exercise can produce cardioprotective effects without an elevation of HSP 72. (+info)

Yellon, D. M.; Hausenloy, D. J. (2007). "Myocardial Reperfusion Injury". New England Journal of Medicine. 357 (11): 1121-1135. ... After MI, the myocardium suffers from reperfusion injury which leads to death of cardiomyocytes and detrimental remodelling of ... Transfection of cardiac myocytes with human HGF reduces ischemic reperfusion injury after MI. The benefits of HGF therapy ... Sala, V.; Crepaldi, T. (2011). "Novel therapy for myocardial infarction: Can HGF/Met be beneficial?". Cellular and Molecular ...

https://en.wikipedia.org/wiki/Human_HGF_plasmid_DNA_therapy

Hausenloy, Derek J.; Yellon, Derek M. (31 July 2008). "Time to Take Myocardial Reperfusion Injury Seriously". New England ... Reperfusion injury, sometimes called ischemia-reperfusion injury (IRI) or reoxygenation injury, is the tissue damage caused ... Reperfusion injury plays a major part in the biochemistry of hypoxic brain injury in stroke. Similar failure processes are ... Reperfusion injury is distinct from cerebral hyperperfusion syndrome (sometimes called "Reperfusion syndrome"), a state of ...

https://en.wikipedia.org/wiki/Reperfusion_injury

H 2S donors reduce myocardial injury and reperfusion complications. Increased H 2S levels within the body will react with ... "Reduction of Ischemia-Reperfusion Mediated Cardiac Injury in Subjects Undergoing Coronary Artery Bypass Graft Surgery". ... Hydrogen sulfide (H 2S) deficiency can be detrimental to the vascular function after an acute myocardial infarction (AMI). AMIs ... PKG also limits smooth muscle cell proliferation, reducing intima thickening following AMI injury, ultimately decreasing ...

https://en.wikipedia.org/wiki/Biological_functions_of_hydrogen_sulfide

May 2010). "Exosome secreted by MSC reduces myocardial ischemia/reperfusion injury". Stem Cell Research. 4 (3): 214-22. doi: ...

https://en.wikipedia.org/wiki/CD9

H 2S therapy reduces myocardial injury and reperfusion complications. Due to its effects similar to NO (without its potential ... Yang X, de Caestecker M, Otterbein LE, Wang B (July 2020). "Carbon monoxide: An emerging therapy for acute kidney injury". ... potential to be used to prevent the development of a series of pathological conditions including ischemia reperfusion injury, ... H 2S deficiency can be detrimental to the vascular function after an acute myocardial infarction (AMI). ...

https://en.wikipedia.org/wiki/Gasotransmitter

"Histone deacetylase inhibition reduces myocardial ischemia-reperfusion injury in mice". FASEB Journal. 22 (10): 3549-60. doi: ... HDIs are also being studied as protection of heart muscle in acute myocardial infarction. Miller TA, Witter DJ, Belvedere S ( ...

https://en.wikipedia.org/wiki/Histone_deacetylase_inhibitor

... a new therapeutic target for myocardial reperfusion injury". Cardiovascular Research. 111 (2): 134-141. doi:10.1093/cvr/cvw100 ... Succinate accumulation under hypoxic conditions has been implicated in the reperfusion injury through increased ROS production ... In animal models, pharmacological inhibition of ischemic succinate accumulation ameliorated ischemia-reperfusion injury. As of ... "Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS". Nature. 515 (7527): 431-5. Bibcode: ...

https://en.wikipedia.org/wiki/Succinic_acid

Alam, M.R.; D. Baetz; M. Ovize (2015). "Cyclophilin D and myocardial ischemia-reperfusion injury: a fresh perspective". J Mol ... Reperfusion injury Reperfusion therapy Eltzschig, H.K. & T. Eckle (2011). "Ischemia and reperfusion-from mechanism to ... Ischemia-reperfusion (IR) tissue injury is the resultant pathology from a combination of factors, including tissue hypoxia, ... IR injury contributes to disease and mortality in a variety of pathologies, including myocardial infarction, ischemic stroke, ...

https://en.wikipedia.org/wiki/Ischemia-reperfusion_injury_of_the_appendicular_musculoskeletal_system

"Effect of trapidil in myocardial ischemia-reperfusion injury in rabbit". Indian Journal of Pharmacology. 46 (2): 207-10. doi: ...

https://en.wikipedia.org/wiki/Trapidil

"Nerve growth factor reduces myocardial ischemia/reperfusion injury in rat hearts". Journal of Basic and Clinical Physiology and ... and traumatic brain injury. Lazarovici also contributed to the characterization of NGF angiogenic properties and ... pan-hematopoietic subpopulation derived from human umbilical cord blood in a traumatic brain injury model". Cytotherapy. 20 (2 ...

https://en.wikipedia.org/wiki/Philip_Lazarovici

"Acute humanin therapy attenuates myocardial ischemia and reperfusion injury in mice". Arteriosclerosis, Thrombosis, and ...

https://en.wikipedia.org/wiki/Humanin

Moens, A.L.; Claeys, M.J.; Timmermans, J.P.; Vrints, C.J. (April 2005). "Myocardial ischemia/reperfusion-injury, a clinical ... However, it is more commonly associated with reperfusion after myocardial injury. AIVR is generally considered to be a benign ... Norris, RM; Mercer, CJ (Mar-Apr 1974). "Significance of idioventricular rhythms in acute myocardial infarction". Progress in ... Accelerated idioventricular rhythm is the most common reperfusion arrhythmia in humans. However, ventricular tachycardia and ...

https://en.wikipedia.org/wiki/Accelerated_idioventricular_rhythm

Yellon, Derek M.; Hausenloy, Derek J. (2007-09-13). "Myocardial Reperfusion Injury". New England Journal of Medicine. 357 (11 ... With reperfusion comes ischemia/reperfusion (IR) injury (IRI), which paradoxically causes cell death in reperfused tissue and ... "Targeting reperfusion injury in patients with ST-segment elevation myocardial infarction: trials and tribulations". European ... "Revisiting Cerebral Postischemic Reperfusion Injury: New Insights in Understanding Reperfusion Failure, Hemorrhage, and Edema ...

https://en.wikipedia.org/wiki/Thrombosis

A deletion of the C-terminal 19 amino acids was found during myocardial ischemia-reperfusion injury in Langendorff perfused rat ... "Troponin I degradation and covalent complex formation accompanies myocardial ischemia/reperfusion injury". Circulation Research ... It was also seen in myocardial stunning in coronary bypass patients. Over-expression of the C-terminal truncated cardiac TnI ( ... Ni CY (2002). "Cardiac troponin I: a biomarker for detection and risk stratification of minor myocardial damage". Clinical ...

https://en.wikipedia.org/wiki/TNNI3

"AGGF1 protects from myocardial ischemia/reperfusion injury by regulating myocardial apoptosis and angiogenesis". Apoptosis. 19 ... Additionally, AGGF1 has been shown to protect against inflammation and ischemic injuries. During embryongenesis, AGGF1 is ... for Blocking Neointimal Formation After Vascular Injury". Journal of the American Heart Association. 6 (6): e005889. doi: ... has also been implicated in treatment after vascular smooth muscle cell damage due to coronary artery disease and myocardial ...

https://en.wikipedia.org/wiki/AGGF1

Such injury would occur when a patient has an acute myocardial infarct followed by reperfusion by either percutaneous coronary ... ZQ, Zhao (August 2003). "Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ... in the area of coronary heart disease in an attempt to limit the injury caused to the heart via ischemia and reperfusion injury ... The second window begins at 24 hours and lasts up to 72 hours after the ischaemia and reperfusion stimulus. In an experimental ...

https://en.wikipedia.org/wiki/Ischemic_preconditioning

Myocardial damage with the resumption of blood flow after an ischemic event is termed "reperfusion injury". The mitochondrial ... Sanada S, Komuro I, Kitakaze M (November 2011). "Pathophysiology of myocardial reperfusion injury: preconditioning, ... specifically as a treatment for ischemic reperfusion injury. The rapid return of myocardial blood supply is critical in order ... reperfusion, and activation of the reperfusion injury salvage kinase pathway (RISK). The mitochondrial accumulation of ...

https://en.wikipedia.org/wiki/Lipid_emulsion

"Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning". ... "New directions for protecting the heart against ischaemia-reperfusion injury: targeting the Reperfusion Injury Salvage Kinase ( ... Brief renal ischemia and reperfusion applied before coronary artery reperfusion reduces myocardial infarct size via endogenous ... These signaling events act on the ROS-generating mitochondria, activate PKCε and the Reperfusion Injury Salvage Kinase (RISK) ...

https://en.wikipedia.org/wiki/Cardioprotection

November 2013). "Role of NADPH oxidase isoforms NOX1, NOX2 and NOX4 in myocardial ischemia/reperfusion injury". Journal of ... which play a role in myocardial reperfusion injury. This was a result of the relation between Nox2 and signaling necessary for ... the protein can be a potential target for drug medication due to its negative effect on myocardial reperfusion. Recent evidence ... It has also been shown to play a part in determining the size of a myocardial infarction due to its connection to ROS, ...

https://en.wikipedia.org/wiki/NOX2

"Protective role of deoxyschizandrin and schisantherin a against myocardial ischemia-reperfusion injury in rats". PLOS ONE. 8 (4 ...

https://en.wikipedia.org/wiki/Deoxyschizandrin

"Cardioprotection with forsythoside B in rat myocardial ischemia-reperfusion injury: relation to inflammation response". ... January 2019). "Protective effect of forsythoside B against lipopolysaccharide-induced acute lung injury by attenuating the ...

https://en.wikipedia.org/wiki/Forsythoside_B

In addition, palmatine might have the antiarrhythmic effect, and provideprotection from myocardial ischemia-reperfusion injury ...

https://en.wikipedia.org/wiki/Palmatine

... protects the isolated rat heart from the myocardial injuries produced by ischemia and reperfusion. Planta Med, 1993 ... Cyclobuxine was in this way able to suppress the damage (myocardial injury) produced by ischemia. As indicated above, research ... cyclobuxine was also found to have a protective effect on myocardial cells against ischemia and reperfusion (in an isolated rat ...

https://en.wikipedia.org/wiki/Cyclobuxine

A major topic of research is the impact of hydrogen sulfide on reducing myocardial ischemia-reperfusion injury. Reperfusion ... "Roles of the nitric oxide signaling pathway in cardiac ischemic preconditioning against myocardial ischemia-reperfusion injury ... Reperfusion triggers an inflammatory response and often results in oxidative damage. H2S decreases injury through many ... The mitochondria has been known to protect the heart from ischemic-reperfusion injury through the opening of the ATP-sensitive ...

https://en.wikipedia.org/wiki/Diallyl_trisulfide

Zheng, Pengfei (2017-02-20). "Plin5 alleviates myocardial ischaemia/reperfusion injury by reducing oxidative stress through ... deficiency in PLIN5 initiates excessive phosforilation of PI3K/Akt which contributes to ischemia-reperfusion injury aggravation ... Wang, Hong (2013). "Cardiomyocyte-specific perilipin 5 overexpression leads to myocardial steatosis and modest cardiac ...

https://en.wikipedia.org/wiki/Perilipin-5

Platelets protect against myocardial dysfunction and injury induced by ischemia and reperfusion in isolated rat hearts. ... Mehta's thesis topic was "studies on experimental myocardial reperfusion" which he completed under the direction of Prof. Tom ... Critical role of AT1 receptor expression after ischemia-reperfusion in isolated rat hearts: Beneficial effect of antisense ... dismutase from myocardial dysfunction and attenuation of vasodilator reserve following coronary occlusion and reperfusion in ...

https://en.wikipedia.org/wiki/Jawahar_L._Mehta

... binding lectin-associated serine protease-2 confers protection from myocardial and gastrointestinal ischemia/reperfusion injury ...

https://en.wikipedia.org/wiki/Collectin

"Reperfusion injury as a therapeutic challenge in patients with acute myocardial infarction". Heart Fail Rev. 12 (3-4): 207-16. ... Myocardial infarction Timeline of myocardial infarction pathology Guanylyl cyclase Rodríguez-Sinovas A, Abdallah Y, Piper HM, ... Reperfusion associated cell death has been modulated (reduced) in animal studies and is an area of active research, which holds ... It is a characteristic histologic finding of a recent myocardial infarction (heart attack) that was partially reperfused. The ...

https://en.wikipedia.org/wiki/Contraction_band_necrosis

"Beta3-Adrenoreceptor Stimulation Ameliorates Myocardial Ischemia-Reperfusion Injury Via Endothelial Nitric Oxide Synthase and ...

https://en.wikipedia.org/wiki/Beta3-adrenergic_agonist

In a mouse model of infarction the A3 selective agonist CP-532,903 protected against myocardial ischemia and reperfusion injury ... "The A3 adenosine receptor agonist CP-532,903 protects against myocardial ischemia/reperfusion injury via the sarcolemmal ATP ... "Cl-IB-MECA Reduces Ischemia/Reperfusion Injury in Mice by Activating the A3 Adenosine Receptor". The Journal of Pharmacology ... it is involved in the inhibition of neutrophil degranulation in neutrophil-mediated tissue injury, it has been implicated in ...

https://en.wikipedia.org/wiki/Adenosine_A3_receptor

"Discrimination between myocardial and skeletal muscle injury by assessment of the plasma ratio of myoglobin over fatty acid- ... "Release of fatty acid-binding protein from isolated rat heart subjected to ischemia and reperfusion or to the calcium paradox ... its rapid release into plasma after myocardial injury - 60 minutes after an ischemic episode, and its relative tissue ... H-FABP is a sensitive biomarker for myocardial infarction and can be detected in the blood within one to three hours of the ...

https://en.wikipedia.org/wiki/Heart-type_fatty_acid_binding_protein

... or during cell injury (such as ischemia-reperfusion injury during heart attacks and strokes) or during developments and ... Braunwald E, Kloner RA (Nov 1985). "Myocardial reperfusion: a double-edged sword?". The Journal of Clinical Investigation. 76 ( ... Most notably, Enodnuclease G is pivotal during oxidative stress by ischemia-reperfusion injury, specifically in the myocardium ... During ischemia reperfusion, ROS release substantially contribute to the cell damage and death via a direct effect on the cell ...

https://en.wikipedia.org/wiki/ENDOG

"SR9009 administered for one day after myocardial ischemia-reperfusion prevents heart failure in mice by targeting the cardiac ... azotemia or acute kidney injury. Studies have also helped elucidate how light has a direct effect on human health through its ... "Short-term disruption of diurnal rhythms after murine myocardial infarction adversely affects long-term myocardial structure ... or reducing adverse light at night in hospitals may improve patient outcomes post-myocardial infarction (heart attack). 2) " ...

https://en.wikipedia.org/wiki/Circadian_rhythm

"Intracellular sodium accumulation during ischemia as the substrate for reperfusion injury". Circulation Research. 84 (12): 1401 ... Létienne R, Bel L, Bessac AM, Vacher B, Le Grand B (December 2009). "Myocardial protection by F 15845, a persistent sodium ... In ischemia, the major damage to the cardiac myocyte, due to hypoxia, is seen following the reperfusion of blood. High ... current blocker, in an ischemia-reperfusion model in the pig". European Journal of Pharmacology. 624 (1-3): 16-22. doi:10.1016/ ...

https://en.wikipedia.org/wiki/F15845

... other A&E/minor injury unit/walk-in centre, treating minor injuries and illnesses Historically, waits for assessment in A&E ... Patients arriving to the emergency department with a myocardial infarction (heart attack) are likely to be triaged to the ... A patient's chance of survival is greatly improved if the patient receives definitive treatment (i.e. surgery or reperfusion) ... These units are for people with non-life-threatening injuries. The use of these units within a department have been shown to ...

https://en.wikipedia.org/wiki/Emergency_department

Obame FN, Zini R, Souktani R, Berdeaux A, Morin D (October 2007). "Peripheral benzodiazepine receptor-induced myocardial ... Solhjoo S, O'Rourke B (January 2015). "Mitochondrial instability during regional ischemia-reperfusion underlies arrhythmias in ... "Neuroprotective effect of Ro5-4864 following brain injury". Experimental Neurology. 214 (2): 201-8. doi:10.1016/j.expneurol. ... improves cardiac functional recovery during postischemia reperfusion in rats". Experimental Biology and Medicine. 235 (4): 478- ...

https://en.wikipedia.org/wiki/Ro5-4864

Reperfusion in acute ST-segment elevation myocardial infarction". CMAJ. 171 (9): 1039-41. doi:10.1503/cmaj.1041417. PMC 526323 ... doi:10.1016/j.injury.2007.03.028. PMID 17640641. Ventura, Christian (20 January 2021). "1: The EMS System". The Emergency ... They have a particular advantage for major trauma injuries. The well-established theory of the golden hour suggests that major ... Increasingly, research into the management of S-T segment elevation myocardial infarctions (STEMI) occurring outside of the ...

https://en.wikipedia.org/wiki/Emergency_medical_services

The resulting neurologic injuries may lead to a persistent subtle decline of cognitive abilities, especially in elderly or very ... Potential adverse effects on cardiovascular activities are listed below: Increase in myocardial oxygen demand due to a rise in ... "Propofol metabolism in man during the anhepatic and reperfusion phases of liver transplantation". Xenobiotica. 22 (1): 105-114 ... blood abnormalities and myocardial dysfunction, etc.) There are also risks of adverse effects related to doses such as ...

https://en.wikipedia.org/wiki/Total_intravenous_anaesthesia

... protects against myocardial ischemia/reperfusion injury via the sarcolemmal ATP-sensitive potassium channel. Journal of ... N-methyluronamides with high selectivity for human adenosine A3 receptors reduce ischemic myocardial injury. American Journal ... and protects against tissue damage following myocardial ischemia, mediated via an interaction with ATP-sensitive potassium ...

https://en.wikipedia.org/wiki/CP-532,903

Rosenkranz, Eliot R.; Buckberg, Gerald D. (1983). "Myocardial protection during surgical coronary reperfusion". Journal of the ... This study called attention to the role of active interventions, including antioxidants, to limit this injury, and provided the ... His research initially centered in the area of myocardial protection and led to the introduction of blood cardioplegia, which ... Hoffman, J. I. E.; Buckberg, G. D. (2014). "The Myocardial Oxygen Supply:Demand Index Revisited". Journal of the American Heart ...

https://en.wikipedia.org/wiki/Gerald_Buckberg

Mechanically unloading the left ventricle before coronary reperfusion reduces left ventricular wall stress and myocardial ... power expenditure of the ventricle and limits the hemodynamic forces that lead to ventricular remodeling after insult or injury ... When the heart is damaged by a myocardial infarction a portion of muscle is permanently lost. The heart has a limited innate ... Clinical research indicates that as the size of the myocardial scar increases, so does the likelihood of the patient to develop ...

https://en.wikipedia.org/wiki/Acute_cardiac_unloading

Thrombolysis in myocardial infarction (TIMI): comparative studies of coronary reperfusion and systemic fibrinogenolysis with ... Reduction of the incidence of amputation in frostbite injury with thrombolytic therapy. Arch Surg. 2007; 142: 546-51. Lijnen HR ... Thrombolysis in Myocardial Infarction (TIMI) Trial, Phase I: A comparison between intravenous tissue plasminogen activator and ... 1984 Dec; 70: 1012-7. The Thrombolysis in Myocardial Infarction (TIMI) trial. Phase I findings. TIMI Study Group. N Engl J Med ...

https://en.wikipedia.org/wiki/Désiré_Collen

... also plays a role in the ischemic cascade due to oxygen reperfusion injury following hypoxia. This cascade ... myocardial infarction, fragile X syndrome, sickle-cell disease, lichen planus, vitiligo, autism, infection, chronic fatigue ... Loffredo L, Violi F (August 2020). "COVID-19 and cardiovascular injury: A role for oxidative stress and antioxidant treatment ... Oxidative stress also contributes to tissue injury following irradiation and hyperoxia, as well as in diabetes. In ...

https://en.wikipedia.org/wiki/Oxidative_stress

... protein kinase and its relationship with localization of intestinal stem cells in rats after ischemia-reperfusion injury". ... April 2007). "VEGFR-1 and -2 regulate inflammation, myocardial angiogenesis, and arteriosclerosis in chronically rejecting ...

https://en.wikipedia.org/wiki/Stem_cell_marker

... mediated diastolic dysfunction in myocardial ischemia-reperfusion injury: therapeutic benefits of Drp1 inhibition to reduce ... Midiv-1 has been demonstrated to attenuate the effects of ischemia reperfusion injury after cardiac arrest. The treatment ... FK506 was shown to also preserve mitochondrial morphology after reperfusion injury. GRCh38: Ensembl release 89: ENSG00000087470 ...

https://en.wikipedia.org/wiki/DNM1L

... traumatic brain injury and spinal cord injury. Excessive amounts of calpain can be activated due to Ca2+ influx after ... Upon reperfusion of the ischemic myocardium, there is development of calcium overload or excess in the heart cell ( ... as well as secondary degeneration resulting from acute cellular stress following myocardial ischemia, cerebral (neuronal) ... or some types of traumatic brain injury such as diffuse axonal injury. Increase in concentration of calcium in the cell results ...

https://en.wikipedia.org/wiki/Calpain

"Regulation of hepatic microRNA expression in response to ischemic preconditioning following ischemia/reperfusion injury in mice ... Wang XH, Qian RZ, Zhang W, Chen SF, Jin HM, Hu RM (February 2009). "MicroRNA-320 expression in myocardial microvascular ...

https://en.wikipedia.org/wiki/Mir-370_microRNA_precursor_family

2007). "Alterations in Myocardial Cardiolipin Content and Composition Occur at the Very Earliest Stages of Diabetes: A Shotgun ... However, the role of CL in aging and ischemia/reperfusion is still controversial. Tangier disease is also linked to CL ... It was first proposed by Otto Heinrich Warburg that cancer originated from irreversible injury to mitochondrial respiration, ... but the structural basis for this injury has remained elusive. Since cardiolipin is an important phospholipid found almost ...

https://en.wikipedia.org/wiki/Cardiolipin

... reperfusion injury MeSH C23.550.767.877.500 - myocardial reperfusion injury MeSH C23.550.767.879 - shock, surgical MeSH C23.550 ...

https://en.wikipedia.org/wiki/List_of_MeSH_codes_(C23)

Her research primarily focuses on the molecular basis of myocardial ischemia/reperfusion injury and in developing ways to ... with particular attention to the molecular basis of myocardial ischemia/reperfusion injury and in developing ways to mitigate ... Her subsequent work has explored the role of proteases and mitochondrial dysfunction in ischemia/reperfusion injury, and most ... "Enhancing Macroautophagy Protects against Ischemia/Reperfusion Injury in Cardiac Myocytes". "Gottlieb Lab". Delbridge, Lea M. D ...

https://en.wikipedia.org/wiki/Roberta_Gottlieb

Myocardial infarction. Retrieved November 28, 2006. Fishbein, M. C. (1990). "Reperfusion injury". Clinical Cardiology. 13 (3): ... Myocardial infarction: diagnosis and investigations - GPnotebook, retrieved November 27, 2006. DE Fenton et al. Myocardial ... Gross examination may reveal signs of myocardial infarction.[citation needed] A one-week-old myocardial infarction of the ... Subepicardial fibrosis (epicardium at top) Myocardial infarction management Myocardial infarction complications For the first ~ ...

https://en.wikipedia.org/wiki/Myocardial_infarction_diagnosis

In the veins above the heart, such as in the head and neck, the venous pressure may be less than atmospheric and an injury may ... The effects of hyperbaric oxygen also counteract the damage that can occur with reperfusion of previously ischemic areas; this ... the coronary capillaries where they can cause myocardial ischaemia or other tissues, where the consequences are usually less ... Early treatment has greatest benefits, but it can be effective as late as 30 hours after the injury. Oxygen first aid treatment ...

https://en.wikipedia.org/wiki/Air_embolism

... especially acute myocardial infarction; however, reperfusion has the potential to exacerbate lethal tissue injury, a process ... Reperfusion is the definitive treatment for acute coronary syndromes, ... "reperfusion injury." Ischemia/reperfusion injury may lead to myocardial infarction, cardiac arrhythmias, and contractile ... Interaction of cardiovascular risk factors with myocardial ischemia/reperfusion injury, preconditioning, and postconditioning ...

https://pubmed.ncbi.nlm.nih.gov/18048761/?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Myocardial ischemia/reperfusion injury (MIRI) is a phenomenon by which the process of myocardial reperfusion can further induce ... Resveratrol increase myocardial Nrf2 expression in type 2 diabetic rats and alleviate myocardial ischemia/reperfusion injury ( ... Dexmedetomidine, Keap1-Nrf2/ARE signal transduction pathway, Myocardial ischemia/reperfusion injury, Oxidative stress ... MIRI is a phenomenon whereby the process of myocardial reperfusion causes more injury compared with simple ischemia [1]. DEX is ...

https://portlandpress.com/bioscirep/article/42/9/BSR20221306/231655/Role-of-Keap1-Nrf2-ARE-signal-transduction-pathway

Evaluation of Serum Serotonin as a Biomarker for Myocardial Infarction and Ischemia/Reperfusion Injury. Appl. Sci.-Basel, 10 ( ... Evaluation of Serum Serotonin as a Biomarker for Myocardial Infarction and Ischemia/Reperfusion Injury ... aggravating myocardial damage and ischemia/reperfusion (I/R) injury. However, serum serotonin and its potential role as a ... We studied whether serum serotonin was associated with I/R injury assessed by ECG analysis and by analysis of TIMI myocardial ...

http://kups.ub.uni-koeln.de/32025/

miR-17-3p Contributes to Exercise-Induced Cardiac Growth and Protects against Myocardial Ischemia-Reperfusion Injury Jing Shi1* ... miR-17-3p Contributes to Exercise-Induced Cardiac Growth and Protects against Myocardial Ischemia-Reperfusion Injury. ... miR-17-3p Contributes to Exercise-Induced Cardiac Growth and Protects against Myocardial Ischemia-Reperfusion Injury. ... miR-17-3p Contributes to Exercise-Induced Cardiac Growth and Protects against Myocardial Ischemia-Reperfusion Injury. ...

https://thno.org/v07p0664

In acute myocardial infarction (AMI), myocardial reperfusion injury may undo part of the recovery after revascularization of ... N2 - In acute myocardial infarction (AMI), myocardial reperfusion injury may undo part of the recovery after revascularization ... AB - In acute myocardial infarction (AMI), myocardial reperfusion injury may undo part of the recovery after revascularization ... abstract = "In acute myocardial infarction (AMI), myocardial reperfusion injury may undo part of the recovery after ...

https://research.tue.nl/en/publications/ultrastructural-characteristics-of-myocardial-reperfusion-injury-

Nature Communications paper showing that Sema7a binds to platelet GPIb and aggravates post-ischemic myocardial tissue injury, ... Red blood cell-derived semaphorin 7A promotes thrombo-inflammation in myocardial ischemia-reperfusion injury through platelet ... Red blood cell-derived semaphorin 7A promotes thrombo-inflammation in myocardial ischemia-reperfusion injury through platelet ... Red blood cell-derived semaphorin 7A promotes thrombo-inflammation in myocardial ischemia-reperfusion injury through platelet ...

https://www.ozgene.com/publications/red-blood-cell-derived-semaphorin-7a-promotes-thrombo-inflammation-in-myocardial-ischemia-reperfusion-injury-through-platelet-gpib/

Induction of beclin-1 signaling can be a potential therapeutic target in myocardial reperfusion-induced microvascular injury. ... Interestingly, beclin1 overexpression increased animal survival and attenuated myocardial infarct size (45 ± 6.13 vs 22 ± 4.37 ... no-reflow area (39 ± 5.22 vs 16 ± 2.54) post-myocardial ischemia reperfusion. ... against injury. TTC and Evans blue dye, western blot, immunofluorescence and immunohistochemistry staining were performed in ...

https://biosignaling.biomedcentral.com/articles/10.1186/s12964-021-00786-z/figures/2

Inhibition of coagulation factor XI attenuates inflammation in myocardial ischemia/reperfusion injury ... A methylation-dependent checkpoint by SETD7 promotes myocardial ischemic injury in mice and men ... Ischaemia-mediated cardiac injury: pathomechanisms and potential treatments. Speakers: Miss Q. Luo, Doctor A. Maier, Doctor J. ... Session: Ischaemia-mediated cardiac injury: pathomechanisms and potential treatments Topic: Ischaemia, Infarction, ...

https://esc365.escardio.org/presentation/252882?resource=abstract

The coronary circulation in acute myocardial ischaemia/reperfusion injury - a target for cardioprotection.. Title. The coronary ... "The coronary circulation in acute myocardial ischaemia/reperfusion injury - a target for cardioprotection.," NEOMED ... provides an overview of strategies to protect the coronary circulation from acute myocardial ischaemia/reperfusion injury. This ... circulation in acute myocardial ischaemia/reperfusion injury - a target for cardioprotection. ...

https://neomed.omeka.net/items/show/4185

Outcome measures included mitochondrial morphology, mitochondrial function, myocardial injury, cardiac function and oxidative ... We hypothesized that inhibition of Drp1 may be effective to reduce MI/R injury in diabetic hearts. High-fat diet and ... Dynamin-related protein 1 (Drp1)-mediated mitochondrial fission plays an important role in MI/R injury under non-diabetic ... The above evidences suggested that Drp1 may be one critical molecule linking diabetes with MI/R injury. ...

https://cardiab.biomedcentral.com/articles/10.1186/s12933-017-0501-2

Combining the natural inflammatory response and reactive oxygen species (ROS) overproduction after reperfusion injury, we ... In a mouse model of myocardial ischemia repefusuin (MI/R) injury, intravenous injection of our formula resulted in the ... the clinical translational potential of systemic administration of RvD1 in the treatment of ischemia-reperfusion injury is ... The resulting formulation enables targeted delivery of RvD1 to the injury site by hijacking circulating chemotactic monocytes, ...

https://jnanobiotechnology.biomedcentral.com/articles/10.1186/s12951-022-01652-x

Quantification of hydroxyl radical and its lack of relevance to myocardial injury during early reperfusion after graded ... Quantification of hydroxyl radical and its lack of relevance to myocardial injury during early reperfusion after graded ...

https://augusta.pure.elsevier.com/en/publications/quantification-of-hydroxyl-radical-and-its-lack-of-relevance-to-m/fingerprints/

Following reperfusion for 6 hours, angiotensin II content of the heart was determined using radioimmunoassay. Myocardial ... telmisartan improved microvascular dysfunction during myocardial I/R injury via the PPARG pathway. ... Myocardial capillaries were examined with transmission electron microscopy. Intercellular adhesion molecule-1 (ICAM-1) and ... injury by activating the peroxisome proliferator-activated receptor gamma (PPARG) pathway. Forty-eight male rabbits were ...

https://bmccardiovascdisord.biomedcentral.com/articles/10.1186/1471-2261-13-39/figures/1

... attenuates lung injury induced by aortic ischemia-reperfusion (IR). Therefore, we hypothesized that GdCl3 may attenuate ... Objectives: Aortic ischemia and reperfusion periods, which are often associated with infrarenal abdominal aortic cross-clamping ... and declamping, cause injury in distant organs including the heart. We recently reported that Kupffer cell blockage with ...

https://avesis.sdu.edu.tr/yayin/cee94348-3c67-4a26-8b75-07d16e0ee371/gadolinium-chloride-attenuates-aortic-occlusion-reperfusion-induced-myocardial-injury-in-rats

Chemerin15 inhibits neutrophil-mediated vascular inflammation and myocardial ischemia-reperfusion injury through ChemR23. EMBO ... Chemerin15 inhibits neutrophil-mediated vascular inflammation and myocardial ischemia-reperfusion injury through ChemR23. Cash ... Chemerin15 inhibits neutrophil-mediated vascular inflammation and myocardial ischemia-reperfusion injury through ChemR23. ... ac.uk/item/8yyzv/chemerin15-inhibits-neutrophil-mediated-vascular-inflammation-and-myocardial-ischemia-reperfusion-injury- ...

https://westminsterresearch.westminster.ac.uk/item/8yyzv/chemerin15-inhibits-neutrophil-mediated-vascular-inflammation-and-myocardial-ischemia-reperfusion-injury-through-chemr23

Elevated Myocardial Creatine Protects Against Ischemia/Reperfusion Injury by Improving Cardiac Energetics ... Elevated Myocardial Creatine Protects Against Ischemia/Reperfusion Injury by Improving Cardiac Energetics ...

https://www.neuroscience.ox.ac.uk/publications/317064?03f5d245-70d6-11ed-a561-061ab7f93640

Effect of N-2-mercaptopropionylglycine in limiting myocardial reperfusion injury following 90 minutes of ischemia in dogs. ... Effect of N-2-mercaptopropionylglycine in limiting myocardial reperfusion injury following 90 minutes of ischemia in dogs. ... mediated reperfusion injury. Twenty dogs underwent 90 min of left anterior descending (LAD) coronary artery occlusion followed ... Reperfusion in control group increased the lipid peroxidation and lowered glutathione (GSH) and superoxide dismutase (SOD) ...

https://imsear.searo.who.int/handle/123456789/108839?locale=th

In this study we investigated the cardioprotective mechanisms of NG-R1 in myocardial ischemia/reperfusion (MI/R) injury in vivo ... Notoginsenoside R1 protects against myocardial ischemia/reperfusion injury in mice via suppressing TAK1-JNK/p38 signaling. ... Notoginsenoside R1 protects against myocardial ischemia/reperfusion injury in mice via sup ... We showed that NG-R1 administration significantly decreased the myocardial infarction area, alleviated myocardial cell damage ...

https://pesquisa.bvsalud.org/portal/resource/pt/mdl-36721009

... of HDAC3-orchestrated circadian clock gene oscillations in diabetic rats following myocardial ischaemia/reperfusion injury * ... of HDAC3-orchestrated circadian clock gene oscillations in diabetic rats following myocardial ischaemia/reperfusion injury * ...

https://www.nature.com/articles/nature07541?error=cookies_not_supported&code=c60635a1-2d4a-44ab-98f8-5a31cf74f50b

Myocardial cell death from ischemia-reperfusion (I/R) injury (e.g. myocardial infarction) continues to be a major cause of ... Protein Kinase C Epsilon PeptideInhibitor Exerts Cardioprotective Effects in Myocardial Ischemia/Reperfusion Injury. Anahi ... Myocardial ischemia/reperfusion injury; Protein kinase C epsilon; Endothelial nitric oxide synthase ... Hausenloy DJ, Yellon DM (2013) Myocardial ischemia-reperfusion injury: a neglected therapeutic target. J Clin Invest 123: 92- ...

https://www.avensonline.org/fulltextarticles/JCB-2332-3671-05-0021.html

The effects of vitamin E and lipoic acid supplementation on myocardial ischemia-reperfusion injury in the rat. FASEB Journal. ... The effects of vitamin E and lipoic acid supplementation on myocardial ischemia-reperfusion injury in the rat. / Coombes, J. S ... The effects of vitamin E and lipoic acid supplementation on myocardial ischemia-reperfusion injury in the rat. In: FASEB ... title = "The effects of vitamin E and lipoic acid supplementation on myocardial ischemia-reperfusion injury in the rat", ...

https://experts.umn.edu/en/publications/the-effects-of-vitamin-e-and-lipoic-acid-supplementation-on-myoca

Reperfusion Injury. Myocardial Reperfusion Injury. Pathologic Processes. Myocardial Ischemia. Heart Diseases. Cardiovascular ... Myocardial reperfusion injury. Myocardial infarct size. ST-elevation myocardial infarction. Remote Ischaemic Conditioning. ... STEMI Myocardial Reperfusion Injury Device: Remote ischemic conditioning Device: Control Not Applicable ... Effect of remote ischaemic conditioning on clinical outcomes in patients with acute myocardial infarction (CONDI-2/ERIC-PPCI): ...

https://clinicaltrials.gov/show/NCT02342522

A MECHANISM FOR CORTICAL BONE STEM CELL-DERIVED EXOSOMES THERAPEUTIC EFFECT ON POST-MYOCARDIAL INFARCTION REPERFUSION INJURY ... Previous studies have shown both that both post-MI and post-ischemia reperfusion (I/R), there is a reduction in scar size and ... Myocardial infarction (MI) is followed by cardiac remodeling involving extensive fibrosis and which can ultimately progress ... of mCBSCs and mCBSC-derived exosomes into the ischemic region of an infarct had a protective effect against I/R injury. ...

https://scholarshare.temple.edu/handle/20.500.12613/6471

Short-Term Administration of Lemon Balm Extract Ameliorates Myocardial Ischemia/Reperfusion Injury: Focus on Oxidative Stress. ... in the rat model of myocardial ischemia/reperfusion (I/R) injury. Thirty-two Wistar rats were randomly divided into a CTRL non- ... treated control group with myocardial I/R injury and three experimental groups of rats treated with 50, 100, or 200 mg/kg of ME ... ME improved cardiodynamic parameters and achieved to preserve cardiac architecture after I/R injury and to decrease fibrosis, ...

https://scidar.kg.ac.rs/handle/123456789/14938

Myocardial ischemia/reperfusion injury 2. *Neurodegeneration 2. *Neurodegenerative Diseases 2. *Neuroinflammation 2 ...

https://works.bepress.com/experts/philadelphia-college-of-osteopathic-medicine/search/?

Exosome secreted by MSC reduces myocardial ischemia/reperfusion injury. Stem Cell Res. 2010, 4, 214-222. [Google Scholar] [ ... Reduction of myocardial infarct size by human mesenchymal stem cell conditioned medium. Stem Cell Res. 2007, 1, 129-137. [ ... also reported that MSC microvesicles, which are secreted membrane vesicles of 80 nm to 1 μm, improve acute kidney injury in a ... Mesenchymal stem cell-derived microvesicles protect against acute tubular injury. J. Am. Soc. Nephrol. 2009, 20, 1053-1067. [ ...

https://www.mdpi.com/1422-0067/22/2/720

Effects of febuxostat and inosine on rat myocardial ischemia/reperfusion injury. Takako Yao Yoshinori Seko ... Non-ST-elevation myocardial infarction complicating carcinoid syndrome. Ayman Elbadawi Erfan Alotaki Islam Y. Elgendy Hend ... Distal left main bronchial injury after catheter ablation for atrial fibrillation: Report of two cases Aaron Sparks James R. ... Sudden cardiac death in a woman with clinical evidence of coronary vasospastic disease and myocardial stunning. A necrospy ...

https://www.oatext.com/Cardiovascular-Disorders-and-Medicine-CDM.php

Protective role of the deSUMOylating enzyme SENP3 in myocardial ischemia-reperfusion injury. Rawlings, N., Lee, L., Nakamura, Y ... Targets and mechanisms of SUMOylation-mediated cardioprotection during ischemia and reperfusion injury. *Henley, Jeremy M ( ...

https://research-information.bris.ac.uk/en/projects/targets-and-mechanisms-of-sumoylation-mediated-cardioprotection-d

l‐α‐Lysophosphatidylinositol (LPI) aggravates myocardial ischemia/reperfusion injury via a GPR55/ROCK‐dependent pathway. Pages ...

https://www.bps.ac.uk/publishing/our-journals/pharmacology-research-perspectives

Activation of an Efferent Cholinergic Pathway Produces Strong Protection Against Myocardial Ischemia/Reperfusion Injury in Rats ... Protective Effects of Melanocortins on Short-Term Changes in a Rat Model of Traumatic Brain Injury: Retraction. March 01, 2023 ...

https://www.medscape.com/viewpublication/767_1

Ischemia/reperfusion injury may lead to myocardial infarction, cardiac arrhythmias, and contractile dysfunction. (nih.gov)
Background: Activated platelets release serotonin during acute myocardial infarction (AMI), aggravating myocardial damage and ischemia/reperfusion (I/R) injury. (uni-koeln.de)
However, serum serotonin and its potential role as a biomarker for myocardial infarction and I/R injury have not been studied so far. (uni-koeln.de)
Methods: In this investigator-initiated pilot study, we examined 38 patients with ST-segment myocardial infarction (STEMI). (uni-koeln.de)
Results: Serum serotonin levels were not elevated in the myocardial infarction group compared to the control cohort and they did not show any timeline kinetics after STEMI. (uni-koeln.de)
Conclusions: Serum serotonin is not suitable as a biomarker after myocardial infarction and in the assessment of I/R injury. (uni-koeln.de)
In acute myocardial infarction (AMI), myocardial reperfusion injury may undo part of the recovery after revascularization of the occluded coronary artery. (tue.nl)
In four isolated Langendorff perfused beating pig hearts, an anterior wall myocardial infarction was created by inflating a balloon in the mid segment of the left anterior descending (LAD) artery. (tue.nl)
Here, we show that platelet-neutrophil complexes (PNCs) are increased in patients with acute myocardial infarction and that this is associated with increased levels of neuronal guidance protein semaphorin 7A (SEMA7A). (ozgene.com)
Agomir of miRNA-30d - a potential new therapeutic target for prevention of ischemic cardiomyopathy after myocardial infarction? (escardio.org)
The coronary circulation is both culprit and victim of acute myocardial infarction. (omeka.net)
However, no-reflow is still a serious complication of reperfused myocardial infarction and carries, independently from infarct size, an unfavourable prognosis. (omeka.net)
Myocardial infarction (MI), a clinical manifestation of coronary heart disease, is the leading cause of cardiovascular-related deaths [ 1 ]. (biomedcentral.com)
In the inflamed microvasculature, C15 rapidly modulates neutrophil physiology inducing adherent cell detachment from the inflamed endothelium, while reducing neutrophil recruitment and heart damage in a murine myocardial infarction model. (westminster.ac.uk)
We showed that NG-R1 administration significantly decreased the myocardial infarction area, alleviated myocardial cell damage and improved cardiac function in MI/R mice . (bvsalud.org)
The results suggest that Myr-PKCε- given at reperfusioneffectively reduces infarct size, improves cardiac function and is aputative treatment that could aid in clinical myocardial infarction/organ transplantation patient recovery. (avensonline.org)
Myocardial cell death from ischemia-reperfusion (I/R) injury (e.g. myocardial infarction) continues to be a major cause of morbidity and mortality in Western nations [ 1 ]. (avensonline.org)
Reperfusion is essential tosalvage ischemic myocardial tissue from infarction. (avensonline.org)
The size of the infarct that results from the combination of the ischemic and reperfusion injury is the major determinant of the prognosis of patients who survive the acute myocardial infarction incident [ 3-7 ]. (avensonline.org)
The purpose of this study is to determine whether remote ischemic conditioning can reduce cardiac death and hospitalization for heart failure at 12 months in patients presenting with a ST-elevation myocardial infarction and treated by percutaneous coronary intervention. (clinicaltrials.gov)
The CONDI2/ERIC-PPCI trial is a randomised controlled clinical trial investigating whether remote ischemic conditioning (RIC) can reduce cardiac death and hospitalization for heart failure at 12 months in 5400 patients presenting with a ST-elevation myocardial infarction (STEMI) and treated by percutaneous coronary intervention (PPCI). (clinicaltrials.gov)
Myocardial infarction (MI) is followed by cardiac remodeling involving extensive fibrosis and which can ultimately progress into heart failure. (temple.edu)
In numerous studies, treatment with recombinant human annexins and annexin analogue peptides have consistently found positive outcomes in animal models of sepsis, myocardial infarction, and ischemia reperfusion injury. (frontiersin.org)
We conclude that, prolongation of acidic conditions during reperfusion by BZ could be responsible for the cardioprotective benefits of reduced infarction and better myocontractile function, through P38MAPK-dependent pathways. (conicet.gov.ar)
13 Recently, our studies prove that hypoxia induction and macrophage migration inhibitory (MIF) modification can strengthen the therapeutic capacity of MSC-derived exosomes on myocardial infarction (MI) through inhibiting apoptosis and promoting angiogenesis. (researchsquare.com)
Ischemia/Reperfusion Injury following Acute Myocardial Infarction: A Critical Issue for Clinicians and Forensic Pathologists. (thieme-connect.de)
Mounting evidence supports that stem cell therapies may be promising in this field on the basis of potential therapeutic use of stem cells in damaged organs such as the myocardium after heart infarction, stroke, spinal cord injury, retina diseases, and damaged liver [ 2 - 4 ]. (hindawi.com)
The goal of the trial was to evaluate treatment with cyclosporine compared with saline in ST-elevation myocardial infarction patients undergoing percutaneous coronary intervention (PCI). (medscape.com)
Cyclosporine will be more effective at decreasing the size of myocardial infarction. (medscape.com)
These side effects will need to be carefully studied in the ST-elevation myocardial infarction patient population since these patients are already at risk of contrast nephropathy. (medscape.com)
Cite this: Effect of Cyclosporine on Reperfusion Injury in Acute Myocardial Infarction (Effect of Cyclosporine on Reperfusion Injury in AMI) - Medscape - Jul 30, 2008. (medscape.com)
Background: Adenosine administered as an adjunct to reperfusion can reduce coronary no-reflow and limit myocardial infarct (MI) size in ST-segment elevation myocardial infarction (STEMI) patients. (uea.ac.uk)
We calculated pooled relative risks using a fixed-effect meta-analysis assessing the impact of adjunctive adenosine therapy on major clinical endpoint including all-cause mortality, non-fatal myocardial infarction, and heart failure. (uea.ac.uk)
Stroke and myocardial infarction are among the most common causes of mortality and disability in the world. (cdc.gov)
Variations in the eicosapentaenoic acid-arachidonic acid ratio associated with age in acute myocardial infarction patients undergoing primary percutaneous coronary intervention. (twmu.ac.jp)
The gadolinium-based contrast agents used for LGE differentiate viable myocardium from scar on the basis of differences in cell membrane integrity for acute myocardial infarction. (cdc.gov)
In chronic myocardial infarction, the scarred tissue enhances much more than normal myocardium due to increases in extracellular volume. (cdc.gov)
When combined with a measure of area at risk like T2-weighted images, CMR can determine infarct size, area at risk, and thus estimate myocardial salvage 1-7 days after acute myocardial infarction. (cdc.gov)
Her past medical history was significant for peripheral vascular disease (PVD), diabetes, myocardial infarction with percutaneous intervention, and ischemic cardiomyopathy. (hindawi.com)

The current review provides an overview of strategies to protect the coronary circulation from acute myocardial ischaemia/reperfusion injury. (omeka.net)
Timely reperfusion therapy can effectively reduce myocardial loss and significantly reduce acute mortality in patients with MI [ 2 ]. (biomedcentral.com)
Acute lung injury (ALI) is an inflammatory disorder. (biomedcentral.com)
Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is severe disorder of lungs with high mortality [ 1 , 2 ]. (biomedcentral.com)
A recent study showed that soluble epoxide hydrolase (sEH) plays a prevailing role in the pathogenesis of acute lung injury (ALI) [ 4 ]. (biomedcentral.com)

Verapamil, a calcium channel blocker, is known to protect the myocardium against ischemia and reperfusion injury. (ekja.org)

Methods: A total of 70 male SD rats were randomly divided into seven equal groups ( n =10): blank control (S group), ischemia/reperfusion injury (C group), DEX preconditioning (DEX group), tertiary butylhydroquinone (tBHQ) control (tBHQ group), combined tBHQ and DEX preconditioning (tBHQ+DEX group), all-trans retinoic acid (ATRA) control (ATRA group), and combined ATRA and DEX preconditioning (ATRA+DEX group). (portlandpress.com)
The aim of these experiments was to determine the effects of combining high levels of vitamin E and lipoic acid supplementation on myocardial performance and arrhythmias during in vivo ischemia and reperfusion (I-R). Female Sprague-Dawley rats (4 months old) were randomly assigned to either a control diet group or a vitamin E and lipoic acid supplementation group. (umn.edu)
Thirty-two Wistar rats were randomly divided into a CTRL non-treated control group with myocardial I/R injury and three experimental groups of rats treated with 50, 100, or 200 mg/kg of ME for 7 days per os. (ac.rs)
Activation of an Efferent Cholinergic Pathway Produces Strong Protection Against Myocardial Ischemia/Reperfusion Injury in Rats: Retraction. (medscape.com)
White R, Holdaway BB, Moody JD, Chang Y. Chronic caffeine administration attenuates vascular injury-induced neointimal hyperplasia in rats. (atsu.edu)
reported that Semen Cassiae may reduce hepatic injury in rats [ 12 ]. (biomedcentral.com)

Methods: We performed an up-to-date search for all RCTs investigating adenosine as an adjunct to reperfusion in STEMI patients. (uea.ac.uk)
Conclusion: We find evidence of improved clinical outcome in terms of less heart failure in STEMI patients administered intracoronary adenosine as an adjunct to reperfusion. (uea.ac.uk)

However, ischaemia and reperfusion cause damage not only in cardiomyocytes but also in the coronary circulation, including microembolisation of debris and release of soluble factors from the culprit lesion, impairment of endothelial integrity with subsequently increased permeability and oedema formation, platelet activation and leukocyte adherence, erythrocyte stasis, a shift from vasodilation to vasoconstriction, and ultimately structural damage to the capillaries with eventual no-reflow, microvascular obstruction and intramyocardial haemorrhage. (omeka.net)

The aim of this review is to show the potential for developing cardioprotective drugs on the basis of endogenous cardioprotection by pre- and postconditioning (i.e., drug applied as trigger or to activate signaling pathways associated with endogenous cardioprotection) and to review the evidence that comorbidities and aging accompanying coronary disease modify responses to ischemia/reperfusion and the cardioprotection conferred by preconditioning and postconditioning. (nih.gov)
Quesnelle KM, Bystrom PV and Toledo-Pereyra LH: Molecular responses to ischemia and reperfusion in the liver. (spandidos-publications.com)

Ischemic preconditioning of myocardium is a well described adaptive response in which brief exposure to ischemia/reperfusion before sustained ischemia markedly enhances the ability of the heart to withstand a subsequent ischemic insult. (nih.gov)
Preconditioning of the myocardium can be induced by several rounds of brief ischemia (i.e. less than 4 min) followed by several rounds of brief reperfusion (i.e. less than 6 min) prior to prolonged ischemia (i.e. 30 min or greater) followed by the final reperfusion period [ 12 ]. (avensonline.org)
Damage to the MYOCARDIUM resulting from MYOCARDIAL REPERFUSION (restoration of blood flow to ischemic areas of the HEART . (bvsalud.org)

Red blood cell-derived semaphorin 7A promotes thrombo-inflammation in myocardial ischemia-reperfusion injury through platelet GPIb. (ozgene.com)
Therapy consists of the restitution of coronary perfusion which is followed by myocardial inflammation. (ozgene.com)
Efficient removal of dead cells and timely resolution of inflammation are exactly the keys to the restoration of cardiac function after myocardial ischemia-reperfusion (MI/R) injury [ 6 , 7 , 8 ]. (biomedcentral.com)
Inflammation is one of the most crucial mechanism underlying hepatic ischemia‑reperfusion injury (HIRI). (spandidos-publications.com)
van Golen RF, Reiniers MJ, Olthof PB, van Gulik TM and Heger M: Sterile inflammation in hepatic ischemia/reperfusion injury: Present concepts and potential therapeutics. (spandidos-publications.com)
The ischemic injury underlying these illnesses is complex, involving intricate interplays among many biological functions including energy metabolism, vascular regulation, hemodynamics, oxidative stress, inflammation, platelet activation, and tissue repair that take place in a context- and time-dependent manner. (cdc.gov)

Most experimental studies on cardioprotection have been undertaken in animal models, in which ischemia/reperfusion is imposed in the absence of other disease processes. (nih.gov)

We hypothesized that inhibition of Drp1 may be effective to reduce MI/R injury in diabetic hearts. (biomedcentral.com)
Delivery of Mdivi-1 into diabetic mice markedly inhibited Drp1 translocation to the mitochondria and reduced mitochondrial fission following MI/R. Inhibition of Drp1 in diabetic hearts improved mitochondrial function and cardiac function following MI/R. Moreover, inhibition of Drp1 reduced myocardial infarct size and serum cardiac troponin I and lactate dehydrogenase activities. (biomedcentral.com)
Pharmacological inhibition of Drp1 prevents mitochondrial fission and reduces MI/R injury in diabetic mice. (biomedcentral.com)
We characterize the effects of inhibition of CA with benzolamide (BZ) during cardiac ischemia-reperfusion (I/R). Langendorff perfused isolated rat hearts were subjected to 30 min of global ischemia and 60 min of reperfusion. (conicet.gov.ar)

In summary, we show that Sema7a binds to platelet GPIb and enhances platelet thrombo-inflammatory activity, aggravating post-ischemic myocardial tissue injury. (ozgene.com)

Selective intracoronary hypothermia is a novel method aimed at reducing myocardial reperfusion injury, but its presumed protective effects in AMI still await further elucidation. (tue.nl)
Many cardioprotective pharmacological agents failed to exert their protective effects in diabetic hearts subjected to myocardial ischemia/reperfusion (MI/R). Identify the molecular basis linking diabetes with MI/R injury is scientifically important and may provide effective therapeutic approaches. (biomedcentral.com)
A 24hr I/R study on 13wk old C57B/L6NJ mice showed that injection of mCBSCs and mCBSC-derived exosomes into the ischemic region of an infarct had a protective effect against I/R injury. (temple.edu)
Protective Effects of Melanocortins on Short-Term Changes in a Rat Model of Traumatic Brain Injury: Retraction. (medscape.com)
Exosomes (Exos) secreted from MSCs have protective against myocardial injury. (researchsquare.com)
To investigate the protective effects and potential mechanisms of estrogen modified human bone marrow mesenchymal stem cells (hBMSC) on high glucose (HG)-induced injury of vascular endothelial cells. (magtech.com.cn)
Estrogen may promote the secretion of NO, VEGF and IL-8 by activating the Akt/eNOS signaling pathway of hBMSC cells, increase the cell viability and migration ability of HUVECs and inhibit the occurrence of apoptosis, play a protective role against the injury of HUVECs induced by HG condition. (magtech.com.cn)
Targeting mitochondrial dynamics by restoring Klf4 might be potentially cardio-protective strategies attenuating I/R injury. (bvsalud.org)
We evaluated the myocardial protective effect of verapamil cardioplegia on the hypertrophied left ventricle during CPB. (ekja.org)
He has advanced our understanding of the mechanisms responsible for injury to the heart during ischemia and reperfusion, opening the way for developing novel protective strategies in patients with ischemic heart disease. (medicalnews.md)

We studied whether serum serotonin was associated with I/R injury assessed by ECG analysis and by analysis of TIMI myocardial perfusion grade (TMP) and myocardial blush grade (MGB). (uni-koeln.de)
Cardiac magnetic resonance (CMR) is a noninvasive imaging method that can determine myocardial anatomy, function, perfusion, and viability in a relative short examination. (cdc.gov)
Single photon emission computed tomography (SPECT) detects viability by imaging a combination of myocardial metabolism and perfusion. (cdc.gov)
Echocardiographic bubble contrast agents represent a relatively pure intravascular perfusion assessment so do not assess myocardial viability or cell membrane integrity per se. (cdc.gov)

Combining the natural inflammatory response and reactive oxygen species (ROS) overproduction after reperfusion injury, we developed a platelet-bionic, ROS-responsive RvD1 delivery platform. (biomedcentral.com)
The generation of reactive oxygen species (ROS) during myocardial ischemia (I)/reperfusion (R) contributes to postreperfusion cardiac injury. (avensonline.org)
In multiple metabolic disorders, maintaining a dynamic balance of mitochondrial number and function is necessary to prevent the overproduction of reactive oxygen species (ROS), which has been proved to be one of the important mechanisms of cardiomyocyte injury due to the mismatching of oxygen consumption and mitochondrial population and finally to heart failure. (dovepress.com)

Additionally, the application of brief repetitive episodes of ischemia/reperfusion at the immediate onset of reperfusion, which has been termed "postconditioning," reduces the extent of reperfusion injury. (nih.gov)
Mdivi-1 (1.2 mg/kg), a small molecule inhibitor of Drp1 or vehicle was administrated 15 min before the onset of reperfusion. (biomedcentral.com)
In control animals (n = 12), 115 ml of saline was infused through left atrium at the onset of reperfusion whereas treated animals (n = 8) received loading dose of MPG (40 mg/kg) infused through left atrium for 1 h followed by maintenance dose (25 mg/kg) for remaining 3 hours. (who.int)
Patients with IC have varied presentations that depend on the onset and duration of injury and extent of involvement. (hindawi.com)

Drp1 is translocated to mitochondria in models of myocardial I/R, resulting in mitochondrial fission and dysfunction. (biomedcentral.com)
Such interventions have been shown to reduce infarct size, attenuate the frequency and severity of reperfusion-induced arrhythmias, and prevent endothelial dysfunction [ 9-13 ]. (avensonline.org)
In early studies Bolli established a primary role of oxygen-free radicals in development of reversible heart dysfunction, or "myocardial stunning. (medicalnews.md)

We hypothesize that a cell permeable PKCε peptide inhibitor, (N-myristic acid-EAVSLKPT, Myr-PKCε-) given at reperfusion will improve postreperfused cardiac function and attenuate infarct size compared to untreated isolated perfused rat hearts subjected to ischemic reperfusion injury. (avensonline.org)
Infarct size (IZ) and myocardial function were assessed, and phosphorylated forms of P38MAPK, Akt and PKCε were evaluated by immunoblotting. (conicet.gov.ar)

In these diseases and aging, the pathological processes are associated with fundamental molecular alterations that can potentially affect the development of ischemia/reperfusion injury per se and responses to cardioprotective interventions. (nih.gov)

Involvement of protein tyrosine phosphatase 1B in insulin-enhanced vascular injury-induced neointima formation 3. (atsu.edu)
Chang Y, Zhuang D, Zhang C, Hassid A. Increase of PTP levels in vascular injury and in cultured aortic smooth muscle cells treated with specific growth factors. (atsu.edu)
The HIRI model was established by occluding the branch of the hepatic pedicle to the left and median liver lobes with an atraumatic vascular clamp for 45 min, followed by reperfusion for 24 h. (spandidos-publications.com)
Reperfusion takes place when there is spontaneous thrombolysis, THROMBOLYTIC THERAPY , collateral flow from other coronary vascular beds, or reversal of vasospasm. (bvsalud.org)

Present study was designed to examine the effectiveness of N-2-mercaptopropionyl glycine (MPG) on oxygen free radical (OFR) mediated reperfusion injury. (who.int)
The aims of premedication are to minimize myocardial oxygen demands by reducing heart rate and systemic arterial pressure and to improve myocardial blood flow with vasodilators. (medscape.com)
We have observed that hydrogen peroxide (H2O2), the dismutated product of superoxide, is a coronary metabolic dilator and couples myocardial oxygen consumption to coronary blood flow. (omeka.net)

METHODS: Loss-of-function and gain-of-function strategies were applied to investigate the role of Klf4 in cardiac I/R injury via genetic ablation or intra-myocardial adenovirus injection. (bvsalud.org)
A number of methods are now clinically available for assessing myocardial viability and there is overlap in the pathophysiological mechanisms that enable each of these diagnostic findings ( Figure 1 ). (cdc.gov)
Thus, all of the major cardiac imaging methods can be used to determine myocardial viability. (cdc.gov)

They were not associated with the severity of coronary artery disease, the outcome of coronary angiography, the extent of I/R injury, or the degree of heart failure. (uni-koeln.de)
In the isolated beating porcine heart model of AMI, reperfusion was associated with additional myocardial injury beyond ischemic injury. (tue.nl)
Resolvin D1 (RvD1) has been shown to provide effective protection against ischemia-reperfusion injury in multiple vital organs such as the heart, brain, kidney. (biomedcentral.com)
However, reperfusion concurrently elicits multiple adverse events, so that a significant proportion of surviving patients eventually head to heart failure. (biomedcentral.com)
Objectives: Aortic ischemia and reperfusion periods, which are often associated with infrarenal abdominal aortic cross-clamping and declamping, cause injury in distant organs including the heart. (sdu.edu.tr)
Previous studies show that notoginsenoside R1 (NG-R1), a novel saponin isolated from Panax notoginseng , protects kidney , intestine , lung , brain and heart from ischemia-reperfusion injury . (bvsalud.org)
These data suggest mat myocardial performance and rhythm disturbances are not affected by vitamin E and lipoic acid supplementation during in vivo ischemia-reperfusion in the rat heart. (umn.edu)

Dynamin-related protein 1 (Drp1)-mediated mitochondrial fission plays an important role in MI/R injury under non-diabetic conditions. (biomedcentral.com)
As mitochondria have been considered as vital cell organelles in cardiomyocytes due to their pivotal role in ATP production required for myocardial contraction and survival, targeting mitochondrial pathological alterations may be one promising strategy against diabetic ischemic injury [ 7 - 9 ]. (biomedcentral.com)
These studies suggest that Drp1-mediated mitochondrial fission plays an important role in myocardial ischemia/reperfusion (MI/R) injury under non-diabetic conditions. (biomedcentral.com)

Annexins A1 and A5 improve organ function and reduce mortality in animal sepsis models, inhibit inflammatory processes, reduce inflammatory mediator release, and protect against ischemic injury. (frontiersin.org)
Several studies have shown that Ac2‑26, the active N ‑terminal peptide of Annexin A1, could modulate anti‑inflammatory processes and protect the organs from ischemia‑reperfusion injury (IRI). (spandidos-publications.com)
Certain medications, chemical injury, collagenous colitis, inflammatory bowel disease, ischemia, and other infectious pathogens can reportedly cause mucosal injury and subsequent pseudomembrane formation. (hindawi.com)

After one hour, two hearts were treated with selective intracoronary hypothermia followed by normal reperfusion (cooled hearts). (tue.nl)

Outcome measures included mitochondrial morphology, mitochondrial function, myocardial injury, cardiac function and oxidative stress. (biomedcentral.com)

Therefore, we hypothesized that GdCl3 may attenuate myocardial injury induced by aortic IR. (sdu.edu.tr)

Collectively, NG-R1 alleviates MI/R injury by suppressing the activity of TAK1, subsequently inhibiting JNK/p38 signaling and attenuating cardiomyocyte apoptosis . (bvsalud.org)

The necessity for effective pharmacological intervention still exists, despite numerous basic studies firmly establishing that I/R injury can be delayed or even reduced by the introduction of cardioprotective agents or strategies prior to a prolonged ischemic insult (preconditioning) or at the start of reperfusion [ 1,8 ]. (avensonline.org)

Notoginsenoside R1 protects against myocardial ischemia/reperfusion injury in mice via suppressing TAK1-JNK/p38 signaling. (bvsalud.org)

However, the clinical translational potential of systemic administration of RvD1 in the treatment of ischemia-reperfusion injury is greatly limited due to biological instability and lack of targeting ability. (biomedcentral.com)

RATIONAL: Excessive mitochondrial fission is considered key process involved in myocardial ischemia/reperfusion (I/R) injury. (bvsalud.org)
This study aims to investigate how Klf4 regulates mitochondrial dynamics and further clarify its underlying mechanism during cardiac I/R injury. (bvsalud.org)
Klf4 deficiency upregulated the expression of ROCK1 at transcriptional level, thus increasing S616-DRP1-mediated mitochondrial fission during I/R. Finally, reconstitution of Klf4 inhibited mitochondrial fission, restored mitochondrial function and alleviated I/R injury. (bvsalud.org)
CONCLUSION: Our study provides the first evidence that Klf4 deficiency exacerbates myocardial I/R injury through regulating ROCK1 expression at transcriptional level to induce DRP1-mediated mitochondrial fission. (bvsalud.org)

In this study we investigated the cardioprotective mechanisms of NG-R1 in myocardial ischemia / reperfusion (MI/R) injury in vivo and in vitro . (bvsalud.org)
Activation of alkalinizing transport mechanisms associated with carbonic anhydrases (CA) leads to myocardial intracellular Ca2+ increase. (conicet.gov.ar)

We recently reported that Kupffer cell blockage with gadolinium chloride (GdCl3) attenuates lung injury induced by aortic ischemia-reperfusion (IR). (sdu.edu.tr)
Xu L, Ge F, Hu Y, Yu Y, Guo K and Miao C: Sevoflurane postconditioning attenuates hepatic ischemia-reperfusion injury by limiting HMGB1/TLR4/NF-kappaB pathway via modulating microRNA-142 in vivo and in vitro. (spandidos-publications.com)
Modified Huangqi Chifeng Decoction Attenuates Proteinuria by Reducing Podocyte Injury in a Rat Model of. (ijddc.com)

Objective: To explore the role and mechanism of the Kelch sample related protein-1-nuclear factor erythroid-2 related factor 2/antioxidant response element (Keap1-Nrf2/ARE) signaling pathway in protection of dexmedetomidine (DEX) preconditioning against myocardial ischemia/reperfusion injury (MIRI). (portlandpress.com)

Importantly, mice injected with miR-17-3p agomir were protected from adverse remodeling after cardiac ischemia/reperfusion injury. (thno.org)
MI/R injury was induced in mice by occluding the left anterior descending coronary artery for 30 min followed by 4 h reperfusion . (bvsalud.org)
To this end, a total of 72 adult C57BL/6 mice were randomly divided into sham operation (sham), ischemia‑reperfusion (I/R), I/R + Ac2‑26 and Ac2‑26 groups. (spandidos-publications.com)

Natural antioxidant can protect against cardiovascular disease - Science Daily, 6/16/12 - 'The enzyme -- glutathione peroxidase, or GPx3 -- is a natural antioxidant that helps protect organisms from oxidant injury and helps the body naturally repair itself. (qualitycounts.com)
As such, new drugs that would complement reperfusion by providing neural and cardiovascular protection and by targeting multiple abnormalities in ischemia are receiving increased attention. (cdc.gov)

Myocardial performance was analyzed by measuring 1) peak arterial pressure development and 2) the rate of change of pressure development by a catheter placed in the arch of the aorta. (umn.edu)

Afterward, hearts were isolated, and cardiodynamic function was assessed via the Langendorff model of global 20 min ischemia and 30 min reperfusion. (ac.rs)

We aimed to investigate the cardioprotective effects of ethanolic Melissa officinalis L. extract (ME) in the rat model of myocardial ischemia/reperfusion (I/R) injury. (ac.rs)

Treatment with anti-Sema7a antibody protected from myocardial tissue injury. (ozgene.com)

The rupture of an epicardial atherosclerotic plaque with superimposed thrombosis causes coronary occlusion, and this occlusion must be removed to induce reperfusion. (omeka.net)
Twenty dogs underwent 90 min of left anterior descending (LAD) coronary artery occlusion followed by 4 h of reperfusion. (who.int)
Occlusion was maintained for 25 minutes followed by a 10 minute period of reperfusion. (umn.edu)

however, reperfusion has the potential to exacerbate lethal tissue injury, a process termed "reperfusion injury. (nih.gov)

Therefore, identify the molecular basis linking diabetes with MI/R injury is scientifically important and may provide effective therapeutic approaches. (biomedcentral.com)

Despite many efforts to treat these injuries, there is still no complete recovery and complete improvement in patients with ischemic stroke. (shefayekhatam.ir)

Anatomy9

Organisms7

Diseases23

Chemicals and Drugs21

Analytical, Diagnostic and Therapeutic Techniques and Equipment27

Phenomena and Processes11

Information Science1

Health Care5

Differential regulation of Bcl-2, AP-1 and NF-kappaB on cardiomyocyte apoptosis during myocardial ischemic stress adaptation. (1/3052)

Reactive oxygen species play an important role in the activation of heat shock factor 1 in ischemic-reperfused heart. (2/3052)

Nonanticoagulant heparin prevents coronary endothelial dysfunction after brief ischemia-reperfusion injury in the dog. (3/3052)

Tumor necrosis factor-alpha contributes to ischemia- and reperfusion-induced endothelial activation in isolated hearts. (4/3052)

Effects of isoproterenol on myocardial structure and function in septic rats. (5/3052)

Formation of 4-hydroxy-2-nonenal-modified proteins in ischemic rat heart. (6/3052)

Metallothionein inhibits ischemia-reperfusion injury in mouse heart. (7/3052)

Acute exercise can improve cardioprotection without increasing heat shock protein content. (8/3052)

Myocardial Reperfusion Injury

Myocardial Reperfusion

Reperfusion Injury

Ischemic Postconditioning

Myocardial Infarction

Myocardium

Creatine Kinase

Cardioplegic Solutions

Myocardial Ischemia

Coronary Circulation

Peroxidase

Cardiotonic Agents

Reperfusion

P-Selectin

Disease Models, Animal

Hemodynamics

Heart

Random Allocation

Rats, Wistar

Rats, Sprague-Dawley

Dogs

Myocardial Contraction

Neutrophils

Thrombectomy

Wounds and Injuries

Ischemic Preconditioning, Myocardial

Suction

Time Factors

Angioplasty, Balloon, Coronary

Electrocardiography

Brain Injuries

Ischemic Preconditioning

Ventricular Function, Left

Perfusion

Heart Arrest, Induced

Thrombolytic Therapy

Coronary Vessels

Coronary Angiography

Necrosis

Ischemia

Creatine Kinase, MB Form

Mitochondria, Heart

Myocytes, Cardiac

Anterior Wall Myocardial Infarction

Coronary Thrombosis

Mitochondrial Membrane Transport Proteins

Percutaneous Coronary Intervention

Athletic Injuries

Treatment Outcome

Microcirculation

Spinal Cord Injuries

Malondialdehyde

Acute Kidney Injury

Warm Ischemia

Lung Injury

Protective Agents

Mice, Inbred C57BL

Rabbits

Immunoglobulin Fab Fragments

Platelet Glycoprotein GPIIb-IIIa Complex

Swine

Echocardiography

Brain Ischemia

Apoptosis

Endothelium, Vascular

Injury Severity Score

Neutrophil Infiltration

Oxidative Stress

L-Lactate Dehydrogenase

Liver

Leg Injuries

Cold Ischemia

Organ Preservation

Kidney

Cytoprotection

Organ Preservation Solutions

Acute Lung Injury

Superoxide Dismutase

Alanine Transaminase

Aspartate Aminotransferases