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)

Methods Mini swine (25-30 kg) were subjected to in situ left anterior descending (LAD) coronary artery ischaemia (60 min) followed by myocardial reperfusion (180 min) at the end of which myocardial infarct size was determined using tetrazolium staining. Animals were randomly assigned to the following experimental protocols: (1) control-no additional intervention; (2) RIPC-four 5-minute cycles of lower limb ischaemia/reperfusion (femoral artery clamping and declamping) were administered before the onset of myocardial ischaemia; (3) RIPC + wort-wortmannin (20 μg/kg, a PI3K inhibitor) was given intravenously 30 s before myocardial reperfusion to RIPC-treated animals; (4) RIPost-four 5-minute cycles of lower limb ischaemia/reperfusion were administered at the end of myocardial ischaemia, one minute before the onset of myocardial reperfusion; (5) RIPost + wort-wortmannin was given 30 s before myocardial reperfusion to RIPost-treated animals. ...
In the present study, we investigated the effect of lipoxin A4 on myocardial ischemia-reperfusion injury (IRI) following cardiac arrest (CA) in a rabbit model. Lipoxin A4 is a metabolite of arachidoni
Ischaemia-reperfusion (IR) injury contributes to the cardiac damage following myocardial infarction and paradoxically reduces the benefits of reperfusion therapy. In patients with ischaemic heart disease, cathepsin-L is elevated in the serum and correlates with disease severity. Our data demonstrate that cathepsin-L released from ex vivo rat hearts after ischaemia, and the cathepsin-L inhibitor CAA0225 improves cardiac function during ischaemia-reperfusion ex vivo. However, the effects of the CAA0225 in in vivo hearts during ischaemia-reperfusion are unknown. We hypothesised that using CAA0225 in an in vivo mouse model of ischaemia-reperfusion would identify the role cathepsin-L plays during ischaemia-reperfusion. Ischaemia-reperfusion injury was induced by 45 min temporary coronary artery ligation and CAA0225 was given by intra-venous injection during ischaemia before reperfusion. Double-dye staining demonstrated no difference in area at risk between groups whereas CAA0225 significantly reduced ...
TY - JOUR. T1 - Bioenergetic effect of liposomal coenzyme Q10 on myocardial ischemia reperfusion injury. AU - Niibori, Koki. AU - Wroblewski, Krzystof P.. AU - Yokoyama, Hitoshi. AU - Crestanello, Juan A.. AU - Whitman, Glenn J.R.. PY - 1999/1/1. Y1 - 1999/1/1. N2 - The antioxidant and bioenergetic effects of CoQ10 are well known but its clinical utility is limited by the requirement for enteral administration. A newly developed liposomal CoQ10 (CoQ) is water soluble and capable of intravenous administration. The purpose of this study is to determine the mechanism by which acute administration CoQ protects myocardium from reperfusion (Rp) injury. Rats were pretreated with CoQ 10 mg/kg i.v. 30 min prior to the experiment. Control rats were pretreated with liposome only. Hearts were excised and subjected to equilibration, 25 min of normothermic ischemia and 40 min of Rp on a Langendorff apparatus. At end Rp, CoQ hearts recovered 74 ± 5% of their DP vs. 50 ± 9% in control (p , 0.05). Aerobic ...
1. Barquera S, Pedroza-Tobías A, Medina C, Hernández-Barrera L,Bibbins-Domingo K, Lozano R,et al. Global overview of the epidemiology ofatherosclerotic cardiovascular disease. Arch Med Res. 2015;46(5):328-38.doi:10.1016/j.arcmed.2015.06.006.. 2. Feigin VL, Parmar PG, Barker-Collo S, Bennett DA, Anderson CS,Thrift AG, et al. Geomagnetic storms can trigger stroke evidence from 6 largepopulation-based studies in Europe and Australasia. Stroke. 2014;45(6):1639-45.doi:10.1161/STROKEAHA.113.004577.. 3. Vencloviene J, Babarskiene R, Slapikas R, Sakalyte G. Theassociation between phenomena on the sun, geomagnetic activity, meteorologicalvariables, and cardiovascular characteristic of patients with myocardialinfarction. Int J Biometeorol. 2013;57(5):797-804.doi:10.1007/s00484-012-0609-8. [MedLine]. 4. Yu L, Sun Y, Cheng L, Jin Z, Yang Y, Zhai M, et al. Melatoninreceptor-mediated protection against myocardial ischemia/reperfusion injury:role of SIRT1. J Pineal Res. ...
BACKGROUND: Preconditioning might protect the myocardium against ischemia/reperfusion injury by reducing infarct size and preventing arrhythmias. Dexmedetomidine (DEX) is a highly selective alpha(2)-agonist used for sedoanalgesia in daily anesthetic practice. The cardioprotective effects of DEX on infarct size and on the incidence of arrhythmias observed after regional ischemia/reperfusion injury in vivo have not been reported. ...
Objective: Ischemia/reperfusion (I/R) injury is an important cause of myocardial damage by means of oxidative, inflammatory, and apoptotic mechanisms. The aim of the present study was to examine the potential cardio protective effects of levosimendan in a diabetic rat model of myocardial I/R injury. ...
TY - JOUR. T1 - Activated platelets contribute importantly to myocardial reperfusion injury. AU - Xu, Yaqin. AU - Huo, Yuqing. AU - Toufektsian, Marie Claire. AU - Ramos, Susan I.. AU - Ma, Yongguang. AU - Tejani, Ankit D.. AU - French, Brent A.. AU - Yang, Zequan. PY - 2006/2/1. Y1 - 2006/2/1. N2 - Platelets become activated during myocardial infarction (MI), but the direct contribution of activated platelets to myocardial reperfusion injury in vivo has yet to be reported. We tested the hypothesis that activated platelets contribute importantly to reperfusion injury during MI in mice. After 30 min of ischemia and 60 min of reperfusion, P-selectin knockout mice had a significantly smaller infarct size than that of wild-type mice P , 0.05). Platelets were detected by P-selectin antibody in the previously ischemic region of wild-type mice as early as 2 min postreperfusion after 45 min, but not 20 min, of ischemia. The appearance of neutrophils in the heart was delayed when compared with platelets. ...
Ischemia/reperfusion (I/R) injury of heart is one of the major causes of acute cardiac injury, which may result in worsening or even loss of heart function. With novel microRNAs being evolutionarily discovered, numbers of them remained functionally unknown. We aimed to discover novel microRNAs with therapeutic or diagnostic potential in the setting of early cardiac I/R injury. Cardiac electrical activity, biochemical detection and histopathology analysis were performed to reveal early changes of cardiac I/R injury. A microRNA array was performed to screen differential microRNAs in the mouse model of cardiac I/R injury. The differentially expressed microRNAs were validated in cardiac tissues and in serum samples. The abnormality in electrocardiogram and increases in serum cTnI levels suggested the successful establishment of cardiac I/R injury in mice. A total of 1882 microRNAs were identified, of which 11 were significantly down-regulated and 41 were significantly up-regulated at 3 h post reperfusion.
TY - JOUR. T1 - Fatty acid analogue accumulation. T2 - A marker of myocyte viability in ischemic-reperfused myocardium. AU - Miller, Donald D. AU - Gill, J. B.. AU - Livni, E.. AU - Elmaleh, D. R.. AU - Aretz, T.. AU - Boucher, C. A.. AU - Strauss, H. W.. PY - 1988/1/1. Y1 - 1988/1/1. N2 - A 3-methyl substituted radioiodinated long chain fatty acid analogue was evaluated as an agent for the nonivasive detection of altered fatty acid uptake in reperfused, postischemic myocardium. This iodinated fatty acid analogue, 15-(para-iodophenyl)-3-methyl pentadecanoic acid, was given intravenously at 3 hours of reperfusion following 15 minutes (Group 1, n = 5 dogs) or 60 minutes (Group 2, n = 5 dogs) of left anterior descending coronary artery occlusion. Myocardial blood flow (MBF) was measured during occlusion and reperfusion with radiolabeled microspheres administered via the left atrium. Paired ultrasonic subendocardial crystals were placed in the ischemic perfusion bed to assess regional left ...
The present study confirms the results of our recent study19 that ischemia followed by reperfusion results in cardiac dysfunction in isolated perfused rat hearts, and the cardiac dysfunction is associated with an increase in total Ang II receptor expression in the myocardium immediately after ischemia/reperfusion. The marked increase in Ang II receptor expression could be accounted for in its entirety by an increase in AT1R expression, since AT2R expression was unchanged. In the present study, we also observed a marked increase in AT1R protein and mRNA expression in hearts exposed to ischemia/reperfusion. Although the beneficial effects of chemical blockade of AT1R have been previously shown,11 19 this is perhaps the first report on the salutary effect of AS-ODNs directed at AT1R mRNA on myocardial ischemia/reperfusion injury. AS-ODNs totally abolished the ischemia/reperfusion-induced increase in myocardial AT1R expression and protected against cardiac dysfunction induced by ischemia/reperfusion ...
Nuclear factor-kappaB (NF-kappaB) plays a central role in myocardial ischemia-reperfusion (MI/R) injury. The inhibitory protein IkappaBalpha prevents its activation. We investigated the effects of adeno-associated viral vector-mediated IkappaBalpha gene transfer in MI/R injury. Male C57BL/6 mice were randomized to receive a recombinant adeno-associated virus (rAAV) encoding the gene for the NF-kappaB inhibitory protein IkappaBalpha (rAAV- IkappaBalpha) or the beta-galactosidase gene (a control and inert gene; rAAV-LacZ), both at a dose of 10(11) copies. Four weeks later anesthetized animals were subjected to total occlusion (45 minutes) of the left main coronary artery followed by 5 hours of reperfusion. MI/R produced a wide infarct size (IF/area-at-risk = 56 +/- 8\%; IF/left ventricle = 44 +/- 5\%) and tissue neutrophil infiltration, studied by means of elastase activity (area-at-risk = 2.5 +/- 0.4 micro g/gm tissue; infarct area = 2.9 +/- 0.6 micro g/gm tissue). Furthermore MI/R caused peak ...
Background: Myocardial ischemia/reperfusion (I/R) injury is common during the treatment of cardiovascular diseases. Neuronal PAS Domain Protein 2 (NPAS2) is one of the core genes that control the rhythm of the biological clock. NPAS2 also regulates the biological rhythm. Results: The rat I/R model showed that the expression of NPAS2 decreased with the increase of reperfusion time. Overexpressing NPAS2 adenovirus (ad-NPAS2) was injected into IR rat which demonstrated that ad-NPAS2 ameliorated rats I/R injury. A hypoxia/reoxygenation (H/R) model in rat cardiomyocytes showed that ad-NPAS2 inhibited cardiomyocyte apoptosis. Co-Immunoprecipitation results showed that there is an interaction between NPAS2 and Cry2. Knockdown of Cry2 aggravated the cardiomyocyte apoptosis induced by H/R. Additionally, NPAS2 directly act on the promoter region of CX3CL1. Knockdown of CX3CL1 reverse the protective effect of ad-NPAS2 on rat myocardial ischemia-reperfusion injury and H/R-induced cardiomyocyte apoptosis. CX3CL1
Figure 5: Honokiol Ameliorates Myocardial Ischemia/Reperfusion Injury in Type 1 Diabetic Rats by Reducing Oxidative Stress and Apoptosis through Activating the SIRT1-Nrf2 Signaling Pathway
Recent studies have demonstrated that intralipid (ILP) conferred myocardial protection against ischemia-reperfusion (IR) injury through activation of reperfusion injury salvage kinase (RISK) pathway. As RISK signal has been shown to be impaired in hypertrophied myocardium, we investigated whether ILP-induced cardiac protection was maintained in hypertrophied rat hearts. Transverse aortic constriction was performed on male Sprague-Dawley rats to induce left ventricular hypertrophy, then sham-operated or hypertrophied rat hearts were isolated and perfused retrogradely by the Langendorff for 30 min (equilibration) followed by 40 min of ischemia and then 120 min of reperfusion ...
INTRODUCTION: Coronary heart disease is the leading cause of death and disability worldwide. According to WHO 7,254,000 deaths worldwide resulted from coronary heart disease (CHD) in 2013.1 The effects of CHD are usually attributable to the detrimental effects of acute myocardial ischemia- reperfusion injury (IRI). IRI typically arises in patients presenting with acute ST-segment elevation myocardial infarction (STEMI).1. The most effective therapeutic intervention for reducing acute myocardial ischemic injury is timely and effective myocardial reperfusion using either thrombolytic therapy or primary percutaneous coronary intervention (PCCI).. However, the process of myocardial reperfusion can itself induce further cardiomyocyte death, a phenomenon known as myocardial reperfusion injury.2. Although the process of myocardial reperfusion continues to improve with more timely and effective reperfusion and with advances in primary percutaneous coronary intervention techonology, antiplatelet and ...
Down-regulation of miR-24 in diabetes: a novel insight into the mechanism of diabetic exacerbation of myocardial ischaemia-reperfusion injury
TY - JOUR. T1 - Progression in attenuating myocardial reperfusion injury: An overview. AU - Bernink, F.J.P.. AU - Timmers, L.. AU - Beek, A.M.. AU - Diamant, M.. AU - Roos, S.T.. AU - van Rossum, A.C.. AU - Appelman, Y.E.A.. PY - 2014. Y1 - 2014. U2 - 10.1016/j.ijcard.2013.11.007. DO - 10.1016/j.ijcard.2013.11.007. M3 - Article. C2 - 24289874. VL - 170. SP - 261. EP - 269. JO - International Journal of Cardiology. JF - International Journal of Cardiology. SN - 0167-5273. IS - 3. ER - ...
Much has been written about myocardial reperfusion injury and the controversies surrounding its existence and clinical relevance in the past 20 to 30 years. Unfortunately, however, there is little published information that integrates research findings with the practical aspects of its management an.... Full description. ...
Acute myocardial infarction contributes significantly to mortality in patients with coronary artery disease. Timely reperfusion of an infarct-related artery within a reas..
Introduction Myocardial ischemia can defined as a state of imbalance between myocardial oxygen supply and demand. This imbalance may be caused by a reduction of blood flow and oxygen supply secondary to increased coronary vascular tone, intracoronary platelet aggregation, thrombus formation, increase heart rate, or microvascular dysfunction [1]. Damage of cardiac cells occurs because of cutting blood flow to the heart and restoration it to myocytes in a state called ischemia reperfusion (I/R) injury [2]. Thus, reperfusion can cause further injury to the myocardium and act like a double--edged sword [3]. It is accepted that the production of reactive oxygen species (ROS) plays an important role in the development (I/R) injury in cardiac cell. (I/R) also have been found to induce myocytes necrosis and apoptosis that seem to be the prevalent modes of cell death during the ischemic period and the reperfusion [4]. Apoptosis is a regulated form of cell death that can potentially be a good approaches ...
Myocardial infarction is the greatest cause of mortality worldwide, and a source of considerable morbidity. Treatment of STCelevation MI (STEMI) has improved enormously with the advent of primary percutaneous coronary intervention (PPCI), but ischaemia/reperfusion (I/R) injury remains an important complication. Evidence from animal studies points to a role for lymphocytes, and in particular T cells, in myocardial I/R injury, but this has not yet been studied in humans. The goal of my PhD was to investigate this phenomenon in human patients treated with PPCI, with particular emphasis on T cell kinetics, their relationship to I/R injury, and the potential mechanisms involved. I retrospectively analysed a large database of MI patients treated with PPCI. I demonstrated that lymphopaenia during admission was an independent predictor of increased longCterm mortality, confirming the prognostic relevance of lymphocytes in this setting for the first time. I then studied a prospectively recruited cohort ...
Reperfusion injury during myocardial infarction accounts for approximately half of final infarct size. Whereas this has been known for decades, efficacious therapy targeting reperfusion injury remains elusive. Many proteins are subject to reversible acetylation, and drugs targeting enzymes that govern these events have emerged in oncology. Among these, small molecules targeting protein deacetylating enzymes, so-called histone deacetylases (HDACs), are approved for human use in rare cancers. Now, work emerging from multiple laboratories, and in both mice and large animals, has documented that HDAC inhibition using compounds approved for clinical use confers robust cardioprotection when delivered at the time of myocardial reperfusion. Here, we summarize the key underpinnings of this science, discuss potential mechanisms, and provide a framework for a first-in-human clinical trial ...
The myocardial infarction is the main cause of morbidity and mortality in cardiovascular diseases around the world. Although the timely and complete reperfusion via Percutaneous Coronary Intervention (PCI) or thrombolysis have distinctly decreased the mortality of myocardial infarction, reperfusion itself may lead to supererogatory irreversible myocardial injury and heart function disorders, namely ischemia-reperfusion (I/R) injury. Extensive studies have indicated that non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs), play important roles in the progress of myocardial I/R injury, which is closely correlative with cardiomyocytes autophagy. Moreover, autophagy plays an important role in maintaining homeostasis and protecting cells in the myocardial ischemia reperfusion and cardiomyocyte hypoxia-reoxygenation (H/R) progress. In this review, we first introduced the biogenesis and functions of ncRNAs, and subsequently summarized the roles and
Background: Reperfusion, although essential for salvage of myocardium in the myocardial infarction, paradoxically causes a wide variety of injuries. The opening of the mitochondrial permeability pore and Ca2+ overload contribute to myocardial ischemia-reperfusion (I/R) injury.. Objectives: Necrosis, the main mechanism of cell death during I/R injury to the myocardium, is an uncontrolled cell death, a pathologic condition accompanying inflammatory responses. We aimed to examine the protective role of this novel necrosis inhibitor against myocardial I/R injury using in vitro and in vivo models through anti-necrosis pathway.. Methods and Results: Rat cardiomyocytes were exposed to hypoxia-reoxygenation injury after pretreatment with dimethyl sulfoxide (vehicle), necrosis inhibitor (NecX), antioxidant (vitamin C) or apoptosis inhibitor (Z-VAD-fmk). NecX-treated cells, compared with vehicle, showed fewer necrosis (Annexin-V/PI) (13.5±1.9% versus 44.1±3.1%; P=0.049) and more viable cells ...
Myocardial Ischemia/Reperfusion (MI/R) injury is a clinical phenomenon including myocardial structural damage, dysfunction and disorders of metabolism..
Fingerprint Dive into the research topics of Effect of estrogen on global myocardial ischemia-reperfusion injury in female rats. Together they form a unique fingerprint. ...
BACKGROUND Oral uptake of lycopene has been shown to be beneficial for preventing myocardial ischemia-reperfusion (I/R) injury. However, the strong first-pass metabolism of lycopene influences its bioavailability and impedes its clinic application. In this study, we determined an intravenous (IV) administration dose of lycopene protects against myocardial infarction (MI) in a mouse model, and investigated the effects of acute lycopene administration on reactive oxygen species (ROS) production and related signaling pathways during myocardial I/R. METHODS In this study, we established both in vitro hypoxia/reoxygenation (H/R) cell model and in vivo regional myocardial I/R mouse model by ligating left anterior artery descending. TTC dual staining was used to assess I/R induced MI in the absence and presence of acute lycopene administration via tail vein injection. RESULTS Lycopene treatment (1 μM) before reoxygenation significantly reduced cardiomyocyte death induced by H/R. Intravenous administration
TY - JOUR. T1 - Polycystin-1 mitigates damage and regulates CTGF expression through AKT activation during cardiac ischemia/reperfusion. AU - Aránguiz, P.. AU - Romero, P.. AU - Vásquez, F.. AU - Flores-Vergara, R.. AU - Aravena, D.. AU - Sánchez, G.. AU - González, M.. AU - Olmedo, I.. AU - Pedrozo, Z.. PY - 2021/1/1. Y1 - 2021/1/1. N2 - During ischemia/reperfusion (I/R), cardiomyocytes activate pathways that regulate cell survival and death and release factors that modulate fibroblast-to-myofibroblast differentiation. The mechanisms underlying these effects are not fully understood. Polycystin-1 (PC1) is a mechanosensor crucial for cardiac function. This work aims to assess the role of PC1 in cardiomyocyte survival, its role in profibrotic factor expression in cardiomyocytes, and its paracrine effects on I/R-induced cardiac fibroblast function. In vivo and ex vivo I/R and simulated in vitro I/R (sI/R) were induced in wild-type and PC1-knockout (PC1 KO) mice and PC1-knockdown (siPC1) ...
Myocardial inflammation is one of the crucial pathophysiological processes in myocardial I/R injury, which can be promoted by the release of various cytokines. The inflammatory responses ultimately aggravate tissue injury (17). Previous studies have demonstrated that the components of adaptive immunity and innate immunity are involved in myocardial I/R injury (18). The heterodimeric cytokine IL-23, primarily secreted by activated dendritic cells and macrophages, functions as a link between innate and adaptive immunity by promoting the proliferation of immune cells and secretion of cytokines (19).. In the present study, it was found that I/R significantly increased the expression of IL-23 in myocardial tissues, which was consistent with the findings of previous studies, indicating that macrophages can rapidly respond to endogenous stimulating factors following tissue injury and have a pathogenic role through their secretion of pro-inflammatory factors (20,21).. In the present study, it was found ...
This study aimed to explore the role of high mobility group [corrected] box 1 (HMGB1) and its receptor toll like receptor 4 (TLR4) on neutrophils in myocardial ischemia reperfusion (I/R) injury. We constructed TLR4-mutant (C3H/HeJ) and control (C3H/HeN) mouse models of myocardial I/R injury and subj …
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This study investigated the cardioprotective effect of vitexin against MIRI and its possible mechanism. Isolated SD rat hearts were subjected to MIRI in a Langendorff perfusion system, and H9c2 cells were subjected to hypoxia/reoxygenation (H/R) in vitro. Ex vivo experiments showed improved left ventricular function and reduced infarct size in the vitexin group. Transmission electron microscopy sh...
TY - JOUR. T1 - Extracellular matrix proteomics in cardiac Ischemia/Reperfusion. T2 - The Search Is on. AU - DeLeon, Kristine Y.. AU - De Castro Brás, Lisandra E.. AU - Lange, Richard A.. AU - Lindsey, Merry L.. PY - 2012/2/14. Y1 - 2012/2/14. KW - Editorials. KW - Extracellular matrix. KW - Extracellular matrix proteomics. KW - Ischemia-reperfusion. KW - Proteomics. UR - http://www.scopus.com/inward/record.url?scp=84857594624&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=84857594624&partnerID=8YFLogxK. U2 - 10.1161/CIRCULATIONAHA.111.086835. DO - 10.1161/CIRCULATIONAHA.111.086835. M3 - Review article. C2 - 22261193. AN - SCOPUS:84857594624. VL - 125. SP - 746. EP - 748. JO - Circulation. JF - Circulation. SN - 0009-7322. IS - 6. ER - ...
Background: Monocyte-mediated inflammation is a major mechanism of myocardial ischemia-reperfusion (IR) injury that hampers reperfusion therapy for acute myocardial infarction (MI); however, no anti-inflammatory therapy has been developed in clinical settings. Pioglitazone, a peroxisome proliferator-activated receptor (PPAR)γ agonist, has unique anti-inflammatory effects on monocytes. Here we tested the hypothesis that nanoparticle-mediated targeting of pioglitazone into IR heart ameliorates IR injury in preclinical animal models.. Methods and Results: We formulated poly(lactic acid/glycolic acid) nanoparticle containing pioglitazone (Pio-NP) and a fluorescence marker FITC (FITC-NP). In a mouse model of myocardial IR injury, intravenous administration of FITC-NP at the time of reperfusion yielded significantly higher FITC signals in the IR myocardium and in monocytes in the circulating blood IR heart. Intravenous treatment with Pio-NPs containing ≥0.1 mg/kg of pioglitazone at the time of ...
Although it is widely accepted from experimental studies that timely reperfusion limits myocardial infarct size, reperfusion by itself may not achieve the greatest possible effect. In a clinical setting, reperfusion, whether by thrombolytic therapy or emergency coronary angioplasty, never can be achieved instantaneously. Thus, adjunctive therapy, which could either slow ischemic metabolism and cellular injury pending successful reperfusion or protect myocytes against undesired, potentially lethal effects of reperfusion (lethal reperfusion injury), should have added clinical benefit for limiting infarct size. Moreover, it would be possible to treat patients at high risk of infarction prophylactically if a safe and effective cardioprotective agent could be developed.. Several endogenous mechanisms or exogenous interventions are known to both slow the rate of ischemic metabolism and delay the onset of lethal myocyte injury. For example, the speed at which ischemic cell injury occurs is markedly ...
DATE: September 19, 2019TIME: 7:00am PDT, 10:00am EDT, 3:00pm BST Cardioprotection by salvage of the infarct-affected myocardium is an unmet yet highly desired therapeutic goal
The Phase II clinical trial of FX06 (F.I.R.E. study) was completed in March 2008, with data indicating a statistically significant reduction in myocardial necrosis following intravenous application of FX06 concurrent with reperfusion. FX06 is a peptide that binds to VE-cadherin, a target on the surfaces of endothelial cells, which form the inner cell layer of blood vessels, thereby preserving blood vessel function. This leads to reduced inflammation, reduced oedema and reduced infarct sizes.. About the study:. The F.I.R.E. (FX06 In Ischemia and REperfusion) trial was conducted between October 2006 and March 2008 as a randomized, double-blind, placebo-controlled study involving 234 patients from 26 leading centres of interventional cardiology in Europe. The study evaluated infarct size in patients undergoing percutaneous coronary intervention (PCI) for acute ST-segment elevation myocardial infarction (STEMI). FX06 was administered intravenously to patients during reperfusion treatment, and the ...
Tytuł projektu: Rozbudowa i przekształcenie bibliograficznej bazy danych AGRO w bazę bibliograficzno-abstraktową z wykorzystaniem oprogramowania YADDA. Nr umowy: POIG 02.03.02-00-031/09 (okres realizacji 2009-2013 ...
Myocardial infarction, Electrocardiography, Arrhythmias, Magnetic resonance imaging, Myocardial reperfusion injury, ELEVATION MYOCARDIAL-INFARCTION, EMISSION-COMPUTED-TOMOGRAPHY, ISCHEMIC CELL-DEATH, ST-SEGMENT RECOVERY, WAVEFRONT PHENOMENON, PRIMARY ANGIOPLASTY, CORONARY-OCCLUSION, FLOW RESTORATION, COLLATERAL FLOW, AT- ...
Co-stimulatory molecules are central for shaping immune responses yet their function following myocardial infarction is not determined. Here, we will test the contribution of two co-stimulatory pathways, namely the CD40/CD40L and CD27/CD70 axes, to morphological and functional outcomes after myocardial infarction in mice. We will examine the cell type-dependent expression and function of these factors determining immune reaction after and recovery from cardiac ischemia/reperfusion injury in mice. By using genetic and pharmacological inhibition this project will help to understand the role of CD40/CD40L and CD27/CD70 following acute myocardial infarction.. ...
Sigma-Aldrich offers abstracts and full-text articles by [Xiaohui Wang, Tuanzhu Ha, Jianghuan Zou, Danyang Ren, Li Liu, Xia Zhang, John Kalbfleisch, Xiang Gao, David Williams, Chuanfu Li].
OBJECTIVE: In recent years, studies have shown that noncoding RNA (circRNA) is an important regulatory molecule involved in cell physiology and pathology.
Hansson MJ, Llwyd O, Morin D, de Paulis D, Arnoux T, Gouarné C, Koul S, Engblom H, Bordet T, Tissier R, Arheden H, Erlinge D, Halestrap AP, Berdeaux A, Pruss RM, Schaller S (2015) Differences in the profile of protection afforded by TRO40303 and mild hypothermia in models of cardiac ischemia/reperfusion injury. Eur J Pharmacol 760:7-19 ...
Zhou H et al. Pathogenesis of cardiac ischemia reperfusion injury is associated with CK2α-disturbed mitochondrial homeostasis via suppression of FUNDC1-related mitophagy. Cell Death Differ. 25, 1080-1093 (2018)(PMID:29540794 ...
TY - JOUR. T1 - Antiarrhythmic effects of ACE inhibitors: a matter of faith or reality?. AU - Gambassi, Giovanni. AU - Carbonin, Pierugo. AU - Pahor, M. PY - 1994. Y1 - 1994. N2 - review article. AB - review article. KW - Angiotensin-Converting Enzyme Inhibitors. KW - Animals. KW - Arrhythmias, Cardiac. KW - Death, Sudden, Cardiac. KW - Dogs. KW - Guinea Pigs. KW - Humans. KW - Hypertrophy, Left Ventricular. KW - Myocardial Reperfusion Injury. KW - Rats. KW - Swine. KW - Angiotensin-Converting Enzyme Inhibitors. KW - Animals. KW - Arrhythmias, Cardiac. KW - Death, Sudden, Cardiac. KW - Dogs. KW - Guinea Pigs. KW - Humans. KW - Hypertrophy, Left Ventricular. KW - Myocardial Reperfusion Injury. KW - Rats. KW - Swine. UR - http://hdl.handle.net/10807/37479. M3 - Article. VL - 28. SP - 173. EP - 182. JO - Cardiovascular Research. JF - Cardiovascular Research. SN - 0008-6363. ER - ...
The aim of the present study was to determine whether curculigoside protects against myocardial ischemia‑reperfusion injury (MIRI) and to investigate the underlying mechanisms. An in vitro model of hypoxia/reoxygenation (H/R) was established by culturing H9c2 cells under hypoxic conditions for 12 h, followed by reoxygenation for 1 h. Cell Counting kit‑8 and lactate dehydrogenase (LDH) assays were subsequently used to examine cell viability and the degree of cell injury. In addition, isolated rat hearts were subjected to 30 min of ischemia followed by 1 h of reperfusion to establish a MIRI model. Triphenyltetrazolium chloride (TTC) staining was performed to measure the infarct size. Furthermore, TUNEL staining and flow cytometry were employed to evaluate cell apoptosis. The opening of the mitochondrial permeability transition pore (MPTP) and changes in the mitochondrial membrane potential (ΔΨm) were assessed. Reverse transcription‑quantitative PCR and western blot analysis were performed ...
TY - JOUR. T1 - Sodium nitroprusside exacerbates myocardial ischemia-reperfusion injury. AU - Cope, Jeffrey T.. AU - Banks, David. AU - Laubach, Victor E.. AU - Binns, Oliver A.R.. AU - King, R. Christopher. AU - Richardson, R. Mark. AU - Shockey, Kimberly S.. AU - Tribble, Curtis G.. AU - Kron, Irving L.. PY - 1997/12/1. Y1 - 1997/12/1. N2 - Background. The role of nitric oxide in myocardial ischemia-reperfusion is controversial. Although many studies claim that nitric oxide ameliorates reperfusion injury, others suggest that it exacerbates such injury, possibly through peroxynitrite production. These discordant results may be attributable to a dose-dependent phenomenon. Methods. Isolated rabbit hearts sustained sequential periods of blood perfusion (20 minutes), warm ischemia (30 minutes), and reperfusion (20 minutes). During reperfusion, four groups underwent intracoronary infusion of saline solution (n = 6), or the nitric oxide donor sodium nitroprusside (100 nm/min [SNP100, n = 6], 1 nmol ...
b,Background,/b, Norepinephrine (NE)-derived free radicals may contribute to myocyte injury after ischemia -reperfusion, so the influence of sympathetic denervation on myocardial ischemia - reperfusion injury was investigated in the present study. ,b,Methods and Results,/b, Cardiac sympathetic denervation was produced in Wistar rats by a solution of 10% phenol 1 week before ischemia. Atenolol (0.5 mg/kg) was intravenously administered 10 min before the coronary occlusion. The left coronary artery was occluded for 30 min and thereafter reperfused. Cardiac interstitial fluid was collected by a microdialysis probe and free radicals in dialysate were determined by electron paramagnetic resonance (EPR) spin trapping, using 5,5-dimethyl-1-pyrroline-N-oxide as a spin trap. The ratio of infarct size to the ischemic area at risk (I/R) was decreased in both the phenol and atenolol groups compared with control (28.5±11.3, 31.8±10.7 vs 50.6±14.7%, p,0.05). During the coronary occlusion, concentrations of ...
Limited microRNAs (miRNAs, miRs) have been reported to be necessary for exercise-induced cardiac growth and essential for protection against pathological cardiac remodeling. Here we determined members of the miR-17-92 cluster and their passenger miRNAs expressions in two distinct murine exercise models and found that miR-17-3p was increased in both. miR-17-3p ... read more promoted cardiomyocyte hypertrophy, proliferation, and survival. TIMP-3 was identified as a direct target gene of miR-17-3p whereas PTEN was indirectly inhibited by miR-17-3p. Inhibition of miR-17-3p in vivo attenuated exercise-induced cardiac growth including cardiomyocyte hypertrophy and expression of markers of myocyte proliferation. Importantly, mice injected with miR-17-3p agomir were protected from adverse remodeling after cardiac ischemia/reperfusion injury. Collectively, these data suggest that miR-17-3p contributes to exercise-induced cardiac growth and protects against adverse ventricular remodeling. miR-17-3p may ...
TY - JOUR. T1 - (−)-Phenserine inhibits neuronal apoptosis following ischemia/reperfusion injury. AU - Chang, Cheng Fu. AU - Lai, Jing Huei. AU - Wu, John Chung Che. AU - Greig, Nigel H.. AU - Becker, Robert E.. AU - Luo, Yu. AU - Chen, Yen Hua. AU - Kang, Shuo Jhen. AU - Chiang, Yung Hsiao. AU - Chen, Kai Yun. PY - 2017/12/15. Y1 - 2017/12/15. N2 - Stroke commonly leads to adult disability and death worldwide. Its major symptoms are spastic hemiplegia and discordant motion, consequent to neuronal cell death induced by brain vessel occlusion. Acetylcholinesterase (AChE) is upregulated and allied with inflammation and apoptosis after stroke. Recent studies suggest that AChE inhibition ameliorates ischemia-reperfusion injury and has neuroprotective properties. (−)-Phenserine, a reversible AChE inhibitor, has a broad range of actions independent of its AChE properties, including neuroprotective ones. However, its protective effects and detailed mechanism of action in the rat middle cerebral ...
article: Dexmedetomidine reduces myocardial ischemia-reperfusion injury in rats through PI3K/AKT/GSK-3β signaling pathway - Minerva Cardioangiologica 2020 February;68(1):58-9 - Minerva Medica - Journals
In this study, we have demonstrated that SIRT1 is a powerful regulator in diabetic MI/R injury. This conclusion is based on several novel findings. First, we have provided evidences that SIRT1 expression was decreased in diabetic heart, and overexpression of SIRT1 alleviated MI/R injury and improved cardiac function in diabetic rats. Second, SIRT1-mediated cardioprotection involved inhibition of oxidative stress. Third, the mechanisms of the cardioprotection were mediated by modulation of eNOS activity.. Overwhelming epidemiological and clinical data have demonstrated that the diabetic heart is more sensitive to I/R injury [6, 29, 30]. It has been demonstrated that diabetes mellitus can exacerbate MIR injury and blunt the protective effect of various therapeutic agents [31, 32]. Thus, novel strategies and targets are urgently needed to reduce myocardial susceptibility to I/R injury in diabetic state. To address this issue, high-fat diet-fed and streptozotocin-induced (HFD-STZ) type 2 diabetic ...
Fingerprint Dive into the research topics of Effect of brief hypoxia on reperfusion arrhythmias and release of Ca,sup,2+,/sup, by rat heart homogenate blocked by ryanodine. Together they form a unique fingerprint. ...
Coronary artery disease is the single largest cause of mortality worldwide, with myocardial infarction being the most serious manifestation. Timely and effective myocardial reperfusion using primary PCI in acute ST elevation myocardial infarction (STEMI) has substantially improved clinical outcomes of patients. Following reopening of the blocked artery, reperfusion itself can cause myocardial injury and cell death (myocardial ischaemia/reperfusion injury). Studies in animal MI models and human therapeutic interventions indicate that ischemia/reperfusion injury is responsible for up to 50% of final infarct size. While CD4 T-lymphocytes (T-cells) have been shown to promote myocardial ischemia/reperfusion injury in the mouse model, their role during STEMI in humans is by large unknown. A low number of lymphocytes following myocardial infarction is a negative predictor of survival, and we have previously shown (PLoS One 2012) that CD4 and CD8 T-cells drop by up to 50% in the peripheral blood during ...
Restoration of blood flow after myocardial infarction (MI), surgery or fibrinolytic therapy is necessary, but can lead to cardiomyocyte dysfunction within a generalised condition commonly known as reperfusion injury. The role of cyclophilins, heat shock proteins (HSP), and the mitochondrial chaperone complex (MCC), was studied in this pathological condition. In vitro and in vivo models were used to replicate conditions of ischaemia/reperfusion (IR) injury. H9c2 and COS-7 cell lines were employed in nitric oxide (NO) donor and transfection applications. Experimental protocols were used to determine mitochondrial membrane potential (MMP), mitochondrial morphology, protein expression, enzyme activity and cell damage in these models. No difference was observed in activity or expression in cyclophilin or expression of the MCC in any of the models. It was noted that in the in vitro model, cell death was predominantly necrotic with only a minority of cells undergoing apoptosis, and as the degree of ...
TY - JOUR. T1 - Changes of endothelin-1 and big endothelin-1 levels and action potential duration during myocardial ischemia-reperfusion in dogs with and without ventricular fibrillation. AU - Vágó, Hajnalka. AU - Soós, Pál. AU - Zima, Endre. AU - Gellér, László. AU - Keltai, Katalin. AU - Róka, Attila. AU - Kékesi, Violetta. AU - Juhász-Nagy, Alexander. AU - Merkely, Béla. PY - 2004/11. Y1 - 2004/11. N2 - Myocardial ischemia-reperfusion is associated with increased production of endothelin-1 (ET-1). Moreover, exogenous ET-1 has arrhythmogenic properties. Our aim was to investigate the correlation between endogenous ET-1, big ET-1 levels and epicardial monophasic action potential duration during myocardial ischemia-reperfusion in anesthetized dogs. Thirty-minute myocardial ischemia was followed by a 90-minute reperfusion period in 18 mongrel dogs. The total incidence of ventricular fibrillation (VF) during ischemia and reperfusion was 11.1% and 33.3%, respectively. During ischemia, ...
TY - JOUR. T1 - Delayed onset of apoptosis following ischemia/reperfusion in rat liver. T2 - Downregulation of BAX gene. AU - Lai, W. Y.. AU - Chien, C. T.. AU - Cheng, C. L.. AU - Yang, B. C.. AU - Hsu, S. M.. AU - Lee, P. H.. PY - 1999/11/1. Y1 - 1999/11/1. UR - http://www.scopus.com/inward/record.url?scp=0032720663&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0032720663&partnerID=8YFLogxK. U2 - 10.1016/S0041-1345(99)00616-8. DO - 10.1016/S0041-1345(99)00616-8. M3 - Article. C2 - 10578340. AN - SCOPUS:0032720663. VL - 31. SP - 2924. EP - 2925. JO - Transplantation Proceedings. JF - Transplantation Proceedings. SN - 0041-1345. IS - 7. ER - ...
Myocardial infarction (MI) is one of the leading causes of death. Wilms' tumor 1-associating protein (WTAP), one of the components of the m6A methyltransferase complex, has been shown to affect gene expression via regulating mRNA modification. Although WTAP has been implicated in various diseases, its role in MI is unclear. In this study, we found that hypoxia/reoxygenation (H/R) time-dependently increased WTAP expression, which in turn promoted endoplasmic reticulum (ER) stress and apoptosis, in human cardiomyocytes (AC16). H/R effects on ER stress and apoptosis were all blocked by silencing of WTAP, promoted by WTAP overexpression, and ameliorated by administration of ER stress inhibitor, 4-PBA. We then investigated the underlying molecular mechanism and found that WTAP affected m6A methylation of ATF4 mRNA to regulate its expression, and that the inhibitory effects of WTAP on ER stress and apoptosis were ATF4 dependent. Finally, WTAP’s effects on myocardial I/R
There is vast literature on the topic of ischemia-reperfusion injury. A summative discussion of the complex pathogenicity will aid practicing physicians in diagnosis and management. We offer a review of this literature as well as a discussion on a rare case of tense edematous bullae as a presentation of ischemia-reperfusion injury. A 65-year-old male underwent a right femoropopliteal bypass for rest pain that had not improved after iliac stent placement. He presented three days after discharge with blistering lesions on the reperfused limb that resembled bullous pemphigoid. This case describes the variability in the presentation of reperfusion injury, as well as the necessity to educate those managing atypical presentations of reperfusion injury.
OBJECTIVE Ischemia reperfusion injury is partly responsible for the high mortality associated with induced myocardial injury and the reduction in the full benefit of myocardial reperfusion. Remote ischemic preconditioning, perconditioning, and postconditioning have all been shown to be cardioprotective. However, it is still unknown which one is the most beneficial. To examine this issue, we used adult male Wistar rat ischemia reperfusion models to compare the cardioprotective effect of these three approaches applied on double-sided hind limbs. METHODS The rats were randomly distributed to the following five groups: sham, ischemia reperfusion, remote preconditioning, remote perconditioning, and remote post-conditioning. The ischemia/reperfusion model was established by sternotomy followed by a 30-min ligation of the left coronary artery and a subsequent 3-h reperfusion. Remote conditioning was induced with three 5-min ischemia/5-min reperfusion cycles of the double-sided hind limbs using a tourniquet.
CCD-WT mice exhibited heightened nociception than pain free mice and nociception tightly correlated with circulating aldehyde (4-HNE) accumulation and cardiac protein carbonylation. CCD induced 4-HNE overload provoked cardiac SIRT1 carbonylative inactivation and impairment the cardioprotection of LKB1-mediated AMPK activation during MI/R, which resulting in enhanced MI/R injury and higher mortality compare with pain free WT mice. In comparison to WT, chronic neuropathic pain enhanced susceptibility to MI/R injury was further exacerbated by ALDH2 deficiency in which associated with more impaired SIRT1-LKB1-AMPK signaling. Further, peripheral injection of 4-HNE induced a sustained allodynia, and increased circulating aldehyde load to the same degree as that seen in CCD-WT mice. The 4-HNE exposure can simulate cardiac SIRT1 carbonylative inactivation and sensitization to MI/R injury, which was observed in CCD-WT mice. However, treatment of CCD-WT mice with ALDH2-selective activator (Alda-1) ...
Mitochondria-mediated cardiomyocyte apoptosis is involved in myocardial ischemia/reperfusion (MI/R) injury. Clematichinenoside (AR) is a triterpenoid saponin isolated from the roots of Clematis chinensis with antioxidant and anti-inflammatory cardioprotection effects against MI/R injury, yet the anti-apoptotic effect and underlying mechanisms of AR in MI/R injury remain unclear. We hypothesize that AR may improve mitochondrial function to inhibit MI/R-induced cardiomyocyte apoptosis. In this study, we replicated an in vitro H9c2 cardiomyocyte MI/R model by hypoxia/reoxygenation (H/R) treatment. The viability of H9c2 cardiomyocytes was determined by MTT assay; apoptosis was evaluated by flow cytometry and TUNEL experiments; mitochondrial permeability transition pore (mPTP) opening was analyzed by a calcein-cobalt quenching method; and mitochondrial membrane potential (ΔΨm) was detected by JC-1. Moreover, we used western blots to determine the mitochondrial cytochrome c translocation to cytosolic and
TY - JOUR. T1 - The harmful effects of ventricular distention during postischemic reperfusion. AU - Lucas, S. K.. AU - Schaff, H. V.. AU - Flaherty, J. T.. AU - Gott, Vincent L. AU - Gardner, T. J.. PY - 1981. Y1 - 1981. N2 - To assess the effects of left ventricular distention during the early reperfusion period following ischemic arrest, 16 canine heart preparations were subjected to 45 minutes of hypothermic (27°C) cardioplegic arrest and normothermic reperfusion. Isovolumic left ventricular developed pressure and rate of rise of left ventricular pressure (dP/dt) were measured with an intraventricular balloon; endocardial/epicardial flow ratios were determined with microspheres; and myocardial gas tensions were monitored with mass spectrometry. During early reperfusion, Group 1 hearts (n=8) were not distended (end-diastolic pressure = 0). Group 2 hearts (n = 8) were subjected to an enddiastolic pressure of 20 mm Hg for the initial 15 minutes of reperfusion. Group 2 hearts demonstrated ...
Objectives. Pharmacological treatment of reperfusion injury using insulin and GSK3β inhibition has been shown to be cardioprotective, however, their interaction with the endogenous cardioprotective strategy, ischemic postconditioning, is not known. Design. Langendorff perfused ex vivo rat hearts were subjected to 30 min of regional ischemia and 120 min of reperfusion. For the first 15 min of reperfusion hearts received either vehicle (Ctr), insulin (Ins) or a GSK3β inhibitor (SB415286; SB41), with or without interruption of ischemic postconditioning (IPost; 3 × 30 s of global ischemia). In addition, the combination of insulin and SB41 for 15 min was assessed. Results. Insulin, SB41 or IPost significantly reduced infarct size versus vehicle treated controls (IPost 33.5 ± 3.3%, Ins 33.5 ± 3.4%, SB41 30.5 ± 3.0% vs. Ctr 54.7 ± 6.8%, p , 0.01). Combining insulin and SB415286 did not confer additional cardioprotection compared to the treatments given alone (SB41 + Ins 26.7 ± 3.5%, ns). ...
The antioxidant properties of flavonols in vivo and their potential benefits in myocardial ischaemia/reperfusion (I/R) injury have been little investigated. We evaluated the ability of a synthetic flavonol, 3,4-dihydroxyflavonol (DiOHF) to scavenge superoxide in post-I/R myocardium and to prevent myocardial I/R injury. 2 Anaesthetized sheep were studied in four groups (n = 5-6): control, ischaemic preconditioning (IPC), vehicle and DiOHF (before reperfusion, 5 mg kg-1, i.v.). The left anterior descending coronary artery was occluded distal to the second diagonal branch for 1 h followed by 2 h of reperfusion. Infarct size, myocardial function, NADPH-activated superoxide generation and biochemical markers of injury were measured. 3 DiOHF (10-8-10-4 M) incubated in vitro with post-I/R myocardium from the vehicle group suppressed superoxide production dose-dependently. DiOHF administered in vivo also significantly reduced superoxide generation in vitro. 4 DiOHF and IPC markedly reduced infarct ...
Experimental and clinical studies have demonstrated that myocardial ischemia induces activation of various components of the renin-angiotensin system (RAS), including angiotensinogen, renin, angiotensin-converting enzyme (ACE), angiotensins, and angi
Early myocardial reperfusion is an effective therapy but ischemia/reperfusion (I/R) causes lethal myocardial injury. The aging heart was reported to show greater cardiac damage after I/R injury than that observed in young hearts. Senescence marker protein 30 (SMP30), whose expression decreases with age, plays a role in reducing oxidative stress and apoptosis. However, the impact of SMP30 on myocardial I/R injury remains to be determined. In this study, the left anterior descending coronary artery was occluded for 30 min, followed by reperfusion in wild-type (WT) and SMP30 knockout (KO) mice. After I/R, cardiomyocyte apoptosis and the ratio of infarct area/area at risk were higher, left ventricular fractional shortening was lower, and reactive oxygen species (ROS) generation was enhanced in SMP30 KO mice. Moreover, the previously increased phosphorylation of GSK-3β and Akt was lower in SMP30 KO mice than in WT mice. In cardiomyocytes, silencing of SMP30 expression attenuated Akt and GSK-3β
Weve investigated the consequences of hypoxia and myocardial ischemia/reperfusion for the framework and function of cytochrome oxidase (CcO). immunoprecipitated CcO complicated. Most oddly enough, both H89 and MPI put into the perfusion moderate dramatically decreased the ischemia/reperfusion problems for the myocardial cells. Our results directed to a thrilling chance for using CcO activity modulators for managing myocardial damage connected with ischemia and oxidative tension circumstances. 404950-80-7 Cytochrome oxidase (CcO)3 may be the terminal oxidase from the mitochondrial 404950-80-7 electron transportation string, whose activity is normally modulated in response to O2 stress and the task load from the tissues (1-6). This rate-limiting enzyme can be an essential site of legislation of mitochondrial respiration and oxidative phosphorylation (7). In the 404950-80-7 SCA12 fungus, changed CcO activity in response to aerobic and anaerobic circumstances is from the differential appearance of ...
TY - JOUR. T1 - Impact of a novel cardioprotective agent on the ischaemia-reperfusion- induced Akt kinase activation. AU - Toth, Ambrus. AU - Kovacs, Krisztina. AU - Deres, Peter. AU - Halmosi, Robert. AU - Czopf, Laszlo. AU - Hanto, Katalin. AU - Kalai, Tamas. AU - Hideg, Kalman. AU - Sumegi, Balazs. AU - Toth, Kalman. PY - 2003/12/1. Y1 - 2003/12/1. N2 - Cardioprotective effect of a free radical-scavenging compound (HO-3073) was examined during ischaemia-reperfusion (IR) in isolated heart perfusion system and its influence on the pro-survival Akt signalling pathway was addressed. Rat hearts were perfused according to the Langendorff method and subjected to a global 25-min ischaemia and 15, 45 and 90-min reperfusion either untreated or treated with HO-3073 (2, 5 and 10μM) and/or wortmannin (100nM, inhibitor of phosphatidylinositol-3-kinase). HO-3073 facilitated the recovery of myocardial energy metabolism as assessed by 31P NMR spectroscopy (creatine phosphate recovery in reperfusion was ...
Ischaemic preconditioning is the most powerful endogenous mechanism for limiting myocardial infarct size in the experimental setting. Its clinical application is limited to scenarios in which the index episode of ischaemia and reperfusion can be anticipated such as in the setting of cardiac surgery • Ischaemic postconditioning represents an endogenous cardioprotective strategy which is applied at the onset of myocardial reperfusion, thereby allowing its use as an adjunct to reperfusion in patients presenting with an acute myocardial infarction • Both ischaemic preconditioning and postconditioning recruit a common signal transduction pathway at the time of myocardial reperfusion, which can be targeted by pharmacological agents administered as adjuncts to reperfusion. ...
TY - JOUR. T1 - S1P 3-mediated cardiac fibrosis in sphingosine kinase 1 transgenic mice involves reactive oxygen species. AU - Takuwa, Noriko. AU - Ohkura, Sei Ichiro. AU - Takashima, Shin Ichiro. AU - Ohtani, Keisuke. AU - Okamoto, Yasuo. AU - Tanaka, Tamotsu. AU - Hirano, Kaoru. AU - Usui, Soichiro. AU - Wang, Fei. AU - Du, Wa. AU - Yoshioka, Kazuaki. AU - Banno, Yoshiko. AU - Sasaki, Motoko. AU - Ichi, Ikuyo. AU - Okamura, Miwa. AU - Sugimoto, Naotoshi. AU - Mizugishi, Kiyomi. AU - Nakanuma, Yasuni. AU - Ishii, Isao. AU - Takamura, Masayuki. AU - Kaneko, Shuichi. AU - Kojo, Shosuke. AU - Satouchi, Kiyoshi. AU - Mitumori, Kunitoshi. AU - Chun, Jerold. AU - Takuwa, Yoh. PY - 2010/2. Y1 - 2010/2. N2 - Aims Sphingosine kinase 1 (SPHK1), its product sphingosine-1-phosphate (S1P), and S1P receptor subtypes have been suggested to play protective roles for cardiomyocytes in animal models of ischaemic preconditioning and cardiac ischaemia/reperfusion injury. To get more insight into roles for SPHK1 in ...
Cardiovascular drugs attenuated myocardial resistance against ischaemia-induced and reperfusion-induced injury in a rat model of repetitive occlusion ...
BACKGROUND: Acute myocardial infarction is one of the leading causes of death. It is caused by a blockage of a coronary artery leading to reduced blood flow to the myocardium and hence ischemic damage. In addition, a second wave of damage after the flow has been restored, named reperfusion injury greatly exacerbate the damage. For the latter, no medical treatment exist. In this study the aim was to characterize Ca(2+) sensitivity in coronary arteries following experimental ischemia/reperfusion injury.. METHODS: Arteries were isolated from hearts exposed to a well-established rat ischemia/reperfusion model. Wire myograph combined with FURA2-AM measurements was applied to study the Ca(2+) dependency of the vasoconstriction.. RESULTS: The results presented herein show that ETB receptors (R) have much weaker Ca(2+)-sensitizing effect than ETA-R and that ETB-R appear to be more dependent on Ca(2+) influx presumably through voltage-gated Ca(2+) channels (VGCC). In addition, we show that there is an ...
Ticlopidin is a well-known antithrombocytic drug used in the prophylaxis of arteriosclerotic diseases. Ticlopidin is supposed to reduce ischemia reperfusion injury with its effects against platelet aggregation which play important roles in ischemia reperfusion injury by means of different mediators. 32 female Sprague-Dawley rats were randomised to four groups one being as control in the study design. Only anesthesia was performed to group 1 (n=8). The right hind limb ischemia was induced by tourniquets applied at the hip level group 2 (n=8). After 4 hours the samples were collected before tourniquets were removed. Group 3 (n=8) and group 4 (n=8) rats were randomised to 2 hours of reperfusion after 4 hours of ischemia. Ticlopidin (50 mg/day) were given five days before the experiment day twice daily to the animals in the group 4. Tissue malondialdehyde levels were recorded by thiobarbutiric acid method as a marker for lipid peroxidation. According to the lung levels of malondialdehide, ticlopidin ...
Our data clearly demonstrate significant cardioprotective activities of the novel small molecule C1 inhibitor (C1s-INH-248) in myocardial ischemia and reperfusion. The cardioprotection exerted by C1s-INH-248 was characterized by a reduction of necrosis and decreased serum CK activity compared with rabbits given the vehicle only. The cardioprotective effect of C1s-INH-248 was dose dependent when administrated as a 0.1-1 mg/kg body weight bolus injection. Even compared with the treatment with the C1 esterase inhibitor (C1-INH) C1s-INH-248 demonstrated superior potency. The protection of C1s-INH-248 also resulted in inhibition of PMN accumulation in the reperfused myocardium. Further, the protective effect could be attributed to decreased deposition of C5b-9 on ischemic reperfused myocardium or vascular endothelial cells. To our knowledge, this is the first study demonstrating cardioprotection with a highly specific synthetic C1 inhibitor following myocardial ischemia and reperfusion.. To date, ...
Background: Cardiac autophagic flux is impaired during myocardial ischemia/reperfusion (MI/R). Impaired autophagic flux may exacerbate MI/R injury. Charged multivesicular body protein 2B (CHMP2B) is a subunit of the endosomal sorting complex required for transport (ESCRT-III) complex that is required for autophagy. However, the reverse role of CHMP2B accumulation in autophagy and MI/R injury has not been established. The objective of this article is to elucidate the roles of AMP-activated protein kinase (AMPK)/atrogin-1 pathways in inhibiting CHMP2B accumulation in ischemia-reperfusion injury. Methods: Male C57BL/6 mice (3-4 months) and H9c2 cardiomyocytes were used to evaluate MI/R and hypoxia/reoxygenation (H/R) injury in vivo and in vitro, respectively. MI/R was built by a left lateral thoracotomy and occluded the left anterior descending artery. H9c2 cells were firstly treated in 95% N2 and 5% CO2 for 15 h and reoxygenation for 1 h. Metformin (100 mg/kg/d) and CHMP2B (Ad-CHMP2B) transfected ...
As progressive organ shortage in cardiac transplantation demands extension of donor criteria, effort is needed to optimize graft survival. Reactive oxygen and nitrogen species, generated during organ procurement, transplantation, and reperfusion, contribute to acute and late graft dysfunction. The combined application of diverse substances acting via different molecular pathways appears to be a reasonable approach to face the complex mechanism of ischemia reperfusion injury. Thus, an antioxidant solution containing |i|α|/i|-ketoglutaric acid, 5-hydroxymethylfurfural, |i|N|/i|-acetyl-L-methionine, and |i|N|/i|-acetyl-selenium-L-methionine was combined with endogenous angiotensin-(1-7). Its capacity of myocardial protection was investigated in isolated Langendorff-perfused rat hearts subjected to warm and cold ischemia. The physiological cardiac parameters were assessed throughout the experiments. Effects were evaluated via determination of the oxidative stress parameters malondialdehyde and carbonyl
TY - JOUR. T1 - Hydrogen Flush After Cold Storage as a New End-Ischemic Ex Vivo Treatment for Liver Grafts Against Ischemia/Reperfusion Injury. AU - Tamaki, Ichiro. AU - Hata, Koichiro. AU - Okamura, Yusuke. AU - Nigmet, Yermek. AU - Hirao, Hirofumi. AU - Kubota, Toyonari. AU - Inamoto, Osamu. AU - Kusakabe, Jiro. AU - Goto, Toru. AU - Tajima, Tetsuya. AU - Yoshikawa, Junichi. AU - Tanaka, Hirokazu. AU - Tsuruyama, Tatsuaki. AU - Tolba, Rene H.. AU - Uemoto, Shinji. PY - 2018/11. Y1 - 2018/11. N2 - Cold storage (CS) remains the gold standard for organ preservation worldwide, although it is inevitably associated with ischemia/reperfusion injury (IRI). Molecular hydrogen (H2) is well known to have antioxidative properties. However, its unfavorable features, ie, inflammability, low solubility, and high tissue/substance permeability, have hampered its clinical application. To overcome such obstacles, we developed a novel reconditioning method for donor organs named hydrogen flush after cold storage ...
TY - JOUR. T1 - Anticoagulant therapy in critical organ ischaemia/reperfusion injury. AU - Loubele, Sarah T. B. G.. AU - ten Cate, Hugo. AU - Spronk, Henri M. H.. PY - 2010/7. Y1 - 2010/7. KW - Ischaemia/reperfusion injury. KW - anti-coagulant therapy. KW - animal models. KW - inflammation. KW - apoptosis. U2 - 10.1160/TH09-08-0582. DO - 10.1160/TH09-08-0582. M3 - Article. VL - 104. SP - 136. EP - 142. JO - Thrombosis and Haemostasis. JF - Thrombosis and Haemostasis. SN - 0340-6245. IS - 1. ER - ...
ABCC6 is expressed mainly in liver and kidney, and phenotypes associated with PXE appear to be complemented by a circulating factor11; thus, restoration of the natural substrate of ABCC6 may be of clinical benefit in the setting of PXE.23 Although Abcc6-deficient mice do not develop myocardial infarction, as noted in some patients with PXE, the data herein demonstrates a significant increase in infarct size using the mouse model subjected to cardiac I/R. This was accompanied by an increased inflammatory infiltrate but no change in cardiac calcification or perfusion, reflected by a similar region at risk following I/R, and no change in baseline cardiac function as determined by echocardiography. Our results suggest that the substrate of ABCC6 may have a wider therapeutic value, including broader use in the setting of myocardial infarction. Importantly, the consequences of Abcc6 deficiency on adverse outcomes following cardiac I/R may occur at the level of the cardiac myocyte, which is a novel ...
Keywords: Ethanol, ischemia-reperfusion injury, preconditioning, heart. Abstract: Epidemiological studies demonstrate that excessive drinking is associated with hypertension, cerebral bleeding and loss of cardiac contractility. Conversely, studies have shown that mortality rates for people who regularly drink ethanol in moderation are lower than in abstainers, primarily due to decreased fatal ischemic heart disease. Further, moderate ethanol consumers have lower rates of myocardial infarction compared with abstainers. These beneficial cardiac effects may be due to pleiotropic effects of ethanol on lipids, platelets, and fibrinolytic activity. During the past decade, studies conducted in several animal models have revealed that light to moderate regular ethanol consumption renders hearts more tolerant to myocardial ischemia-reperfusion injury; to a degree similar to cardiac ischemic preconditioning (brief episodes of ischemia dramatically limit infarct size following prolonged ischemia). Recent ...
Abstract. Objective: To investigate the effect of ischemic postconditioning on protein aggregation caused by transient ischemia and reperfusion and to clarify its underlying mechanism.. Methods: Two-vessel-occluded transient global ischemia rat model was used. The rats in ischemic postconditioning group were subjected to three cycles of 30-s/30-s reperfusion/clamping after 15min of ischemia. Neuronal death in the CA1 region was observed by hematoxylin-eosin staining, and number of live neurons was assessed by cell counting under a light microscope. Succinyl-LLVY-AMC was used as substrate to assay proteasome activity in vitro. Protein carbonyl content was spectrophotometrically measured to analyze protein oxidization. Immunochemistry and laser scanning confocal microscopy were used to observe the distribution of ubiquitin in the CA1 neurons. Western blotting was used to analyze the quantitative alterations of protein aggregates, proteasome, hsp70 and hsp40 in cellular fractions under different ...
In the present study, dogs were pretreated with intravenous digoxin, 0.0125 mg/kg/day, for 6 to 7 consecutive days to achieve clinically relevant serum concentrations; untreated animals were used as control subjects. After pretreatment, nine digoxin-
TY - JOUR. T1 - Acute inflammatory reaction after myocardial ischemic injury and reperfusion. Development and use of a neutrophil-specific antibody. AU - Hawkins, Hal K.. AU - Entman, Mark L.. AU - Zhu, Jessica Y.. AU - Youker, Keith A.. AU - Berens, Kurt. AU - Doré, Monique. AU - Smith, C. Wayne. PY - 1996/6. Y1 - 1996/6. N2 - Reperfusion of the infarcted canine myocardium after 1 hour of ischemia is associated with an acute inflammatory infiltrate at the border of the infarct. In this paper, we demonstrate that early margination and emigration of neutrophils originate in thin-walled (∼5-μm) venous cisterns that average 200 μm in length and vary from 10 to 70 μm in width and show strong constitutive expression of both ICAM-1 and P-selectin; this class of vessels (venous cisterns) appears to be a unique feature in heart. A monoclonal antibody (SG8H6) with specificity for canine neutrophils was developed that allowed much more sensitive immunohistochemical detection of neutrophils in tissue ...
Despite prompt reperfusion by primary percutaneous coronary intervention (PPCI), the mortality and morbidity of patients presenting with an acute ST-segment elevation myocardial infarction (STEMI) remain significant with 9% death and 10% heart failure at 1 year. In these patients, one important neglected therapeutic target is myocardial reperfusion injury, a term given to the cardiomyocyte death and microvascular dysfunction which occurs on reperfusing ischaemic myocardium. A number of cardioprotective therapies (both mechanical and pharmacological), which are known to target myocardial reperfusion injury, have been shown to reduce myocardial infarct (MI) size in small proof-of-concept clinical studies-however, being able to demonstrate improved clinical outcomes has been elusive ...
Introduction: Ischemia/Reperfusion (IR) injury mainly causes the increase of enzymes involved in myocytes injury including CK-MB (creatine kinase-MB) isoenzyme and LDH (lactate dehydrogenase). Leakage of CK-MB isoenzyme and LDH from myocardial tissues to blood is indicator of acute myocardial infarction. The aim of this study was to assess the effect of HEMADO on IR injury and its relationship with mitochondrial ATP-sensitive K+ channels (mitoKATP) in rat heart. Methods: Twenty eight male Wistar rats (250-300g) were divided into four groups (seven members in each group): control (without ischemia), I/R (with ischemia+without HEMADO), ischemia received HEMADO (HEMADO), ischemia received HEMADO and 5-HD (5-hydroxydecanoate, specific mitoKATP channel blocker) (HEMADO+5-HD). The animals were anesthetized and the hearts were quickly removed and mounted on Langendorff apparatus and perfused by Krebs-Henseleit solution under constant pressure and temperature of 37ºC. After 20 minutes of stabilization,
Yellon, Derek M.; Hausenloy, Derek J. (2007-09-13). "Myocardial Reperfusion Injury". New England Journal of Medicine. 357 (11 ... Targeting ischemia/reperfusion injury[edit]. Main article: Reperfusion injury. With reperfusion comes ischemia/reperfusion (IR ... Myocardial infarction[edit]. Main article: Myocardial infarction. Myocardial infarction (MI) or heart attack, is caused by ... "Targeting reperfusion injury in patients with ST-segment elevation myocardial infarction: trials and tribulations". European ...
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 ...
H 2S donors reduce myocardial injury and reperfusion complications. Increased H 2S levels within the body will react with ... Non-safety related ) "Reduction of Ischemia-Reperfusion Mediated Cardiac Injury in Subjects Undergoing Coronary Artery Bypass ... 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 ...
H 2S donors reduce myocardial injury and reperfusion complications. Increased H 2S levels within the body will react with ... Nitric oxide can contribute to reperfusion injury when an excessive amount produced during reperfusion (following a period of ... "Endogenous sulfur dioxide protects against isoproterenol-induced myocardial injury and increases myocardial antioxidant ... Non-safety related ) "Reduction of Ischemia-Reperfusion Mediated Cardiac Injury in Subjects Undergoing Coronary Artery Bypass ...
May 2010). "Exosome secreted by MSC reduces myocardial ischemia/reperfusion injury". Stem Cell Research. 4 (3): 214-22. doi: ...
"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 ( ...
... 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: ...
"Effect of trapidil in myocardial ischemia-reperfusion injury in rabbit". Indian Journal of Pharmacology. 46 (2): 207-10. doi: ...
"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 ...
"Acute humanin therapy attenuates myocardial ischemia and reperfusion injury in mice". Arteriosclerosis, Thrombosis, and ...
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 ...
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 ...
"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 ...
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 lasting up to 72 hours post the ischaemia and reperfusion stimulus. In an experimental ...
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 ...
"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) ...
... which play a role in myocardial reperfusion injury. This was a result of the relation between Nox2 and signaling necessary for ... NOX2 and NOX4 in myocardial ischemia/reperfusion injury". Journal of Molecular and Cellular Cardiology. 64: 99-107. doi:10.1016 ... It has also been shown to play a part in determining the size of a myocardial infarction due to its connection to ROS, ... Since Nox2 was shown to play a huge part in determining the size of a myocardial infarction, this transforms the protein into a ...
"Protective role of deoxyschizandrin and schisantherin a against myocardial ischemia-reperfusion injury in rats". PLOS ONE. 8 (4 ...
"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 ...
... 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 ...
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 ...
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 ...
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 ...
"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 ...
... binding lectin-associated serine protease-2 confers protection from myocardial and gastrointestinal ischemia/reperfusion injury ...
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 ...
Prevents Spontaneous Ventricular Arrhythmias and Reduces Infarct Size During Myocardial Ischemia/Reperfusion Injury in Open- ...
Lauver DA, Booth EA, White AJ, Poradosu E, Lucchesi BR (2005). "Sulodexide attenuates myocardial ischemia/reperfusion injury ... recent research has also demonstrated the beneficial effects of sulodexide in animal models of reperfusion injury and the ...
... effect of the alcoholic extract of Terminalia arjuna bark in an in vivo model of myocardial ischemic reperfusion injury". Life ...
Oxidants interfere with the normal brain chemistry and cause further damage (this is known as "reperfusion injury"). ... Hyperbaric oxygen therapy is being evaluated with the reduction in total and myocardial creatine phosphokinase levels showing a ... which have a role in reperfusion injury after asphyxia.[26] Research by Ola Didrik Saugstad and others led to new international ... Brain injury may still occur in a TIA lasting only a few minutes. Having a TIA is a risk factor for eventually having a stroke. ...
Influence on Vitamin C Bioavailability and Capacity to Protect Against Ischemia-Reperfusion Injury". Nutrition and Metabolic ... A 2013 meta-analysis found no evidence that vitamin C supplementation reduces the risk of myocardial infarction, stroke, ...
... and cardiodepressant properties in ischemic preconditioning and myocardial ischemia-reperfusion induced cardiac injury. Journal ...
Mechanical: vascular injury, pneumothorax (by placing pulmonary artery catheter), tracheal injury/stenosis (result of ... fat emboli and reperfusion pulmonary edema after lung transplantation or pulmonary embolectomy. However, the majority of these ... Cardiac: abnormal heart rhythms, myocardial dysfunction. *Kidney: acute kidney failure, positive fluid balance ... Comparison of two fluid-management strategies in acute lung injury". N Engl J Med. 354 (24): 2564-2575. doi:10.1056/ ...
... on myocardial ischemic reperfusion injury' in Molecular and Cellular Biochemistry vol. 289 (2006) pp. 55-63. PMID 16628469 ...
Endothelial injury: Injury to the endothelial causing platelet activation and aggregation *Common causes include: trauma, ... Main articles: Thrombolysis, Thrombosis prophylaxis, and Reperfusion therapy. This section needs more medical references for ... This means that cerebral stroke, myocardial infarction, or any other organ can be affected. ... A thrombus is a healthy response to injury intended to prevent bleeding, but can be harmful in thrombosis, when clots obstruct ...
Ischemia-reperfusion injury of the appendicular musculoskeletal system. ReferencesEdit. *^ a b c GRCh38: Ensembl release 89: ... elevated myoglobin has low specificity for acute myocardial infarction (AMI) and thus CK-MB, cardiac Troponin, ECG, and ... Myoglobin is a sensitive marker for muscle injury, making it a potential marker for heart attack in patients with chest pain.[ ... In humans, myoglobin is only found in the bloodstream after muscle injury. It is an abnormal finding, and can be diagnostically ...
Endothelial injury: Injury to the endothelium (interior surface of blood vessel), causing platelet activation and aggregation; ... Main articles: Thrombolysis, Thrombosis prophylaxis, and Reperfusion therapy. Anticoagulants are drugs used to prevent the ... This means that cerebral stroke, myocardial infarction, or any other organ can be affected. ... A thrombus is a healthy response to injury intended to prevent bleeding, but can be harmful in thrombosis, when clots obstruct ...
A medical emergency is an acute injury or illness that poses an immediate risk to a person's life or long-term health, ... In addition, there is a direct relationship between time-to-treatment and the success of reperfusion (restoration of blood flow ... stroke and myocardial infarction (heart attack). In the case of stroke, there is a window of three hours within which the ...
"MRL mice fail to heal the heart in response to ischemia-reperfusion injury". Wound Repair and Regeneration. 13 (2): 205-8. doi: ... MRL mice are not protected against myocardial infarction; heart regeneration in adult mammals (neocardiogenesis) is limited, ... One of the most studied regenerative responses in humans is the hypertrophy of the liver following liver injury.[89][90] For ... MRL mice show the same amount of cardiac injury and scar formation as normal mice after a heart attack.[84] However, recent ...
Most notably, SOD1 is pivotal in reactive oxygen species (ROS) release during oxidative stress by ischemia-reperfusion injury, ... "Myocardial reperfusion: a double-edged sword?". The Journal of Clinical Investigation. 76 (5): 1713-9. doi:10.1172/JCI112160. ... "Past and present course of cardioprotection against ischemia-reperfusion injury". Journal of Applied Physiology. 103 (6): 2129- ... SOD1 has been implicated in cardioprotection against ischemia-reperfusion injury, such as during ischemic preconditioning of ...
"Effect of low-level laser therapy on lung injury induced by hindlimb ischemia/reperfusion in rats". Lasers in Medical Science ... Ad, N. (2001-10-01). "Impact of low level laser irradiation on infarct size in the rat following myocardial infarction". ... "Low-level laser irradiation improves functional recovery and nerve regeneration in sciatic nerve crush rat injury model". PloS ...
... and reperfusion injury[24] (damage occurring after ischemia when blood flow returns to tissue), after myocardial infarction[25] ... clinical study in Europe to determine its ability to ameliorate neuronal cellular damage and reperfusion injury (phase III) in ... Ciclosporin has been investigated as a possible neuroprotective agent in conditions such as traumatic brain injury, and has ... This multi-center study is being organized by NeuroVive Pharma and the European Brain Injury Consortium using NeuroVive's ...
Reperfusion injury. *Machine perfusion. *Perfusionist. *Myocardial perfusion imaging. *rCBF. *Cerebral edema. References[edit] ... 99mTc labelled Tetrofosmin and Sestamibi for myocardial perfusion imaging with SPECT ... 82Rb-chloride for measuring myocardial perfusion with PET (absolute quantification is possible) ... "Fully quantitative cardiovascular magnetic resonance myocardial perfusion ready for clinical use: a comparison between ...
This blood clot may then restrict blood flow within the heart, leading to heart tissue damage, or a myocardial infarction, also ... thrombus aspiration as reperfusion strategy. *platelet P2Y12 receptor inhibitors: The CURE trial in 2001 determined that the ... Also applicable is the Virchow's triad of blood stasis, endothelial injury, and hypercoagulable state. Atherosclerosis ... Due to the large number of cases of myocardial infarction leading to death and disease in the world, there has been extensive ...
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.. *^ "What Does a Super Paramedic Do? (BBC News website)". 30 June 2005. ... 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 ...
Reperfusion injury, i.e. postpulmonary thromboendartectomy or lung transplantation. *Swimming induced pulmonary edema also ... It is most often precipitated by acute myocardial infarction or mitral regurgitation, but can be caused by aortic regurgitation ... Acute lung injury may also cause pulmonary edema through injury to the vasculature and parenchyma of the lung. Acute lung ... This damage may be direct injury or injury mediated by high pressures within the pulmonary circulation. When directly or ...
... such as ischemia-reperfusion injury.,[2] hepatic inflammatory processes,[3] acute hepatotoxicity [4] etc. TxB2, a stable ... If the cap of a vulnerable plaque erodes or ruptures, as in myocardial infarction, platelets stick to the damaged lining of the ... Yokoyama Y (2005). "Role of thromboxane in producing hepatic injury during a hepatic stress disorder". Arch. Surg. 140 (8): 801 ... Cavar I (2011). "Anti-thromboxane B2 antibodies protect against acetaminophen-induced liver injury in mice". Journal of ...
Crucial Role of Endogenous Interleukin-10 Production in Myocardial Ischemia/Reperfusion Injury, Circulation., 2000; 101: 1019- ...
... such as ischemia-reperfusion injury.,[2] hepatic inflammatory processes,[3] acute hepatotoxicity [4] etc. TxB2, a stable ... It is believed that this shift in balance lowers the incidence of myocardial infarction (heart attack) and stroke. ... Yokoyama Y (2005). "Role of thromboxane in producing hepatic injury during a hepatic stress disorder". Arch Surg. 140 (8): 801- ... Cavar I (2011). "Anti-thromboxane B2 antibodies protect against acetaminophen-induced liver injury in mice". Journal of ...
... protects against myocardial ischemia/reperfusion injury via the sarcolemmal ATP-sensitive potassium channel". J. Pharmacol. Exp ... reduces ischemia/reperfusion injury in mice by activating the A3 adenosine receptor". The Journal of Pharmacology and ...
... reperfusion injury and the generation of reactive oxygen species. These later stages are characterised by Th2 polarity. ... myocardial infarction, heart failure, and rarely haemolytic anaemia, aplastic anaemia, serum sickness, severe skin conditions, ... myocardial infarction, QT interval prolongation, renal failure and hypersensitivity. ...
Myocardial infarction[edit]. Absolute contraindications:[10] *Any previous history of hemorrhagic stroke, ischemic stroke ... Thrombolysis can also play an important part in reperfusion therapy that deals specifically with blocked arteries. ... Recent (within 30 days) trauma with internal injuries or ulcerative wounds.. *Gastrointestinal or urinary tract haemorrhage ... ST elevation myocardial infarction: Large trials have shown that mortality can be reduced using thrombolysis (particularly ...
Main article: Myocardial infarction. Patients arriving to the emergency department with a myocardial infarction (heart attack) ... Type 3 A&E department - other A&E/ minor injury unit/ walk-in centre, treating minor injuries and illnesses [20] ... A patient's chance of survival is greatly improved if the patient receives definitive treatment (i.e. surgery or reperfusion) ... Superficial injury, contusion. 213,000 FreestandingEdit. In addition to the normal hospital based emergency departments a trend ...
... (from the Greek νέκρωσις "death, the stage of dying, the act of killing" from νεκρός "dead") is a form of cell injury ... In the case of ischemia, which includes myocardial infarction, the restriction of blood supply to tissues causes hypoxia and ... Eum HA, Cha YN, Lee SM (2007). "Necrosis and apoptosis: sequence of liver damage following reperfusion after 60 min ischemia in ... Structural signs that indicate irreversible cell injury and the progression of necrosis include dense clumping and progressive ...
... a new therapeutic target for myocardial reperfusion injury". Cardiovascular Research. 111 (2): 134-141. doi:10.1093/cvr/cvw100 ... Ischemia reperfusion injuryEdit. Succinate accumulation under hypoxic conditions has been implicated in the reperfusion injury ... In animal models, pharmacological inhibition of ischemic succinate accumulation ameliorated ischemia-reperfusion injury.[29] As ... "Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS". Nature. 515 (7527): 431-5. Bibcode: ...
Ischemia-reperfusion injury of the appendicular musculoskeletal system. References[edit]. .mw-parser-output .reflist{font-size: ... Myoglobin is not specific for myocardial necrosis, however, especially in the presence of skeletal muscle injury and renal ... Chung MJ, Brown DL (July 2018). "Diagnosis of acute myocardial infarction.". In Brown DL (ed.). Cardiac Intensive Care-E-Book. ... Myoglobin is a sensitive marker for muscle injury, making it a potential marker for heart attack in patients with chest pain.[ ...
"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 ...
... 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 ...
In fact, this damage properly constitutes a partial diastolic depolarization or injury, i.e., a moderate reduction of the rest ... we present some considerations on the myocardial damage due to a deficit of oxygen supply. ... Ischemia-reperfusion myocardial injury] Arch Cardiol Mex. Oct-Dec 2003;73(4):284-90. ... Myocardial Reperfusion Injury* / metabolism * Myocardial Reperfusion Injury* / pathology * Myocardial Reperfusion Injury* / ...
Lethal myocardial reperfusion injury attenuates the full benefits of myocardial reperfusion in terms of MI size reduction and ... This figure illustrates the individual contributions of acute myocardial ischemic injury and myocardial reperfusion injury to ... a phenomenon known as myocardial reperfusion injury (1-3). Although the process of myocardial reperfusion continues to improve ... there is still no effective therapy for preventing myocardial reperfusion injury. In this respect, myocardial reperfusion ...
... including myocardial ischemia-reperfusion injury (IRI), but the molecular basis of UPS impairment remains poorly understood. ... When subject to regional myocardial ischemia-reperfusion, young Ubqln1-CKO mice showed substantially exacerbated cardiac ... Ubqln1-CKO impairs myocardial UPS performance without affecting proteasome peptidase activities at 3 weeks of age. ... Myocardial proteasomal peptidase activity assays. Crude protein extracts from the ventricular myocardium of homozygous Ubqln1- ...
"Sivelestat reduces myocardial ischemia and reperfusion injury in rat hearts even when administered after onset of myocardial ... "Postconditioning attenuates myocardial ischemia-reperfusion injury by inhibiting events in the early minutes of reperfusion," ... Sivelestat Attenuates Myocardial Reperfusion Injury during Brief Low Flow Postischemic Infusion. Sverre E. Aune,1 Steve T. Yeh, ... B. R. Lucchesi, "Myocardial ischemia, reperfusion and free radical injury," American Journal of Cardiology, vol. 65, no. 19, pp ...
... including myocardial ischemia-reperfusion injury (IRI), but the molecular basis of UPS impairment remains poorly understood. ... When subject to regional myocardial ischemia-reperfusion, young Ubqln1-CKO mice showed substantially exacerbated cardiac ... and increased myocardial ubiquitinated proteins without altering proteasome activities, resulting in late-onset cardiomyopathy ... ubiquitination-proteasome coupling and that an inadequacy in the coupling represents a major pathogenic factor for myocardial ...
We investigated whether necroptosis is involved in myocardial ischemia-reperfusion... ... We investigated whether necroptosis is involved in myocardial ischemia-reperfusion injury in isolated guinea pig hearts and, if ... Caspase inhibition and limitation of myocardial infarct size: protection against lethal reperfusion injury. Br J Pharmacol. ... Necroptosis is involved in myocardial ischemia-reperfusion injury, and simultaneous inhibition of necroptosis and apoptosis ...
... Shiao Ding, Yang Yang, and Ju Mei ... Shiao Ding, Yang Yang, and Ju Mei, "Protective Effects of L-Malate against Myocardial Ischemia/Reperfusion Injury in Rats," ...
Pathophysiology of myocardial reperfusion injury: preconditioning, postconditioning, and translational aspects of protective ... Myocardial Reperfusion Injury/pathology. *Myocardial Reperfusion Injury/physiopathology*. *Myocardial Reperfusion Injury/ ... Preliminary exploration into the pathophysiology of ischemia-reperfusion injury, together with the accumulation of clinical ... The subcellular pathophysiological mechanism of ischemia-reperfusion injury and preconditioning-induced cardioprotection is not ...
However, reperfusion itself may contribute to myocardial cell death. The current review outlines the multifocal mechanisms of ... Prompt reperfusion therapy in acute myocardial infarction enhances clinical outcome. ... Prompt reperfusion therapy in acute myocardial infarction enhances clinical outcome. However, reperfusion itself may contribute ... to myocardial cell death. The current review outlines the multifocal mechanisms of reperfusion injury and focuses on ...
Sulfonylurea receptor 1 subunits of ATP-sensitive potassium channels and myocardial ischemia/reperfusion injury.. Lefer DJ1, ... Myocardial Reperfusion Injury/etiology. *Myocardial Reperfusion Injury/metabolism*. *Myocardial Reperfusion Injury/prevention ... Sulfonylurea Receptor 1 Subunits of ATP-Sensitive Potassium Channels and Myocardial Ischemia/Reperfusion Injury ... and a surprising protection from myocardial ischemia/reperfusion in SUR1-null mice. Here, we review some of the extra- ...
... injury to the heart is accompanied by the upregulation and posttranslational modification of a number of proteins normally ... Cyclin-dependent kinase 2 signaling regulates myocardial ischemia/reperfusion injury J Mol Cell Cardiol. 2008 Nov;45(5):610-6. ... Ischemia/reperfusion (I/R) injury to the heart is accompanied by the upregulation and posttranslational modification of a ... To confirm that Rb was the critical target in Cdk2-mediated I/R injury, we determined the consequences of I/R injury in cardiac ...
Minimizing Reperfusion Injury in Patients With Acute Myocardial Infarction (PCinAMI). The safety and scientific validity of ...
Myocardial Ischemia. Reperfusion Injury. Myocardial Reperfusion Injury. Pathologic Processes. Necrosis. Heart Diseases. ... Efficacy of FX06 in the Prevention of Myocardial Reperfusion Injury. The safety and scientific validity of this study is the ... Efficacy of FX06 in the Prevention of Myocardial Reperfusion Injury) trial. J Am Coll Cardiol. 2009 Feb 24;53(8):720-9. doi: ... the Efficacy of FX06 in the prevention of myocardial reperfusion injury trial. EuroIntervention. 2010 Apr;5(8):946-52. doi: ...
Timely reperfusion of an infarct-related artery within a reas.. ... Acute Myocardial Injury: A Perspective on Lethal Reperfusion ... Acute myocardial infarction contributes significantly to mortality in patients with coronary artery disease. ... Sharma V, Bell RM, Yellon DM (2012) Targeting reperfusion injury in acute myocardial infarction: a review of reperfusion injury ... Consequences of Reperfusion of the Infarct-Related Artery. Lethal reperfusion injury. Lethal reperfusion injury refers ...
This is the first study to show that the anticancer drug Doxorubicin exacerbates myocardial ischaemia reperfusion injury. ... the cellular mechanism via which Doxorubicin mediates increased myocardial injury in conditions of ischaemia-reperfusion. ... Cellular injury was subsequently determined by measurement of live/death ratio and apoptosis using flow cytometry. ... Studies were undertaken in Langendorff hearts and adult/neonatal ventricular myocytes subjected to ischaemia-reperfusion. ...
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 ... Myocardial Ischemic Reperfusion Injury; Injuries, Myocardial Reperfusion; Myocardial Reperfusion Injuries; Reperfusion Injuries ... Myocardial Reperfusion Injury. Subscribe to New Research on Myocardial Reperfusion Injury Damage to the MYOCARDIUM resulting ...
Myocardial infarction (MI) induces cardiac remodeling. This may increase the susceptibility of the infarcted heart to ... the acute effects of angiotensin II in ischemia-reperfusion injury (IR) remains unclear. In the present study, we tested ... Myocardial infarction (MI) induces cardiac remodeling. This may increase the susceptibility of the infarcted heart to ... 30 minutes of reperfusion) during vehicle or angiotensin II infusions (10(-7) M). MI hearts were dilated and had reduced ...
... injury contributes to adverse cardiac outcomes after myocardial ischemia, cardiac surgery, or circulatory arrest. In this study ... therapy to protect heart cells from myocardial IR injury. Adult male SD rats (n = 8/each group) were randomized: group 1 (sham- ... operated control), group 2 (IR, 30-min ischemia/72 h reperfusion), group 3 (IR-SS31 (2 mg intra-peritoneal injection at 30 min/ ... demonstrates that the combined SS31-Mito therapy is superior to either therapy alone for protecting myocardium from IR injury ...
Increased myocardial ischemia-reperfusion injury in renal failure involves cardiac adiponectin signal deficiency.. [Yanbin Song ... The present study was designed to determine the role of APN in myocardial ischemia-reperfusion (MI/R) injury in mice with renal ... The present study demonstrates that renal dysfunction increases cardiac susceptibility to ischemic-reperfusion injury, which is ... Moreover, SN increased myocardial NO metabolites, superoxide, and their cytotoxic reaction product peroxynitrite, upregulated ...
The present study was designed to investigate the protective effect of Rg1 on heart ischemia and reperfusion (I/R) injury, with ... These results indicated that Rg1 had protective potential against I/R-induced myocardial injury, which may be related to ... These results indicated that Rg1 had protective potential against I/R-induced myocardial injury, which may be related to ... Rg1 prevented I/R-elicited insults in myocardium, including myocardial infarction and apoptosis, decreased myocardial blood ...
Evidence from animal studies points to a role for lymphocytes, and in particular T cells, in myocardial I/R injury, but this ... but ischaemia/reperfusion (I/R) injury remains an important complication. ... Myocardial infarction is the greatest cause of mortality worldwide, and a source of considerable morbidity. Treatment of ... These findings identify a possible therapeutic target in I/R injury postCPPCI, opening up a new avenue for further research and ...
Ischaemia-reperfusion (IR) injury contributes to the cardiac damage following myocardial infarction and paradoxically reduces ... 1 The cathepsin-L inhibitor CAA0225 protects against myocardial ischaemia-reperfusion injury ... 1 The cathepsin-L inhibitor CAA0225 protects against myocardial ischaemia-reperfusion injury ... Ischaemia-reperfusion injury was induced by 45 min temporary coronary artery ligation and CAA0225 was given by intra-venous ...
Although early reperfusion is essential for myocardial salvage, it induces reperfusion injury, which reduces the benefits of ... Activating PI3K/Akt at the time of reperfusion has been demonstrated to provide protection against myocardial I/R injury (4,18, ... Myocardial ischemia-reperfusion injury: a neglected therapeutic target. J Clin Invest 2013; 123: 92-100, doi: 10.1172/JCI62874 ... Lipopolysaccharide-induced myocardial protection against ischaemia/reperfusion injury is mediated through a PI3K/Akt-dependent ...
Luteolin Inhibits Ischemia/Reperfusion-Induced Myocardial Injury in Rats via Downregulation of microRNA-208b-3p.. [Chen Bian, ... LUT pretreatment conveys anti-apoptotic effects after myocardial I/R injury by decreasing miR-208b-3p and increasing Ets1 ... there have no reports on whether LUT can exert protective effects against myocardial I/R injury through the actions of specific ... LUT pretreatment reduced miR-208b-3p expression in myocardial tissue, as compared to the I/R group. And LUT decreased miR-208b- ...
Tissue Inhibitor of Metalloproteinase-4 and Matrix Metalloproteinases During Acute Myocardial Ischemia-Reperfusion Injury. ... Tissue Inhibitor of Metalloproteinase-4 and Matrix Metalloproteinases During Acute Myocardial Ischemia-Reperfusion Injury ... Tissue Inhibitor of Metalloproteinase-4 and Matrix Metalloproteinases During Acute Myocardial Ischemia-Reperfusion Injury ... Tissue Inhibitor of Metalloproteinase-4 and Matrix Metalloproteinases During Acute Myocardial Ischemia-Reperfusion Injury ...
... we investigated the effect of lipoxin A4 on myocardial ischemia-reperfusion injury (IRI) following cardiac arrest (CA) in a ... Pathogenesis of myocardial ischemia-reperfusion injury and rationale for therapy. The American Journal of Cardiology 106(3): ... Treating myocardial ischemia-reperfusion injury by targeting endothelial cell transcription. The Annals of Thoracic Surgery 68( ... In the present study, we investigated the effect of lipoxin A4 on myocardial ischemia-reperfusion injury (IRI) following ...
Role of cyclophilins and heat shock proteins in myocardial ischaemia/reperfusion injury ... In vitro and in vivo models were used to replicate conditions of ischaemia/reperfusion (IR) injury. H9c2 and COS-7 cell lines ... "reperfusion injury". The role of cyclophilins, heat shock proteins (HSP), and the mitochondrial chaperone complex (MCC), was ... Restoration of blood flow after myocardial infarction (MI), surgery or fibrinolytic therapy is necessary, but can lead to ...
Acetaminophen to Prevent Ischemic Oxidative Reperfusion Injury During Percutaneous Coronary Intervention for Acute Myocardial ... Home » Topics » Reperfusion » Research » Acetaminophen to Prevent Ischemic Oxidative Reperfusion Injury During Percutaneous ... "Acetaminophen to Prevent Ischemic Oxidative Reperfusion Injury During Percutaneous Coronary Intervention for Acute Myocardial ... reperfusion after percutaneous revascularization for acute myocardial infarction.. Study Design. Allocation: Randomized, ...
Complement activation augments myocardial cell injury and apoptosis during ischemia/reperfusion (I/R), whereas complement ... Anti-apoptotic role for C1 inhibitor in ischemia/reperfusion-induced myocardial cell injury.. Fu, Jinrong ... The aim of this study was to determine whether C1INH protects against myocardial cell injury via an anti-apoptotic activity or ... improves outcome in I/R-mediated myocardial cell injury via an anti-apoptotic activity independent of serine protease ...
... reperfusion, so the influence of sympathetic denervation on myocardial ischemia - reperfusion injury was investigated in the ... Canine myocardial reperfusion injury : Its reduction by the combined administration of superoxide dismutase and catalase JOLLY ... Novel Rat Model of Ischemic Cardiomyopathy Induced by Repetitive Myocardial Ischemia/Reperfusion Injury While Conscious ... Contributes to Myocardial Ischemia-Reperfusion Injury * * NONOMURA Makoto * The Second Department of Internal Medicine, Toyama ...
  • This phenomenon is characteristic of the acute phase of the myocardial infarction syndrome and is responsible for the main electrical manifestations appearing in this phase: disorders of rhythm and conduction, as well as a reduced contractility of the involved myocardial fibers. (nih.gov)
  • These changes can present again, more exaggerated, in a following phase of evolution of the myocardial infarction due to myocardial reperfusion. (nih.gov)
  • Acute myocardial infarction (MI) is a major cause of death and disability worldwide. (jci.org)
  • IRI typically arises in patients presenting with an acute ST-segment elevation myocardial infarction (STEMI), in whom the most effective therapeutic intervention for reducing acute myocardial ischemic injury and limiting the size of myocardial infarction (MI) is timely and effective myocardial reperfusion using either thrombolytic therapy or primary percutaneous coronary intervention (PPCI). (jci.org)
  • Alternation in the coronary blood flow velocity pattern in patients with no reflow and reperfused acute myocardial infarction," Circulation , vol. 94, no. 6, pp. 1269-1275, 1996. (hindawi.com)
  • These findings may provide a novel, additive strategy for cardioprotection in acute myocardial infarction. (springer.com)
  • Qiao S, Xie H, Wang C, Wu X, Liu H, Liu C. Delayed anesthetic preconditioning protects against myocardial infarction via activation of nuclear factor-κB and upregulation of autophagy. (springer.com)
  • Heart diseases due to myocardial ischemia, such as myocardial infarction or ischemic heart failure, are major causes of death in developed countries, and their number is unfortunately still growing. (nih.gov)
  • Clinical perspectives on reperfusion injury in acute myocardial infarction. (biomedsearch.com)
  • Prompt reperfusion therapy in acute myocardial infarction enhances clinical outcome. (biomedsearch.com)
  • The purpose of the study is to evaluate whether FX06 is capable of limiting infarct size following balloon catheterization for acute myocardial infarction. (clinicaltrials.gov)
  • Single index lesion with complete occlusion [thrombolysis in myocardial infarction (TIMI) flow 0/I] of one target vessel. (clinicaltrials.gov)
  • Acute myocardial infarction contributes significantly to mortality in patients with coronary artery disease. (omicsonline.org)
  • Effects of acute angiotensin II on ischemia reperfusion injury following myocardial infarction. (biomedsearch.com)
  • Myocardial infarction (MI) induces cardiac remodeling. (biomedsearch.com)
  • Rg1 prevented I/R-elicited insults in myocardium, including myocardial infarction and apoptosis, decreased myocardial blood flow (MBF) and heart function, and alteration in myocardium structure. (frontiersin.org)
  • Myocardial infarction is the greatest cause of mortality worldwide, and a source of considerable morbidity. (bl.uk)
  • Ischaemia-reperfusion (IR) injury contributes to the cardiac damage following myocardial infarction and paradoxically reduces the benefits of reperfusion therapy. (bmj.com)
  • reperfusion after percutaneous revascularization for acute myocardial infarction. (bioportfolio.com)
  • The objective of the present study is to establish the safety and efficacy of Prochymal® following first acute myocardial infarction. (bioportfolio.com)
  • In the setting of reperfusion therapy in an acute myocardial infarction using primary percutaneous intervention (PCI), the body's own inflammatory system involving the complement cascade m. (bioportfolio.com)
  • Efficacy of zofenopril in combination with amlodipine in patients with acute myocardial infarction: a pooled individual patient data analysis of four randomized, double-blind, controlled, prospective studies. (bioportfolio.com)
  • In the four SMILE (Survival of Myocardial Infarction Long-Term Evaluation) studies, early administration of zofenopril in acute myocardial infarction (AMI) showed beneficial effects as compared to pla. (bioportfolio.com)
  • Prognostic value of hematological parameters in patients with acute myocardial infarction: Intrahospital outcomes. (bioportfolio.com)
  • The intensity of the inflammatory response and hemodynamic repercussion in acute myocardial infarction causing the presence in the peripheral circulation of nucleated red blood cells (NRBCs), increase. (bioportfolio.com)
  • Use of objective evidence of myocardial ischemia to facilitate the diagnostic and prognostic distinction between type 2 myocardial infarction and myocardial injury. (bioportfolio.com)
  • First, describe how acute myocardial infarction criteria are used to diagnose type 1 (T1MI) and 2 (T2MI) myocardial infarction. (bioportfolio.com)
  • Impact of a High-Intensity Training on Ventricular Function in Rats After Acute Myocardial Infarction. (bioportfolio.com)
  • Physical exercise should be part of the treatment of post-acute myocardial infarction (AMI) patients. (bioportfolio.com)
  • Diabetes Mellitus and Cardiogenic Shock Complicating Acute Myocardial Infarction. (bioportfolio.com)
  • Diabetes mellitus (diabetes) increases the risk of acute myocardial infarction, which can result in cardiogenic shock. (bioportfolio.com)
  • MYOCARDIAL INFARCTION in which the anterior wall of the heart is involved. (bioportfolio.com)
  • Anterior wall myocardial infarction is often caused by occlusion of the left anterior descending coronary artery. (bioportfolio.com)
  • It can be categorized as anteroseptal or anterolateral wall myocardial infarction. (bioportfolio.com)
  • A myocardial infarction that does not produce elevations in the ST segments of the ELECTROCARDIOGRAM. (bioportfolio.com)
  • ST segment elevation of the ECG is often used in determining the treatment protocol (see also ST Elevation Myocardial Infarction). (bioportfolio.com)
  • In a rat model of acute myocardial infarction (AMI) induced by I/R, administration of C1INH protected against cardiomyocytic apoptosis via normalization of ratio of the Bcl-2/Bax expression in the myocardial infarct area. (diva-portal.org)
  • The myocardial infarction was confirmed by electrocardiogram and cardiac ultrasound. (snmjournals.org)
  • 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). (acc.org)
  • Cyclosporine will be more effective at decreasing the size of myocardial infarction. (acc.org)
  • 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. (acc.org)
  • Ischaemia contributes to the pathophysiology of many conditions, including myocardial infarction, peripheral vascular insufficiency, stroke, and hypovolemic shock. (termedia.pl)
  • Currently, substantial expenditure in the health service is directed towards restoring blood flow in patients with acute myocardial infarction (AMI) in order to limit myocardial injury. (findaphd.com)
  • Myocardial I/R injury can lead to the impairment of cardiac function and damage of myocardial cells, which increases the risk of cardiovascular events, such as myocardial infarction and arrhythmia, and seriously affects the prognosis of underlying diseases 2 , 3 . (scielo.br)
  • Acute myocardial infarction (AMI) mainly occurs upon coronary occlusion, which is caused by detachment and rupture of unstable atherosclerotic plaques ( 3 , 4 ). (spandidos-publications.com)
  • Although puerarin is generally considered as a protective agent for cardio-cerebrovascular diseases, the exact effect on reducing myocardial infarction reperfusion injury (MIRI) is not well understood. (medscimonit.com)
  • To assess the therapeutic effects of protective effects of puerarin on myocardial infarction reperfusion injury, the outcome indicators which were reported in at least 3 original studies were extracted and pooled, including size of myocardial ischemia (MIS) and myocardial infarction (MIN), creatine kinase (CK), methylene dioxyamphetamine (MDA), and superoxide dismutase (SOD). (medscimonit.com)
  • Epinephrine versus norepinephrine for cardiogenic shock after acute myocardial infarction. (eurekaselect.com)
  • Randomized control of sympathetic drive with continuous intravenous esmolol in patients with acute st-segment elevation myocardial infarction: The beta-blocker therapy in acute myocardial infarction (BEAT-AMI) Trial. (eurekaselect.com)
  • Reperfusion, although essential for salvage of myocardium in the myocardial infarction, paradoxically causes a wide variety of injuries. (ahajournals.org)
  • The novel necrosis inhibitor demonstrates a significant protective effect against myocardial I/R injury and has advantages over CsA, based more on the direct necrosis inhibition on cardiomyocytes, indicating that it is a promising candidate for cardioprotective adjunctive therapy with reperfusion in patients with myocardial infarction. (ahajournals.org)
  • It mainly occurs after myocardial infarction and by-pass surgery, and is one major issue in clinic. (alliedacademies.org)
  • Mineralocorticoid receptor antagonist pre-treatment and early post-treatment to minimize reperfusion injury after ST-elevation myocardial infarction: The MINIMIZE STEMI trial. (whiterose.ac.uk)
  • Background: Mineralocorticoid receptor antagonist (MRA) therapy has been shown to prevent adverse left ventricular (LV) remodeling in ST-segment elevation myocardial infarction (STEMI) patients with heart failure. (whiterose.ac.uk)
  • Methods: STEMI patients presenting within 12 hours and with a proximal coronary artery occlusion with Thrombolysis In Myocardial Infarction flow grade 0 were consented and randomized to either an intravenous bolus of potassium canrenoate, followed by oral spironolactone for 3 months or matching placebo. (whiterose.ac.uk)
  • The authors investigated the hypothesis that isoflurane modulates nitric oxide (NO) synthesis and protection against myocardial infarction through time-dependent changes in expression of key NO regulatory proteins, guanosine triphosphate cyclohydrolase (GTPCH)-1, the rate-limiting enzyme involved in the biosynthesis of tetrahydrobiopterin and endothelial nitric oxide synthase (eNOS). (asahq.org)
  • Extracorporeal circulation and coronary bypass surgery are usually employed to improve myocardial ischemia after myocardial infarction occurs. (peerj.com)
  • Mitochondrial dysfuntion due to oxidative stress seems to be crucial in cell death and tissue damage caused by ischaemia-reperfusion injury during myocardial infarction. (unipd.it)
  • Coronary collateralisation, occurring particularly in the presence of coronary artery disease (CAD), is considered protective in the case of myocardial infarction. (bmj.com)
  • Myocardial infarct size is a major determinant of prognosis in patients with IHD, and development of a novel strategy to limit infarction is of great clinical importance. (biomedcentral.com)
  • It accounts for a great proportion of cell loss associated with myocardial infarction (MI) and / or ischemia-reperfusion (IR). (biomedcentral.com)
  • Fifty eight people with acute ST elevation myocardial infarction were randomised to an intravenous bolus of 2.5 mg of ciclosporin per kg of body weight, or saline, before undergoing percutaneous coronary intervention. (bmj.com)
  • Myocardial ischemia-reperfusion (I/R) injury is an important health concern in myocardial infarction and situations such as angioplasty and cardiac surgeries. (usask.ca)
  • The coronary circulation is both culprit and victim of acute myocardial infarction. (vumc.nl)
  • However, no-reflow is still a serious complication of reperfused myocardial infarction and carries, independently from infarct size, an unfavourable prognosis. (vumc.nl)
  • Reperfusion injury during myocardial infarction accounts for approximately half of final infarct size. (uab.edu)
  • Early revascularization in acute myocardial infarction decreases infarct size and improves outcomes. (kcl.ac.uk)
  • Compared with the untreated group, Bulbus Allii Caespitosi and trimetazidine could improve the activity of myocardial cells after myocardial infarction (P0.05). (bvsalud.org)
  • Human HGF plasmid DNA therapy of cardiomyocytes is being examined as a potential treatment for coronary artery disease (a major cause of myocardial infarction (MI)), as well as treatment for the damage that occurs to the heart after MI. (wikipedia.org)
  • Although the process of myocardial reperfusion continues to improve with more timely and effective reperfusion and with advances in PCI technology and antiplatelet and antithrombotic agents for maintaining the patency of the infarct-related coronary artery, there is still no effective therapy for preventing myocardial reperfusion injury. (jci.org)
  • When subject to regional myocardial ischemia-reperfusion, young Ubqln1-CKO mice showed substantially exacerbated cardiac malfunction and enlarged infarct size, and conversely, mice with transgenic Ubqln1 overexpression displayed attenuated IRI. (jci.org)
  • Genetic or pharmacological inhibition of Cdk2 activity in vivo during I/R injury led to a 36% reduction in infarct size (IFS), when compared to control mice, associated with a reduction in apoptotic myocytes. (nih.gov)
  • Timely reperfusion of an infarct-related artery within a reasonable time-frame after acute coronary occlusion continues to be the most effective intervention in patients to reduce morbidity and mortality. (omicsonline.org)
  • The occurrence of reperfusion injury may be inevitable but restoration of blood flow to the infarct-related artery is critical to ensure salvage of reversibly injured myocytes within the area at risk. (omicsonline.org)
  • Debate concerning prevalence of reperfusion injury continues but no true experimental model is presently available to distinguish damage caused by restoration of flow to the perfusion bed of the infarct related artery compared to that present at the end of ischemia. (omicsonline.org)
  • Timely reperfusion of the infarct-related artery continues to be the most effective means to limit development of cellular necrosis. (omicsonline.org)
  • Compared with sham-operated mice, cardiac function was significantly depressed, and myocardial infarct size and apoptosis increased in SN mice following MI/R. The aggravated MI/R injury was further intensified in APN-knockout mice and markedly ameliorated by treatment with gAd but not fAd. (sigmaaldrich.com)
  • Myocradial blood flow and heart function were monitored over the period of I/R. Myocardial infarct size, structure and apoptosis, energy metabolism, and change in RhoA signaling pathway were evaluated 90 min after reperfusion. (frontiersin.org)
  • At the end of reperfusion, myocardial infarct size and biochemical changes were compared. (scielo.br)
  • Some inflammatory factors (IL-1β, IL-6, TNF-α, and IL-10), NF-κB p65, infarct ratios, apoptotic index, cardiac troponin I (cTnI), hemodynamic and myocardial structures were measured or observed in different groups. (springer.com)
  • C1INH improved parameters of cardiac function and hemodynamics and reduced myocardial infarct size (MIS). (diva-portal.org)
  • In conclusion, EMPA can trigger AMPK signaling pathways and modulate myocardial contractility and reduce myocardial infarct size caused by ischemia and reperfusion independent of hypoglycemic effect. (medworm.com)
  • Valsartan inhibited Toll-like receptor 4 (TLR-4) and nuclear factor-kappa B (NF-B) expressions concomitant with an improvement in myocardial injury, such as smaller infarct size, reduced release of myocardial enzymes, and proinflammatory mediators. (termedia.pl)
  • At the end of reperfusion, the cardiac function indexes, serum lactate dehydrogenase (LDH) and creatine kinase (CK) levels, heart weight (HW)/body weight (BW) ratio and infarct size, and expressions of phosphatidylinositol-3 kinase/serine-threonine protein kinase (PI3K/AKT) and glycogen synthase kinase-3β (GSK-3β) proteins and the phosphorylated forms (p-AKT, p-GSK-3β) were determined. (scielo.br)
  • Curculigoside pre‑treatment significantly improved cell viability, decreased cell apoptosis and LDH activity, and reduced the infarct size and myocardial apoptosis in vitro and ex vivo, respectively. (spandidos-publications.com)
  • After reperfusion, infarct sizes in the area-at-risk and serum cardiac troponin-I levels were determined. (eurekaselect.com)
  • Results: Esmolol during reperfusion resulted in robust cardioprotection (esmolol vs. saline: 24.3±8% vs. 40.6±3% infarct size), which was abolished by epinephrine co-administration (38.1±15% infarct size). (eurekaselect.com)
  • We tested the hypothesis that conditional depletion of pro-inflammatory macrophages and dendritic cells may dampen excessive inflammatory response in the infarct myocardium, and thus attenuate MI/R injury. (ahajournals.org)
  • Whether initiating MRA therapy prior to primary percutaneous coronary intervention (PPCI) accrues additional benefit of reducing myocardial infarct size and preventing adverse LV remodeling is not known. (whiterose.ac.uk)
  • We aimed to investigate whether MRA therapy initiated prior to reperfusion reduces myocardial infarct (MI) size and prevents adverse LV remodeling in STEMI patients. (whiterose.ac.uk)
  • At the end of the experiment, the rats were sacrificed to measure the myocardial Infarct Size (IS) and sample the myocardial tissue to detect the content of ADP. (alliedacademies.org)
  • Infarct size, myocardial function, NADPH-activated superoxide generation and biochemical markers of injury were measured. (edu.au)
  • To evaluate differences in cardiac resistance against myocardial ischaemia and reperfusion injury, cardiac surrogate parameters including maximal ST-elevation, arrhythmias and infarct size were assessed. (bmj.com)
  • BACKGROUND: Preconditioning might protect the myocardium against ischemia/reperfusion injury by reducing infarct size and preventing arrhythmias. (bezmialem.edu.tr)
  • The cardioprotective effects of DEX on infarct size and on the incidence of arrhythmias observed after regional ischemia/reperfusion injury in vivo have not been reported. (bezmialem.edu.tr)
  • Myocardial infarct size was determined with triphenyltetrazolium chloride staining. (biomedcentral.com)
  • However, abrupt restoration of coronary flow results in myocardial reperfusion injury and increased final infarct size. (kcl.ac.uk)
  • We hypothesized that a low-dose HMGB1 treatment would improve myocardial functional recovery and decrease infarct size after global I/R injury in association with increased levels of cardioprotective paracrine factors and decreased inflammation. (elsevier.com)
  • At the end of reperfusion, the hearts were sectioned and incubated in triphenyltetrazolium chloride to assess myocardial infarct size or homogenized to measure levels of inflammatory cytokines and growth factors. (elsevier.com)
  • Results: Postischemic treatment with 200-ng HMGB1 significantly improved myocardial functional recovery after global I/R in association with decreased infarct size and decreased interleukin-1 (IL-1), IL-6, IL-10, and vascular endothelial growth factor (VEGF) levels. (elsevier.com)
  • Conclusion: In the setting of global I/R, 200-ng postischemic HMGB1 treatment improves myocardial function and decreases infarct size in association with suppressed myocardial inflammation. (elsevier.com)
  • We investigated whether necroptosis is involved in myocardial ischemia-reperfusion injury in isolated guinea pig hearts and, if so, whether simultaneous inhibition of necroptosis and apoptosis confers enhanced cardioprotection. (springer.com)
  • Necroptosis is involved in myocardial ischemia-reperfusion injury, and simultaneous inhibition of necroptosis and apoptosis enhances the cardioprotective effect. (springer.com)
  • Apoptosis in myocardial ischemia-reperfusion. (springer.com)
  • Necrostatin-1 suppresses autophagy and apoptosis in mice traumatic brain injury model. (springer.com)
  • articles concerning reperfusion injury (lethal and otherwise), ischemia-reperfusion injury, apoptosis, microvascular injury, ischemic conditioning and different combinations thereof were consulted. (omicsonline.org)
  • Cellular injury was subsequently determined by measurement of live/death ratio and apoptosis using flow cytometry. (bmj.com)
  • These results indicated that Rg1 had protective potential against I/R-induced myocardial injury, which may be related to inhibiting myocardial apoptosis and modulating energy metabolism through binding to RhoA. (frontiersin.org)
  • Complement activation augments myocardial cell injury and apoptosis during ischemia/reperfusion (I/R), whereas complement system inhibition with C1 inhibitor (C1INH), a serine protease inhibitor, exerts markedly cardioprotective effects. (diva-portal.org)
  • The major mechanisms of ischaemic reperfusion injury are oxidative stress (mainly oxygen-free radicals), apoptosis, neutrophil-endothelium interactions, and hypercontracture (i.e. myocyte Ca2+ over loading), endothelial cell activation with microvascular dysfunction, and altered myocardial metabolism. (termedia.pl)
  • Lactate dehydrogenase, casein kinase, malondialdehyde assay, reactive oxygen species (ROS) detection and cell apoptosis analysis measured cell damage and cell apoptosis in H9c2 cells under hypoxia/reperfusion (H/R) treatment. (termedia.pl)
  • Previous studies have reported that the structural and functional damage to myocardial cells may primarily result from apoptosis during MIRI. (spandidos-publications.com)
  • Rat cardiomyocytes were exposed to hypoxia-reoxygenation injury after pretreatment with dimethyl sulfoxide (vehicle), necrosis inhibitor (NecX), antioxidant (vitamin C) or apoptosis inhibitor (Z-VAD-fmk). (ahajournals.org)
  • Ultrasonic cardiogram was used to evaluate cardiac functions, while serum enzyme and myocardial apoptosis were detected by ELISA and TUNEL assays respectively. (alliedacademies.org)
  • CONCLUSIONS: Intravenous administration of rhEpo protects the heart against cold global I/R. Apoptosis does not seem to play a major role in the process of tissue injury in this model. (uzh.ch)
  • Transferase-mediated dUTP-X nick end labeling assay was performed to evaluate the effect TAX on myocardial apoptosis. (peerj.com)
  • Furthermore, TAX up-regulated the Bcl-2 protein level but down-regulated the levels of Bax, Cyt-c, caspase 3 and 9 protein, thereby inhibits the myocardial apoptosis. (peerj.com)
  • Hence, TAX has a cardioprotective effect against I/R injury by modulating mitochondrial apoptosis pathway. (peerj.com)
  • Apoptosis involves programmed cell death, which is the vital pathological process in acute reperfusion injury ( Konstantinidis, Whelan & Kitsis, 2012 ). (peerj.com)
  • These results suggest that intake of germinated brown rice may effectively to protect cell proliferation and apoptosis and may provide important nutrients to prevent heart failure due to myocardial ischemia . (bvsalud.org)
  • By reducing oxidative stress, inflammation, and apoptosis, IMD may represent a promising novel therapeutic target mitigating diabetic ischemic heart injury. (biomedcentral.com)
  • In the present investigation, the effect of Curcuma longa (Cl) and Ocimum sanctum (Os) on myocardial apoptosis and cardiac function was studied in an ischemia and reperfusion (I-R) model of myocardial injury. (biomedcentral.com)
  • It has been reported that these programmed cell death pathways can be inhibited by antioxidants [ 6 , 7 ] However, there are few studies addressing the inhibition of apoptosis and it's directs on myocardial contractility. (biomedcentral.com)
  • It is produced and proteolytically cleaved to its active state in response to cellular injury or during apoptosis. (wikipedia.org)
  • Acute occlusion of the coronary artery in the STEMI patient subjects the myocardium supplied by that vessel to acute myocardial ischemia, thereby demarcating the area at risk (AAR) of potential MI, should the acute coronary occlusion be sustained or permanent. (jci.org)
  • The current review outlines the multifocal mechanisms of reperfusion injury and focuses on understanding the potential role of each element and its contribution to the injury pattern inflicted upon the myocardium. (biomedsearch.com)
  • Finally, we explore promising innovative strategies targeting novel reperfusion injury pathways to protect ischemic myocardium during reperfusion. (biomedsearch.com)
  • Although issues relating to Doxorubicin and cardiac safety have been well established in normal conditions, the effects of this drug on the myocardium during ischaemia-reperfusion have not been investigated in detail to date. (bmj.com)
  • Damage to the MYOCARDIUM resulting from MYOCARDIAL REPERFUSION (restoration of blood flow to ischemic areas of the HEART. (curehunter.com)
  • The present study demonstrates that renal dysfunction increases cardiac susceptibility to ischemic-reperfusion injury, which is associated with downregulated APN/AdipoR1/AMPK signaling and increased oxidative/nitrative stress in local myocardium, and provides the first evidence for the protective role of exogenous supplement of gAd on MI/R outcomes in renal failure. (sigmaaldrich.com)
  • Several studies indicated that Que, when given before ischemia (preconditioning), protects the myocardium from I/R injury through its antioxidant and anti-inflammatory activities ( 12 , 13 ). (scielo.br)
  • To identify the potential target proteins of XST, two-dimensional gel electrophoresis (2-DE)-based proteomics was utilized to analyze the protein profile of myocardium in rats with myocardial ischemia/reperfusion (I/R) injury. (rsc.org)
  • This is the first study on the proteomic expression of XST-treated myocardium with I/R injury to reveal that the cardioprotective effects of XST may be attributed to the PDH-mediated restoration of aerobic glucose oxidation. (rsc.org)
  • In conclusion, the recombinant serine protease inhibitor, LEX032, appears to be an effective agent for attenuating MI/R injury by inhibiting neutrophil-accumulation into the ischemic-reperfused myocardium and by inactivating cytotoxic metabolites (proteases and superoxide radical) released from neutrophils. (aspetjournals.org)
  • Moreover, inflammatory cytokines, such as TNF-α, MCP-1 and IFN-γ in the infracted myocardium as well as myocardial nitrotyrosine level, an index of oxidative and nitrative stresses, were dramatically decreased in CD11c-DTR mice than those in WT mice. (ahajournals.org)
  • Necrosis, the main mechanism of cell death during I/R injury to the myocardium, is an uncontrolled cell death, a pathologic condition accompanying inflammatory responses. (ahajournals.org)
  • We evaluated the ability of a synthetic flavonol, 3',4'-dihydroxyflavonol (DiOHF) to scavenge superoxide in post-I/R myocardium and to prevent myocardial I/R injury. (edu.au)
  • APC favorably modulated a NO biosynthetic pathway by up-regulating GTPCH-1 and eNOS, and this action contributed to protection of myocardium against ischemia and reperfusion injury. (asahq.org)
  • The timely restoration of blood flow to the ischemic myocardium (reperfusion) became the standard treatment for these patients. (peerj.com)
  • The purpose of this study is to determine the mechanism by which acute administration CoQ protects myocardium from reperfusion (Rp) injury. (elsevier.com)
  • After MI, the myocardium suffers from reperfusion injury which leads to death of cardiomyocytes and detrimental remodelling of the heart, consequently reducing proper cardiac function. (wikipedia.org)
  • K. Okajima, N. Harada, M. Uchiba, and M. Mori, "Neutrophil elastase contributes to the development of ischemia-reperfusion- induced liver injury by decreasing endothelial production of prostacyclin in rats," American Journal of Physiology-Gastrointestinal and Liver Physiology , vol. 287, no. 6, pp. (hindawi.com)
  • Shiao Ding, Yang Yang, and Ju Mei, "Protective Effects of L-Malate against Myocardial Ischemia/Reperfusion Injury in Rats," Evidence-Based Complementary and Alternative Medicine , vol. 2016, Article ID 3803657, 9 pages, 2016. (hindawi.com)
  • Adult male SD rats ( n = 8/each group) were randomized: group 1 (sham-operated control), group 2 (IR, 30-min ischemia/72 h reperfusion), group 3 (IR-SS31 (2 mg intra-peritoneal injection at 30 min/24 h/48 h after IR)), group 4 (IR-mitochondria (2 mg/derived from donor liver/intra-venous administration/30 min after IR procedure)), and group 5 (IR-SS31-mitochondria). (mdpi.com)
  • Male Sprague-Dawley rats were subjected to 30 min of occlusion of left coronary anterior descending artery followed by reperfusion for 90 min. (frontiersin.org)
  • Male Sprague-Dawley rats were randomly allocated to 5 groups (20 animals/group): sham, I/R, Que postconditioning, Que+LY294002 [a phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway inhibitor], and LY294002+I/R. I/R was produced by 30-min coronary occlusion followed by 2-h reperfusion. (scielo.br)
  • Luteolin Inhibits Ischemia/Reperfusion-Induced Myocardial Injury in Rats via Downregulation of microRNA-208b-3p. (sigmaaldrich.com)
  • 2009. Role of lipoxygenases and the lipoxin A(4)/annexin 1 receptor in ischemia-reperfusion-induced gastric mucosal damage in rats. (springer.com)
  • Male Sprague-Dawley rats underwent a 45-min transient left coronary artery occlusion, followed by reperfusion. (snmjournals.org)
  • To investigate the effect of astragaloside IV (As-IV) on myocardial ischemia-reperfusion (I/R) injury in rats and reltaed mechanisms. (scielo.br)
  • As-IV can alleviate the myocardial I/R injury in rats through regulating PI3K/AKT/GSK-3β signaling pathways. (scielo.br)
  • Therefore, the study was carried out to investigate the protective effect of As-IV on myocardial I/R injury in rats and the relations with PI3K/AKT/GSK-3β signaling pathways. (scielo.br)
  • An additional 18 hearts were subjected to the same protocol, and sevoflurane (n=9) or desflurane (n=9) was added to the perfusion medium during the first 30 min of reperfusion in a concentration corresponding to 1.5 MAC in rats. (springer.com)
  • Des coeurs de rats isolés dans une préparation de Langendorff (n=9) ont été arrêtés par la perfusion d'une solution cardioplégique HTK et soumis pendant 30 min à une ischémie globale suivie de 60 min de reperfusion (témoins). (springer.com)
  • D'autres coeurs (18) ont été soumis au même protocole, mais du sévoflurane (n=9) ou du desflurane (n=9) a été ajouté au liquide de perfusion pendant les 30 premières min de la reperfusion selon une concentration correspondant à 1,5 CAM chez les rats. (springer.com)
  • We tried to determine whether trimucrin is cardioprotective in rats subjected to myocardial ischemia-reperfusion (I-R) injury. (ovid.com)
  • The left anterior descending coronary artery of anesthetized rats was subjected to 1 h occlusion and 3 h reperfusion. (ovid.com)
  • 2 Subsequent reports demonstrated that breathing nitric oxide could decrease neointima formation after carotid artery injury (rats), 3 decrease thrombosis after thrombolysis (dogs), 4 and reduce reperfusion injury after mesenteric artery ischemia (cats) 5 or cardiac ischemia-reperfusion (mice 6 and pigs 7 ). (asahq.org)
  • The study was to evaluate the roles of Adiponectin (ADP) in alleviating myocardial ischemia-reperfusion injury in rats with Remote Ischemic Postconditioning (RIP). (alliedacademies.org)
  • A total of 57 healthy male SD rats were randomly divided into 3 groups (the sham operation group (S), the myocardial ischemia-reperfusion group (I/R), and the RIP group (R). The myocardial ischemia-reperfusion injury model was established by ligating the left coronary artery for 30 min followed by 180-min reperfusion. (alliedacademies.org)
  • ADP is involved in RIP that can alleviate the myocardial ischemia-reperfusion injury in rats. (alliedacademies.org)
  • In this study, we established the rat RIP model and the M-I/R model, aiming to observe the myocardial protective roles of RIP and the serum and myocardial ADP changes in rats. (alliedacademies.org)
  • Two weeks after the intervention, rats underwent a single, sustained LAD occlusion followed by reperfusion. (bmj.com)
  • In this study on ischaemia-induced and reperfusion-induced injury, we found that the most widely used cardioprotective drugs in CAD unfavourably impacted the cardiac outcomes in rats after ischaemic preconditioning. (bmj.com)
  • Four weeks streptozotocin (STZ)-induced diabetic (D) and non-diabetic (C) Sprague-Dawley rats were randomly assigned to receive 30 or 45 min of left anterior descending artery ligation followed by 2 or 3 hours of reperfusion, respectively. (biomedcentral.com)
  • On the 31st day, in the rats of the control IR, Cl-IR and Os-IR groups LAD occlusion was undertaken for 45 min, and reperfusion was allowed for 1 h. (biomedcentral.com)
  • Role of mitochondrial ATP-sensitive potassium channel-mediated PKC-ε in delayed protection against myocardial ischemia/reperfusion injury in isolated hearts of sevoflurane-preconditioned rats. (elsevier.com)
  • D, E ) Expression levels of WTAP, cleaved PARP, cleaved Caspase-3, ATF4 and CHOP in myocardial cells of rats. (aging-us.com)
  • In patients with MI, the treatment of choice for reducing acute myocardial ischemic injury and limiting MI size is timely and effective myocardial reperfusion using either thombolytic therapy or primary percutaneous coronary intervention (PPCI). (jci.org)
  • Treatment of STCelevation MI (STEMI) has improved enormously with the advent of primary percutaneous coronary intervention (PPCI), but ischaemia/reperfusion (I/R) injury remains an important complication. (bl.uk)
  • In addition to prompt reperfusion (usually by percutaneous coronary intervention (PCI)) there is an urgent need for effective adjunctive therapies that limit myocardial injury due to IRI. (findaphd.com)
  • Rg1 (5 mg/kg/h) was continuously administrated intravenously 30 min before occlusion until the end of reperfusion. (frontiersin.org)
  • At the end of 8-week exercise training, mice underwent 30-min left anterior descending coronary artery occlusion followed by 60-min or 24-h reperfusion. (iupui.edu)
  • The rupture of an epicardial atherosclerotic plaque with superimposed thrombosis causes coronary occlusion, and this occlusion must be removed to induce reperfusion. (vumc.nl)
  • To investigate the effects of allopurinol in an XO-free model and determine whether pretreat- ment is necessary, 12 domestic pigs (15 kg to 20 kg) underwent occlusion of the left circum- flex for 8 minutes followed by reperfusion for 4 hours. (ecu.edu)
  • free Management of Myocardial Reperfusion Injury management werden know a public local consulting. (odserver.com)
  • Management of Myocardial Reperfusion Injury will tackle these issues in a modern and systematic way and the information will be delivered in a fashion that will be appealing to the reader. (ebook-dl.com)
  • Our data demonstrate that cathepsin-L released from ex vivo rat hearts after ischaemia, and the cathepsin-L inhibitor CAA0225 improves cardiac function during ischaemia-reperfusion ex vivo . (bmj.com)
  • Trimucrin also improved cardiac function and survival rates after I-R injury. (ovid.com)
  • These results demonstrate that trimucrin exerts cardioprotective property against myocardial I-R injury mediated through antiplatele, anti-inflammatory, anti-apoptotic mechanism, as well as improvements in cardiac function. (ovid.com)
  • These data indicate that the decreased infiltration of pro-inflammatory macrophages /dendritic cells and subsequent ameliorated inflammation may contribute to attenuated reperfusion injury and better reserved cardiac function in CD11c-DTR mice. (ahajournals.org)
  • Background: Cardiovascular disease is still the most frequent cause of death in both developed and developing countries while metabolic syndrome and myocardial ischemia reperfusion (I/R) injury are the common risk factors responsible for the impaired cardiac function. (eurekaselect.com)
  • In vitro reversible myocardial I/R for postischemic cardiac function and in vivo regional myocardial I/R for MI were performed. (elsevier.com)
  • The current study investigated whether Que postconditioning has any protective effects on myocardial ischemia/reperfusion (I/R) injury in vivo and its potential cardioprotective mechanisms. (scielo.br)
  • suggested that valsartan plays an essential role in the protective effects on myocardial ischemic reperfusion injury, and the possible protection mechanism is due to its anti-inflammation function via TLR-4/NF-B signalling pathway [5]. (termedia.pl)
  • In addition, the previous studies have shown that As-IV has the protective effects on myocardial I/R injury, and the mechanisms are various 12 - 16 . (scielo.br)
  • Exercise-induced cardioprotection against myocardial ischemia-reperfusion injury. (semanticscholar.org)
  • article{Powers2008ExerciseinducedCA, title={Exercise-induced cardioprotection against myocardial ischemia-reperfusion injury. (semanticscholar.org)
  • Myocardial ischemia-reperfusion (IR) injury contributes to adverse cardiac outcomes after myocardial ischemia, cardiac surgery, or circulatory arrest. (mdpi.com)
  • Excessive infiltration of pro-inflammatory monocytes /macrophages early after myocardial ischemia/reperfusion (MI/R) contributes to myocardial injury and cardiac dysfunction. (ahajournals.org)
  • In the present study, we hypothesized that exercise-induced acceleration of myocardial tissue oxygenation recovery contributes to this protection. (iupui.edu)
  • Here, we report that mice with a cardiomyocyte-restricted knockout of Ubiquilin1 (Ubqln1-CKO mice) accumulated a surrogate UPS substrate (GFPdgn) and increased myocardial ubiquitinated proteins without altering proteasome activities, resulting in late-onset cardiomyopathy and a markedly shortened life span. (jci.org)
  • Recent data, however, demonstrated the presence of SUR1 subunits in mouse cardiac tissue (particularly in atria) and a surprising protection from myocardial ischemia/reperfusion in SUR1-null mice. (nih.gov)
  • To confirm that Rb was the critical target in Cdk2-mediated I/R injury, we determined the consequences of I/R injury in cardiac-specific Rb-deficient mice (CRb(L/L)). IFS was increased 140% in CRb(L/L) mice compared to CRb+/+ controls. (nih.gov)
  • TUNEL positive nuclei and caspase-3 activity were augmented by 92% and 36%, respectively, following injury in the CRb(L/L) mice demonstrating that loss of Rb in the heart significantly exacerbates I/R injury. (nih.gov)
  • The present study was designed to determine the role of APN in myocardial ischemia-reperfusion (MI/R) injury in mice with renal failure and delineate the underlying mechanisms. (sigmaaldrich.com)
  • These data demonstrate for the first time that CAA0225 protects against ischaemia-reperfusion injury in mice and the mechanism relates to the normalisation of abnormal calcium handling following ischaemia-reperfusion injury. (bmj.com)
  • Adult cardiomyocytes from wild-type littermates (WT) or gene-deficient mice were pretreated with vehicle (V) or rosiglitazone (RSG) for 6 h followed by simulated ischemia-reperfusion (SI/R, 3 h/12 h). (scialert.net)
  • Myocytes from adiponectin receptor 1 knockdown (AdipoR1-KD) or AdipoR1-KD/AdipoR2-KO mice had slightly increased SI/R injury, but the difference was not statistically significant. (scialert.net)
  • Moreover, the elevated expression of miR-214-5p by adenovirus injection protected cardiac cells from I/R injury in mice (n = 6/per group). (termedia.pl)
  • Methods: C57BL/6J mice were subjected to 60 min of myocardial ischemia and 120 min of reperfusion. (eurekaselect.com)
  • Mice received either saline, esmolol (0.4 mg/kg/h), epinephrine (0.05 mg/kg/h), or esmolol combined with epinephrine (esmolol: 0.4 mg/kg/h or 0.8 mg/kg/h and epinephrine: 0.05 mg/kg/h) during reperfusion. (eurekaselect.com)
  • Voluntary running in mice beneficially modulates myocardial ischemic tolerance, signaling kinases, and gene expression patterns. (semanticscholar.org)
  • Now, work emerging from multiple laboratories, and in both mice and large animals, has documented that HDAC inhibition using compounds approved for clinical use confers robust cardioprotection when delivered at the time of myocardial reperfusion. (uab.edu)
  • The effect of myocardial I/R was examined in young adult wild-type (WT) and ZmRacD transgenic (TG) mice. (elsevier.com)
  • Importantly, acute regional myocardial I/R (30-min ischemia and 24-h reperfusion) caused significantly larger MI in TG mice compared with WT mice. (elsevier.com)
  • More importantly, impaired UPS performance plays a major role in cardiac pathogenesis, including myocardial ischemia-reperfusion injury (IRI), but the molecular basis of UPS impairment remains poorly understood. (jci.org)
  • Ischemia and reperfusion (I/R) injury is a pathogenesis process consisting of a spectrum of episodes, among which mitochondria dysfunction plays a central role. (frontiersin.org)
  • Myocardial ischemia-reperfusion (I/R) injury is the lesion in which the blood perfusion is restored after the myocardial blood supply is interrupted for a certain period, leading to the injury or dysfunction in ischemic area 1 . (scielo.br)
  • Background: Animal studies on cardiac arrest found that a combination of epinephrine with esmolol attenuates post-resuscitation myocardial dysfunction. (eurekaselect.com)
  • Epinephrine increases the severity of postresuscitation myocardial dysfunction. (eurekaselect.com)
  • Myocardial Ischemia/Reperfusion (MI/R) injury is a clinical phenomenon including myocardial structural damage, dysfunction and disorders of metabolism and electrophysiology after re-perfusion of ischemic heart tissues. (alliedacademies.org)
  • The reperfusion of ischemic tissues is often associated with microvascular dysfunction. (peerj.com)
  • Thus these findings provide direct evidence that increased levels of active myocardial Rac renders the heart susceptible to increased postischemic contractile dysfunction and MI following acute I/R. (elsevier.com)
  • We investigated the potential of telmisartan to improve microvascular dysfunction induced by myocardial ischemia/reperfusion (I/R) injury by activating the peroxisome proliferator-activated receptor gamma (PPARG) pathway. (biomedcentral.com)
  • Except for the typical effects of angiotensin II-receptor blocker, telmisartan improved microvascular dysfunction during myocardial I/R injury via the PPARG pathway. (biomedcentral.com)
  • 10 ] showed that an angiotensin type 1 receptor (AGTR1) blockade prevents microvascular dysfunction induced by I/R injury. (biomedcentral.com)
  • The purpose of this study was to monitor the presence and time course of regional myocardial GLP-1R expression after MI/R with noninvasive PET. (snmjournals.org)
  • Moreover, SN increased myocardial NO metabolites, superoxide, and their cytotoxic reaction product peroxynitrite, upregulated inducible NO synthase expression, and decreased endothelial NOS phosphorylation. (sigmaaldrich.com)
  • 1999. Treating myocardial ischemia-reperfusion injury by targeting endothelial cell transcription. (springer.com)
  • 001). Treatment with propranolol neither preserved endothelial function after cholesterol feeding nor reduced neutrophil accumulation in ischemic-reperfused myocardial tissue. (aspetjournals.org)
  • Moreover, carvedilol treatment significantly preserved aortic endothelial function and markedly reduced neutrophil accumulation in ischemic-reperfused myocardial tissue. (aspetjournals.org)
  • These results indicate that in addition to its beta blocking activity, the antioxidant and endothelial protective activities of carvedilol contributed significantly to its cardiac protective effects after ischemia and reperfusion. (aspetjournals.org)
  • However, ischaemia and reperfusion cause damage not only in cardiomyocytes but also in the coronary circulation, including microembolization 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 leucocyte adherence, erythrocyte stasis, a shift from vasodilation to vasoconstriction, and ultimately structural damage to the capillaries with eventual no-reflow, microvascular obstruction (MVO), and intramyocardial haemorrhage (IMH). (vumc.nl)
  • Activated endothelial cells produce more reactive oxygen species but less nitric oxide following reperfusion, and the imbalance results in a subsequent inflammatory response. (wikipedia.org)
  • All the mentioned phenomena are due to a defect of the myocardial energetic mechanisms, owing to the mitochondrial alterations in myocytes: early reduction of the nicotinamide adenine nucleotides, accumulation of calcium ("calcium overload") into mitochondria, and a drop in oxidative phosphorylation. (nih.gov)
  • In this review, we discuss the current findings regarding the fundamental pathophysiological mechanisms of ischemia-reperfusion injury, the associated protective mechanisms of ischemic pre- and postconditioning, and the potential seeds for molecular, pharmacological, or mechanical treatments against ischemia-reperfusion injury, as well as subsequent adverse outcomes by modulation of subcellular signaling mechanisms (especially mitochondrial function). (nih.gov)
  • The goal of my PhD was to investigate this phenomenon in human patients treated with PPCI, with particular emphasis on T cell kinetics, their relationship to I/R injury, and the potential mechanisms involved. (bl.uk)
  • In this study, we determined the effect of asiatic acid on myocardial ischemia/reperfusion injury and investigated the underlying mechanisms, using an in vitro rat H9c2 cardiomyocytes model of oxygen-glucose deprivation/reoxygenation (OGD/R) injury. (mdpi.com)
  • We will extend this work to investigate the mechanisms by which nitrite protects the heart against reperfusion injury. (findaphd.com)
  • The aim of the present study was to determine whether curculigoside protects against myocardial ischemia‑reperfusion injury (MIRI) and to investigate the underlying mechanisms. (spandidos-publications.com)
  • This study aimed to evaluate its effect and potential mechanisms on myocardial ischemia/reperfusion (I/R) injury. (peerj.com)
  • The objective of the present study was to determine the cardio-protective effects of GBR and to elucidate the mechanisms underlying these effects in a model of simulated myocardial ischemic/ reperfusion injury (sI/R). (bvsalud.org)
  • Diabetic patients, through incompletely understood mechanisms, endure exacerbated ischemic heart injury compared to non-diabetic patients. (biomedcentral.com)
  • Therefore, the aims of the current study were 1) to determine whether IMD1-53 may protect diabetic hearts against MI/R injury, and if so, 2) to determine the underlying responsible mechanisms. (biomedcentral.com)
  • The pathophysiology and molecular mechanisms of reperfusion injury are complex and, regarding diagnosis, individual diagnostic techniques have been proposed but without a proper assessment of the relative values of these methods. (ebook-dl.com)
  • However, the process of reperfusion can itself induce cardiomyocyte death, known as myocardial reperfusion injury, for which there is still no effective therapy. (jci.org)
  • CREBH influence knockdown was also studied using short hairpin RNA specifically CREBH (Ad-CREBHi) .We found that proinflammatory cytokines affect MC and hepatocytes during myocardial ischemia to induce cleavage CREBH, activate the acute phase response in the liver, and cause injury superimposed on MCs. (wetp.org)
  • Eighteen New Zealand White rabbits were divided into 3 groups and the left circumflex coronary artery was ligated to induce myocardial ischemia . (bvsalud.org)
  • Tissue samples were obtained after 4 h reperfusion to determine expression of receptor-interacting protein 1 (RIP1) and activated caspase 3 by Western blot analysis. (springer.com)
  • LUT pretreatment reduced miR-208b-3p expression in myocardial tissue, as compared to the I/R group. (sigmaaldrich.com)
  • Although restoration of blood flow to an ischaemic organ is essential to prevent irreversible cellular injury, reperfusion may enhance tissue injury in excess of that produced by ischaemia alone [1]. (termedia.pl)
  • Electron paramagnetic resonance oximetry was performed to measure myocardial tissue oxygenation. (iupui.edu)
  • The oximetry study demonstrated that exercise markedly shortened myocardial tissue oxygenation recovery time following reperfusion. (iupui.edu)
  • Together, our study demonstrated that exercise training up-regulated Kir6.1, improved tissue oxygenation recovery, and protected the heart against I/R injury. (iupui.edu)
  • Nowadays, tissue injury induced by I/R is a major factor, which often cause death. (peerj.com)
  • These data demonstrate the significant influence of dietary nitrite and nitrate intake on the maintenance of steady-state tissue nitrite/nitroso levels and illustrate the consequences of nitrite deficiency on the pathophysiology of MI/R injury. (institut-environnement.fr)
  • The objectives of this study were to 1) determine the extent to which ascorbate or catechin alone at levels which could be in blood after dietary supplementation, can protect myocardial tissue in the reperfusion phase of I/R injury, and 2) evaluate the possible cooperative or synergistic protective effect of ascorbate and catechin when given together. (usask.ca)
  • Transfection with HGF plasmids in damaged cardiac tissue also promotes angiogenesis (increased capillary density compared to control subjects), as well as decreasing detrimental remodelling of the tissue at the site of injury (decreased fibrotic deposition). (wikipedia.org)
  • Reperfusion injury, sometimes called ischemia-reperfusion injury (IRI) or reoxygenation injury, is the tissue damage caused when blood supply returns to tissue (re- + perfusion) after a period of ischemia or lack of oxygen (anoxia or hypoxia). (wikipedia.org)
  • Ischemic tissue would have decreased function of these scavengers because of cell injury. (wikipedia.org)
  • Left ventricular (LV) developed pressure and creatine kinase (CK) release were determined as indices of myocardial performance and cellular injury, respectively. (springer.com)
  • 3 ml of jugular venous blood was sampled at the 180 min after reperfusion for the detection of serum ADP, creatine kinase-MB (CK-MB) activity, and cTnI concentration. (alliedacademies.org)
  • Plasma Creatine kinase-MB (CK-MB), Lactate dehydrogenase (LDH) release, myocardial nitric oxide(NO) content and nitrotyrosine formation, 15-F 2t -Isoprostane and plasma superoxide dismutase (SOD) were measured with colorimetric assays. (biomedcentral.com)
  • 2010. Lipoxin A4 analogue protects brain and reduces inflammation in a rat model of focal cerebral ischemia reperfusion. (springer.com)
  • The aim of this study was to determine whether C1INH protects against myocardial cell injury via an anti-apoptotic activity or anti-inflammatory effect. (diva-portal.org)
  • In experimental studies, it has been shown that nitrite protects against myocardial ischaemia reperfusion injury. (findaphd.com)
  • However, whether IMD protects against diabetic myocardial ischemia/reperfusion (MI/R) injury is unknown. (biomedcentral.com)
  • These data suggest that Cdk2 signaling pathways are critical regulators of cardiac I/R injury in vivo and support a cardioprotective role for Rb. (nih.gov)
  • However, the effects of the CAA0225 in in vivo hearts during ischaemia-reperfusion are unknown. (bmj.com)
  • We hypothesised that using CAA0225 in an in vivo mouse model of ischaemia-reperfusion would identify the role cathepsin-L plays during ischaemia-reperfusion. (bmj.com)
  • Ex vivo isolated rat cardiomyocytes demonstrated that ischemia-reperfusion increased calcium influx through L-type calcium channels, reduced sarcolemmal NCX extrusion and SERCA activity. (bmj.com)
  • However, it is unclear whether Que postconditioning has a protective effect against myocardial I/R injury in vivo . (scielo.br)
  • In the present study, Que postconditioning was used as an adjuvant to attenuate myocardial I/R injury in an in vivo rat model. (scielo.br)
  • In vitro and in vivo models were used to replicate conditions of ischaemia/reperfusion (IR) injury. (bl.uk)
  • In vivo PET was performed to determine myocardial uptake of 18 F-FBEM-Cys 40 -exendin-4 at different time points after reperfusion. (snmjournals.org)
  • Schlack W, Preckel B, Barthel H, Obal D, Thämer V . Halothane reduces reperfusion injury after regional ischaemia in the rabbit heart in vivo . (springer.com)
  • The effects of a novel serine protease inhibitor (serpin), LEX032, were investigated in a murine model of MI (20 min) and R (24 hr) injury in vivo. (aspetjournals.org)
  • We aimed to examine the protective role of this novel necrosis inhibitor against myocardial I/R injury using in vitro and in vivo models through anti-necrosis pathway. (ahajournals.org)
  • OBJECTIVE: Cardioprotective properties of recombinant human Erythropoietin (rhEpo) have been shown in in vivo regional or ex vivo global models of ischemia-reperfusion (I/R) injury. (uzh.ch)
  • The aim of this study was to characterize the cardioprotective potential of rhEPO in an in vivo experimental model of global I/R approximating the clinical cardiac surgical setting and to gain insights into the myocardial binding sites of rhEpo and the mechanism involved in its cardioprotective effect. (uzh.ch)
  • The antioxidant properties of flavonols in vivo and their potential benefits in myocardial ischaemia/reperfusion (I/R) injury have been little investigated. (edu.au)
  • We analyzed the regulatory effect of circRNA-68566 on I/R injury and found that circRNA-68566 promoted the proliferation of injured cardiomyocytes in vitro and in vivo. (europeanreview.org)
  • WTAP knockdown inhibits I/R injury in vivo . (aging-us.com)
  • The absence of oxygen halts oxidative phosphorylation, leading to mitochondrial membrane depolarization, ATP depletion, and inhibition of myocardial contractile function. (jci.org)
  • Melatonin confers cardioprotective effect against myocardial ischemia/reperfusion (MI/R) injury by reducing oxidative stress. (ovid.com)
  • In summary, our results demonstrate that melatonin treatment attenuates MI/R injury by reducing oxidative stress damage via activation of SIRT1 signaling in a receptor-dependent manner. (ovid.com)
  • Various forms of reperfusion injury can include myocardial and vascular stunning, microvascular injury and no-reflow, arrhythmias, etc. (omicsonline.org)
  • Cardiac MRI analysis revealed a significant relationship between postCreperfusion effector T cell kinetics and microvascular obstruction (MVO), a component of I/R injury, raising the possibility of a mechanistic link. (bl.uk)
  • This is an observational study investigating the role of inflammation in myocardial microvascular injury following coronary angioplasty and stenting. (isrctn.com)
  • Reperfusion of ischemic tissues is often associated with microvascular injury, particularly due to increased permeability of capillaries and arterioles that lead to an increase of diffusion and fluid filtration across the tissues. (wikipedia.org)
  • Following 20-min global ischemia and 45-min reperfusion, postischemic cardiac contractile function and heart rate were significantly reduced in TG hearts compared with WT hearts. (elsevier.com)
  • Although early reperfusion is essential for myocardial salvage, it induces reperfusion injury, which reduces the benefits of myocardial reperfusion ( 1 , 2 ). (scielo.br)
  • Activation of silent information regulator 1 (SIRT1) signaling also reduces MI/R injury. (ovid.com)
  • Transfection of cardiac myocytes with human HGF reduces ischemic reperfusion injury after MI. (wikipedia.org)
  • Conclusions RO led to an increased myocardial resistance against ischaemia and reperfusion injury. (bmj.com)
  • In this article, the pathophysiology of myocardial lRI and the emerging therapeutic strategies for protecting the heart from its detrimental effects are reviewed. (jci.org)
  • Pathophysiology of myocardial reperfusion injury: preconditioning, postconditioning, and translational aspects of protective measures. (nih.gov)
  • Preliminary exploration into the pathophysiology of ischemia-reperfusion injury, together with the accumulation of clinical evidence, led to the discovery of ischemic preconditioning, which has been the main hypothesis for over three decades for how ischemia-reperfusion injury can be attenuated. (nih.gov)
  • Objective: The diverse studies have revealed multifunctional roles of TRP channels in the physiological conditions and various diseases while some members of TRP channel superfamily are demonstrated to participate in the pathophysiology of cardiometabolic diseases and myocardial ischemia reperfusion injury. (eurekaselect.com)
  • The role of nitric oxide in myocardial ischemia-reperfusion is controversial. (elsevier.com)
  • We evaluate the spectrum of contemporary therapies that have been tested in an attempt to reduce myocardial injury. (biomedsearch.com)
  • Remote Ischemic Postconditioning (RIP) refers to repeated short-term intermittent remote organ reperfusion and re-ischemia before the reperfusion toward one long-term myocardial ischemic period, and it can reduce myocardial ischemia/reperfusion (M-I/R) injury and enhance myocardial tolerance against relatively long-time ischemia and hypoxia [ 1 - 3 ]. (alliedacademies.org)
  • This suggests that acute administration of liposomal CoQ improves myocardial tolerance to I/R via its role as an antioxidant as well as improving oxygen utilization and high energy phosphate production. (elsevier.com)
  • Postconditioning attenuates myocardial ischemia-reperfusion injury by inhibiting events in the early minutes of reperfusion," Cardiovascular Research , vol. 62, no. 1, pp. 74-85, 2004. (hindawi.com)
  • Carvedilol, a new beta adrenoreceptor blocker and free radical scavenger, attenuates myocardial ischemia-reperfusion injury in hypercholesterolemic rabbits. (aspetjournals.org)
  • A number of new therapeutic strategies currently under investigation for preventing myocardial reperfusion injury have the potential to improve clinical outcomes in patients with acute MI treated with PPCI. (jci.org)
  • Recent researches have suggested that LUT can carry out cardioprotective effects during ischemia/reperfusion (I/R). However, there have no reports on whether LUT can exert protective effects against myocardial I/R injury through the actions of specific microRNAs (miRs). (sigmaaldrich.com)
  • Glucagonlike peptide (GLP-1) and its receptor (GLP-1R) exhibit cardioprotective effects after myocardial ischemia and reperfusion (MI/R) in both animal studies and clinical trials. (snmjournals.org)
  • The cardioprotective effects of XST were further validated in H9c2 cardiac muscle cells with hypoxia/reoxygenation injury. (rsc.org)
  • Further studies are being undertaken to determine the cellular mechanism via which Doxorubicin mediates increased myocardial injury in conditions of ischaemia-reperfusion. (bmj.com)
  • T cells were acutely depleted from the circulation within minutes of reperfusion, with highly differentiated effector cells showing the greatest changes. (bl.uk)
  • During the initial ischemia phase, as well as during reperfusion, metabolic therapy can be very useful as, for example, glucose-insulin-potassium solutions (G-I-K). These could act as scavengers of the free radicals derived from oxygen and avoid or reduce the myocardial damage due to reperfused myocytes. (nih.gov)
  • Myocardial 'reperfusion injury' has been partly attributed to the production of free radicals which are cytotoxic towards cells. (curehunter.com)
  • Norepinephrine (NE)-derived free radicals may contribute to myocyte injury after ischemia -reperfusion, so the influence of sympathetic denervation on myocardial ischemia - reperfusion injury was investigated in the present study. (nii.ac.jp)
  • Cardiac denervation protected myocyte against ischemia - reperfusion injury through decreasing direct NE toxicity, but not through decreasing NE-derived free radicals. (nii.ac.jp)
  • Oxygen-derived free radicals play a critical role in atherogenesis and reperfusion injury. (aspetjournals.org)
  • The subcellular pathophysiological mechanism of ischemia-reperfusion injury and preconditioning-induced cardioprotection is not well understood, but extensive research into components, including autacoids, ion channels, receptors, subcellular signaling cascades, and mitochondrial modulators, as well as strategies for modulating these components, has made evolutional progress. (nih.gov)
  • Thioredoxin-interacting protein and myocardial mitochondrial function in ischemia-reperfusion injury. (harvard.edu)
  • The opening of the mitochondrial permeability pore and Ca 2+ overload contribute to myocardial ischemia-reperfusion (I/R) injury. (ahajournals.org)
  • To determine whether sevoflurane or desflurane offer additional protective effects against myocardial reperfusion injury after protecting the heart against the ischemic injury by cardioplegic arrest. (springer.com)
  • Lycopene can protect rat cardiomyocytes from MI/R injury, possibly via activation of Sirt1 signaling pathway to decrease reactive stress response after MI/R injury and subsequent amelioration of inflammatory injury. (alliedacademies.org)
  • Connexin43(CX43) is the most abundant member of Cx family in the heart, the normal expression of Cx43 is important for heart development, electrically coupled cardiomyocytes activities and coordination of myocardial function. (eurekaselect.com)
  • The increased production of HGF by transfected cardiomyocytes during injury has also shown to be a powerful chemo-attractant of adult mesenchymal stem cells via HGF/c-Met binding. (wikipedia.org)
  • Bulbus Allii Caespitosi can improve myocardial metabolism after ischemia and reperfusion in swines. (bvsalud.org)
  • However, coronary reperfusion can cause secondary damage to ischemic tissues, which is known as myocardial ischemia reperfusion injury (MIRI). (spandidos-publications.com)