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, 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 ...
Hausenloy, Derek J.; Yellon, Derek M. (31 July 2008). "Time to Take Myocardial Reperfusion Injury Seriously". New England ... Reperfusion injury, sometimes called ischemia-reperfusion injury (IRI) or reoxygenation injury, is the tissue damage caused ... Reperfusion injury plays a major part in the biochemistry of hypoxic brain injury in stroke. Similar failure processes are ... Reperfusion injury is distinct from cerebral hyperperfusion syndrome (sometimes called "Reperfusion syndrome"), a state of ...
H 2S donors reduce myocardial injury and reperfusion complications. Increased H 2S levels within the body will react with ... "Reduction of Ischemia-Reperfusion Mediated Cardiac Injury in Subjects Undergoing Coronary Artery Bypass Graft Surgery". ... Hydrogen sulfide (H 2S) deficiency can be detrimental to the vascular function after an acute myocardial infarction (AMI). AMIs ... PKG also limits smooth muscle cell proliferation, reducing intima thickening following AMI injury, ultimately decreasing ...
May 2010). "Exosome secreted by MSC reduces myocardial ischemia/reperfusion injury". Stem Cell Research. 4 (3): 214-22. doi: ...
H 2S therapy reduces myocardial injury and reperfusion complications. Due to its effects similar to NO (without its potential ... Yang X, de Caestecker M, Otterbein LE, Wang B (July 2020). "Carbon monoxide: An emerging therapy for acute kidney injury". ... potential to be used to prevent the development of a series of pathological conditions including ischemia reperfusion injury, ... H 2S deficiency can be detrimental to the vascular function after an acute myocardial infarction (AMI). ...
"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: ...
Alam, M.R.; D. Baetz; M. Ovize (2015). "Cyclophilin D and myocardial ischemia-reperfusion injury: a fresh perspective". J Mol ... Reperfusion injury Reperfusion therapy Eltzschig, H.K. & T. Eckle (2011). "Ischemia and reperfusion-from mechanism to ... Ischemia-reperfusion (IR) tissue injury is the resultant pathology from a combination of factors, including tissue hypoxia, ... IR injury contributes to disease and mortality in a variety of pathologies, including myocardial infarction, ischemic stroke, ...
"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 ...
Yellon, Derek M.; Hausenloy, Derek J. (2007-09-13). "Myocardial Reperfusion Injury". New England Journal of Medicine. 357 (11 ... With reperfusion comes ischemia/reperfusion (IR) injury (IRI), which paradoxically causes cell death in reperfused tissue and ... "Targeting reperfusion injury in patients with ST-segment elevation myocardial infarction: trials and tribulations". European ... "Revisiting Cerebral Postischemic Reperfusion Injury: New Insights in Understanding Reperfusion Failure, Hemorrhage, and Edema ...
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 and lasts up to 72 hours after 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) ...
November 2013). "Role of NADPH oxidase isoforms NOX1, NOX2 and NOX4 in myocardial ischemia/reperfusion injury". Journal of ... which play a role in myocardial reperfusion injury. This was a result of the relation between Nox2 and signaling necessary for ... the protein can be a potential target for drug medication due to its negative effect on myocardial reperfusion. Recent evidence ... It has also been shown to play a part in determining the size of a myocardial infarction due to its connection to ROS, ...
"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 ...
In addition, palmatine might have the antiarrhythmic effect, and provideprotection from myocardial ischemia-reperfusion injury ...
... 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 ...
... binding lectin-associated serine protease-2 confers protection from myocardial and gastrointestinal ischemia/reperfusion injury ...
"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 ...
"Beta3-Adrenoreceptor Stimulation Ameliorates Myocardial Ischemia-Reperfusion Injury Via Endothelial Nitric Oxide Synthase and ...
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 ...
"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 ...
"SR9009 administered for one day after myocardial ischemia-reperfusion prevents heart failure in mice by targeting the cardiac ... azotemia or acute kidney injury. Studies have also helped elucidate how light has a direct effect on human health through its ... "Short-term disruption of diurnal rhythms after murine myocardial infarction adversely affects long-term myocardial structure ... or reducing adverse light at night in hospitals may improve patient outcomes post-myocardial infarction (heart attack). 2) " ...
"Intracellular sodium accumulation during ischemia as the substrate for reperfusion injury". Circulation Research. 84 (12): 1401 ... Létienne R, Bel L, Bessac AM, Vacher B, Le Grand B (December 2009). "Myocardial protection by F 15845, a persistent sodium ... In ischemia, the major damage to the cardiac myocyte, due to hypoxia, is seen following the reperfusion of blood. High ... current blocker, in an ischemia-reperfusion model in the pig". European Journal of Pharmacology. 624 (1-3): 16-22. doi:10.1016/ ...
... other A&E/minor injury unit/walk-in centre, treating minor injuries and illnesses Historically, waits for assessment in A&E ... Patients arriving to the emergency department with a myocardial infarction (heart attack) are likely to be triaged to the ... A patient's chance of survival is greatly improved if the patient receives definitive treatment (i.e. surgery or reperfusion) ... These units are for people with non-life-threatening injuries. The use of these units within a department have been shown to ...
Obame FN, Zini R, Souktani R, Berdeaux A, Morin D (October 2007). "Peripheral benzodiazepine receptor-induced myocardial ... Solhjoo S, O'Rourke B (January 2015). "Mitochondrial instability during regional ischemia-reperfusion underlies arrhythmias in ... "Neuroprotective effect of Ro5-4864 following brain injury". Experimental Neurology. 214 (2): 201-8. doi:10.1016/j.expneurol. ... improves cardiac functional recovery during postischemia reperfusion in rats". Experimental Biology and Medicine. 235 (4): 478- ...
Reperfusion in acute ST-segment elevation myocardial infarction". CMAJ. 171 (9): 1039-41. doi:10.1503/cmaj.1041417. PMC 526323 ... doi:10.1016/j.injury.2007.03.028. PMID 17640641. Ventura, Christian (20 January 2021). "1: The EMS System". The Emergency ... They have a particular advantage for major trauma injuries. The well-established theory of the golden hour suggests that major ... Increasingly, research into the management of S-T segment elevation myocardial infarctions (STEMI) occurring outside of the ...
The resulting neurologic injuries may lead to a persistent subtle decline of cognitive abilities, especially in elderly or very ... Potential adverse effects on cardiovascular activities are listed below: Increase in myocardial oxygen demand due to a rise in ... "Propofol metabolism in man during the anhepatic and reperfusion phases of liver transplantation". Xenobiotica. 22 (1): 105-114 ... blood abnormalities and myocardial dysfunction, etc.) There are also risks of adverse effects related to doses such as ...
... protects against myocardial ischemia/reperfusion injury via the sarcolemmal ATP-sensitive potassium channel. Journal of ... N-methyluronamides with high selectivity for human adenosine A3 receptors reduce ischemic myocardial injury. American Journal ... and protects against tissue damage following myocardial ischemia, mediated via an interaction with ATP-sensitive potassium ...
Rosenkranz, Eliot R.; Buckberg, Gerald D. (1983). "Myocardial protection during surgical coronary reperfusion". Journal of the ... This study called attention to the role of active interventions, including antioxidants, to limit this injury, and provided the ... His research initially centered in the area of myocardial protection and led to the introduction of blood cardioplegia, which ... Hoffman, J. I. E.; Buckberg, G. D. (2014). "The Myocardial Oxygen Supply:Demand Index Revisited". Journal of the American Heart ...
Mechanically unloading the left ventricle before coronary reperfusion reduces left ventricular wall stress and myocardial ... power expenditure of the ventricle and limits the hemodynamic forces that lead to ventricular remodeling after insult or injury ... When the heart is damaged by a myocardial infarction a portion of muscle is permanently lost. The heart has a limited innate ... Clinical research indicates that as the size of the myocardial scar increases, so does the likelihood of the patient to develop ...
Thrombolysis in myocardial infarction (TIMI): comparative studies of coronary reperfusion and systemic fibrinogenolysis with ... Reduction of the incidence of amputation in frostbite injury with thrombolytic therapy. Arch Surg. 2007; 142: 546-51. Lijnen HR ... Thrombolysis in Myocardial Infarction (TIMI) Trial, Phase I: A comparison between intravenous tissue plasminogen activator and ... 1984 Dec; 70: 1012-7. The Thrombolysis in Myocardial Infarction (TIMI) trial. Phase I findings. TIMI Study Group. N Engl J Med ...
... also plays a role in the ischemic cascade due to oxygen reperfusion injury following hypoxia. This cascade ... myocardial infarction, fragile X syndrome, sickle-cell disease, lichen planus, vitiligo, autism, infection, chronic fatigue ... Loffredo L, Violi F (August 2020). "COVID-19 and cardiovascular injury: A role for oxidative stress and antioxidant treatment ... Oxidative stress also contributes to tissue injury following irradiation and hyperoxia, as well as in diabetes. In ...
... protein kinase and its relationship with localization of intestinal stem cells in rats after ischemia-reperfusion injury". ... April 2007). "VEGFR-1 and -2 regulate inflammation, myocardial angiogenesis, and arteriosclerosis in chronically rejecting ...
... mediated diastolic dysfunction in myocardial ischemia-reperfusion injury: therapeutic benefits of Drp1 inhibition to reduce ... Midiv-1 has been demonstrated to attenuate the effects of ischemia reperfusion injury after cardiac arrest. The treatment ... FK506 was shown to also preserve mitochondrial morphology after reperfusion injury. GRCh38: Ensembl release 89: ENSG00000087470 ...
... traumatic brain injury and spinal cord injury. Excessive amounts of calpain can be activated due to Ca2+ influx after ... Upon reperfusion of the ischemic myocardium, there is development of calcium overload or excess in the heart cell ( ... as well as secondary degeneration resulting from acute cellular stress following myocardial ischemia, cerebral (neuronal) ... or some types of traumatic brain injury such as diffuse axonal injury. Increase in concentration of calcium in the cell results ...
"Regulation of hepatic microRNA expression in response to ischemic preconditioning following ischemia/reperfusion injury in mice ... Wang XH, Qian RZ, Zhang W, Chen SF, Jin HM, Hu RM (February 2009). "MicroRNA-320 expression in myocardial microvascular ...
2007). "Alterations in Myocardial Cardiolipin Content and Composition Occur at the Very Earliest Stages of Diabetes: A Shotgun ... However, the role of CL in aging and ischemia/reperfusion is still controversial. Tangier disease is also linked to CL ... It was first proposed by Otto Heinrich Warburg that cancer originated from irreversible injury to mitochondrial respiration, ... but the structural basis for this injury has remained elusive. Since cardiolipin is an important phospholipid found almost ...
... reperfusion injury MeSH C23.550.767.877.500 - myocardial reperfusion injury MeSH C23.550.767.879 - shock, surgical MeSH C23.550 ...
Her research primarily focuses on the molecular basis of myocardial ischemia/reperfusion injury and in developing ways to ... with particular attention to the molecular basis of myocardial ischemia/reperfusion injury and in developing ways to mitigate ... Her subsequent work has explored the role of proteases and mitochondrial dysfunction in ischemia/reperfusion injury, and most ... "Enhancing Macroautophagy Protects against Ischemia/Reperfusion Injury in Cardiac Myocytes". "Gottlieb Lab". Delbridge, Lea M. D ...
Myocardial infarction. Retrieved November 28, 2006. Fishbein, M. C. (1990). "Reperfusion injury". Clinical Cardiology. 13 (3): ... Myocardial infarction: diagnosis and investigations - GPnotebook, retrieved November 27, 2006. DE Fenton et al. Myocardial ... Gross examination may reveal signs of myocardial infarction.[citation needed] A one-week-old myocardial infarction of the ... Subepicardial fibrosis (epicardium at top) Myocardial infarction management Myocardial infarction complications For the first ~ ...
In the veins above the heart, such as in the head and neck, the venous pressure may be less than atmospheric and an injury may ... The effects of hyperbaric oxygen also counteract the damage that can occur with reperfusion of previously ischemic areas; this ... the coronary capillaries where they can cause myocardial ischaemia or other tissues, where the consequences are usually less ... Early treatment has greatest benefits, but it can be effective as late as 30 hours after the injury. Oxygen first aid treatment ...
... especially acute myocardial infarction; however, reperfusion has the potential to exacerbate lethal tissue injury, a process ... Reperfusion is the definitive treatment for acute coronary syndromes, ... "reperfusion injury." Ischemia/reperfusion injury may lead to myocardial infarction, cardiac arrhythmias, and contractile ... Interaction of cardiovascular risk factors with myocardial ischemia/reperfusion injury, preconditioning, and postconditioning ...
Myocardial ischemia/reperfusion injury (MIRI) is a phenomenon by which the process of myocardial reperfusion can further induce ... Resveratrol increase myocardial Nrf2 expression in type 2 diabetic rats and alleviate myocardial ischemia/reperfusion injury ( ... Dexmedetomidine, Keap1-Nrf2/ARE signal transduction pathway, Myocardial ischemia/reperfusion injury, Oxidative stress ... MIRI is a phenomenon whereby the process of myocardial reperfusion causes more injury compared with simple ischemia [1]. DEX is ...
Evaluation of Serum Serotonin as a Biomarker for Myocardial Infarction and Ischemia/Reperfusion Injury. Appl. Sci.-Basel, 10 ( ... Evaluation of Serum Serotonin as a Biomarker for Myocardial Infarction and Ischemia/Reperfusion Injury ... aggravating myocardial damage and ischemia/reperfusion (I/R) injury. However, serum serotonin and its potential role as a ... We studied whether serum serotonin was associated with I/R injury assessed by ECG analysis and by analysis of TIMI myocardial ...
miR-17-3p Contributes to Exercise-Induced Cardiac Growth and Protects against Myocardial Ischemia-Reperfusion Injury Jing Shi1* ... miR-17-3p Contributes to Exercise-Induced Cardiac Growth and Protects against Myocardial Ischemia-Reperfusion Injury. ... miR-17-3p Contributes to Exercise-Induced Cardiac Growth and Protects against Myocardial Ischemia-Reperfusion Injury. ... miR-17-3p Contributes to Exercise-Induced Cardiac Growth and Protects against Myocardial Ischemia-Reperfusion Injury. ...
In acute myocardial infarction (AMI), myocardial reperfusion injury may undo part of the recovery after revascularization of ... N2 - In acute myocardial infarction (AMI), myocardial reperfusion injury may undo part of the recovery after revascularization ... AB - In acute myocardial infarction (AMI), myocardial reperfusion injury may undo part of the recovery after revascularization ... abstract = "In acute myocardial infarction (AMI), myocardial reperfusion injury may undo part of the recovery after ...
Nature Communications paper showing that Sema7a binds to platelet GPIb and aggravates post-ischemic myocardial tissue injury, ... Red blood cell-derived semaphorin 7A promotes thrombo-inflammation in myocardial ischemia-reperfusion injury through platelet ... Red blood cell-derived semaphorin 7A promotes thrombo-inflammation in myocardial ischemia-reperfusion injury through platelet ... Red blood cell-derived semaphorin 7A promotes thrombo-inflammation in myocardial ischemia-reperfusion injury through platelet ...
Induction of beclin-1 signaling can be a potential therapeutic target in myocardial reperfusion-induced microvascular injury. ... Interestingly, beclin1 overexpression increased animal survival and attenuated myocardial infarct size (45 ± 6.13 vs 22 ± 4.37 ... no-reflow area (39 ± 5.22 vs 16 ± 2.54) post-myocardial ischemia reperfusion. ... against injury. TTC and Evans blue dye, western blot, immunofluorescence and immunohistochemistry staining were performed in ...
Inhibition of coagulation factor XI attenuates inflammation in myocardial ischemia/reperfusion injury ... A methylation-dependent checkpoint by SETD7 promotes myocardial ischemic injury in mice and men ... Ischaemia-mediated cardiac injury: pathomechanisms and potential treatments. Speakers: Miss Q. Luo, Doctor A. Maier, Doctor J. ... Session: Ischaemia-mediated cardiac injury: pathomechanisms and potential treatments Topic: Ischaemia, Infarction, ...
The coronary circulation in acute myocardial ischaemia/reperfusion injury - a target for cardioprotection.. Title. The coronary ... "The coronary circulation in acute myocardial ischaemia/reperfusion injury - a target for cardioprotection.," NEOMED ... provides an overview of strategies to protect the coronary circulation from acute myocardial ischaemia/reperfusion injury. This ... circulation in acute myocardial ischaemia/reperfusion injury - a target for cardioprotection. ...
Outcome measures included mitochondrial morphology, mitochondrial function, myocardial injury, cardiac function and oxidative ... We hypothesized that inhibition of Drp1 may be effective to reduce MI/R injury in diabetic hearts. High-fat diet and ... Dynamin-related protein 1 (Drp1)-mediated mitochondrial fission plays an important role in MI/R injury under non-diabetic ... The above evidences suggested that Drp1 may be one critical molecule linking diabetes with MI/R injury. ...
Combining the natural inflammatory response and reactive oxygen species (ROS) overproduction after reperfusion injury, we ... In a mouse model of myocardial ischemia repefusuin (MI/R) injury, intravenous injection of our formula resulted in the ... the clinical translational potential of systemic administration of RvD1 in the treatment of ischemia-reperfusion injury is ... The resulting formulation enables targeted delivery of RvD1 to the injury site by hijacking circulating chemotactic monocytes, ...
Quantification of hydroxyl radical and its lack of relevance to myocardial injury during early reperfusion after graded ... Quantification of hydroxyl radical and its lack of relevance to myocardial injury during early reperfusion after graded ...
Following reperfusion for 6 hours, angiotensin II content of the heart was determined using radioimmunoassay. Myocardial ... telmisartan improved microvascular dysfunction during myocardial I/R injury via the PPARG pathway. ... Myocardial capillaries were examined with transmission electron microscopy. Intercellular adhesion molecule-1 (ICAM-1) and ... injury by activating the peroxisome proliferator-activated receptor gamma (PPARG) pathway. Forty-eight male rabbits were ...
... attenuates lung injury induced by aortic ischemia-reperfusion (IR). Therefore, we hypothesized that GdCl3 may attenuate ... Objectives: Aortic ischemia and reperfusion periods, which are often associated with infrarenal abdominal aortic cross-clamping ... and declamping, cause injury in distant organs including the heart. We recently reported that Kupffer cell blockage with ...
Chemerin15 inhibits neutrophil-mediated vascular inflammation and myocardial ischemia-reperfusion injury through ChemR23. EMBO ... Chemerin15 inhibits neutrophil-mediated vascular inflammation and myocardial ischemia-reperfusion injury through ChemR23. Cash ... Chemerin15 inhibits neutrophil-mediated vascular inflammation and myocardial ischemia-reperfusion injury through ChemR23. ... ac.uk/item/8yyzv/chemerin15-inhibits-neutrophil-mediated-vascular-inflammation-and-myocardial-ischemia-reperfusion-injury- ...
Elevated Myocardial Creatine Protects Against Ischemia/Reperfusion Injury by Improving Cardiac Energetics ... Elevated Myocardial Creatine Protects Against Ischemia/Reperfusion Injury by Improving Cardiac Energetics ...
Effect of N-2-mercaptopropionylglycine in limiting myocardial reperfusion injury following 90 minutes of ischemia in dogs. ... Effect of N-2-mercaptopropionylglycine in limiting myocardial reperfusion injury following 90 minutes of ischemia in dogs. ... mediated reperfusion injury. Twenty dogs underwent 90 min of left anterior descending (LAD) coronary artery occlusion followed ... Reperfusion in control group increased the lipid peroxidation and lowered glutathione (GSH) and superoxide dismutase (SOD) ...
In this study we investigated the cardioprotective mechanisms of NG-R1 in myocardial ischemia/reperfusion (MI/R) injury in vivo ... Notoginsenoside R1 protects against myocardial ischemia/reperfusion injury in mice via suppressing TAK1-JNK/p38 signaling. ... Notoginsenoside R1 protects against myocardial ischemia/reperfusion injury in mice via sup ... We showed that NG-R1 administration significantly decreased the myocardial infarction area, alleviated myocardial cell damage ...
... of HDAC3-orchestrated circadian clock gene oscillations in diabetic rats following myocardial ischaemia/reperfusion injury * ... of HDAC3-orchestrated circadian clock gene oscillations in diabetic rats following myocardial ischaemia/reperfusion injury * ...
Myocardial cell death from ischemia-reperfusion (I/R) injury (e.g. myocardial infarction) continues to be a major cause of ... Protein Kinase C Epsilon PeptideInhibitor Exerts Cardioprotective Effects in Myocardial Ischemia/Reperfusion Injury. Anahi ... Myocardial ischemia/reperfusion injury; Protein kinase C epsilon; Endothelial nitric oxide synthase ... Hausenloy DJ, Yellon DM (2013) Myocardial ischemia-reperfusion injury: a neglected therapeutic target. J Clin Invest 123: 92- ...
The effects of vitamin E and lipoic acid supplementation on myocardial ischemia-reperfusion injury in the rat. FASEB Journal. ... The effects of vitamin E and lipoic acid supplementation on myocardial ischemia-reperfusion injury in the rat. / Coombes, J. S ... The effects of vitamin E and lipoic acid supplementation on myocardial ischemia-reperfusion injury in the rat. In: FASEB ... title = "The effects of vitamin E and lipoic acid supplementation on myocardial ischemia-reperfusion injury in the rat", ...
Reperfusion Injury. Myocardial Reperfusion Injury. Pathologic Processes. Myocardial Ischemia. Heart Diseases. Cardiovascular ... Myocardial reperfusion injury. Myocardial infarct size. ST-elevation myocardial infarction. Remote Ischaemic Conditioning. ... STEMI Myocardial Reperfusion Injury Device: Remote ischemic conditioning Device: Control Not Applicable ... Effect of remote ischaemic conditioning on clinical outcomes in patients with acute myocardial infarction (CONDI-2/ERIC-PPCI): ...
A MECHANISM FOR CORTICAL BONE STEM CELL-DERIVED EXOSOMES THERAPEUTIC EFFECT ON POST-MYOCARDIAL INFARCTION REPERFUSION INJURY ... Previous studies have shown both that both post-MI and post-ischemia reperfusion (I/R), there is a reduction in scar size and ... Myocardial infarction (MI) is followed by cardiac remodeling involving extensive fibrosis and which can ultimately progress ... of mCBSCs and mCBSC-derived exosomes into the ischemic region of an infarct had a protective effect against I/R injury. ...
Short-Term Administration of Lemon Balm Extract Ameliorates Myocardial Ischemia/Reperfusion Injury: Focus on Oxidative Stress. ... in the rat model of myocardial ischemia/reperfusion (I/R) injury. Thirty-two Wistar rats were randomly divided into a CTRL non- ... treated control group with myocardial I/R injury and three experimental groups of rats treated with 50, 100, or 200 mg/kg of ME ... ME improved cardiodynamic parameters and achieved to preserve cardiac architecture after I/R injury and to decrease fibrosis, ...
Myocardial ischemia/reperfusion injury 2. *Neurodegeneration 2. *Neurodegenerative Diseases 2. *Neuroinflammation 2 ...
Exosome secreted by MSC reduces myocardial ischemia/reperfusion injury. Stem Cell Res. 2010, 4, 214-222. [Google Scholar] [ ... Reduction of myocardial infarct size by human mesenchymal stem cell conditioned medium. Stem Cell Res. 2007, 1, 129-137. [ ... also reported that MSC microvesicles, which are secreted membrane vesicles of 80 nm to 1 μm, improve acute kidney injury in a ... Mesenchymal stem cell-derived microvesicles protect against acute tubular injury. J. Am. Soc. Nephrol. 2009, 20, 1053-1067. [ ...
Effects of febuxostat and inosine on rat myocardial ischemia/reperfusion injury. Takako Yao Yoshinori Seko ... Non-ST-elevation myocardial infarction complicating carcinoid syndrome. Ayman Elbadawi Erfan Alotaki Islam Y. Elgendy Hend ... Distal left main bronchial injury after catheter ablation for atrial fibrillation: Report of two cases Aaron Sparks James R. ... Sudden cardiac death in a woman with clinical evidence of coronary vasospastic disease and myocardial stunning. A necrospy ...
Protective role of the deSUMOylating enzyme SENP3 in myocardial ischemia-reperfusion injury. Rawlings, N., Lee, L., Nakamura, Y ... Targets and mechanisms of SUMOylation-mediated cardioprotection during ischemia and reperfusion injury. *Henley, Jeremy M ( ...
l‐α‐Lysophosphatidylinositol (LPI) aggravates myocardial ischemia/reperfusion injury via a GPR55/ROCK‐dependent pathway. Pages ...
Activation of an Efferent Cholinergic Pathway Produces Strong Protection Against Myocardial Ischemia/Reperfusion Injury in Rats ... Protective Effects of Melanocortins on Short-Term Changes in a Rat Model of Traumatic Brain Injury: Retraction. March 01, 2023 ...
  • Ischemia/reperfusion injury may lead to myocardial infarction, cardiac arrhythmias, and contractile dysfunction. (nih.gov)
  • Background: Activated platelets release serotonin during acute myocardial infarction (AMI), aggravating myocardial damage and ischemia/reperfusion (I/R) injury. (uni-koeln.de)
  • However, serum serotonin and its potential role as a biomarker for myocardial infarction and I/R injury have not been studied so far. (uni-koeln.de)
  • Methods: In this investigator-initiated pilot study, we examined 38 patients with ST-segment myocardial infarction (STEMI). (uni-koeln.de)
  • Results: Serum serotonin levels were not elevated in the myocardial infarction group compared to the control cohort and they did not show any timeline kinetics after STEMI. (uni-koeln.de)
  • Conclusions: Serum serotonin is not suitable as a biomarker after myocardial infarction and in the assessment of I/R injury. (uni-koeln.de)
  • In acute myocardial infarction (AMI), myocardial reperfusion injury may undo part of the recovery after revascularization of the occluded coronary artery. (tue.nl)
  • In four isolated Langendorff perfused beating pig hearts, an anterior wall myocardial infarction was created by inflating a balloon in the mid segment of the left anterior descending (LAD) artery. (tue.nl)
  • Here, we show that platelet-neutrophil complexes (PNCs) are increased in patients with acute myocardial infarction and that this is associated with increased levels of neuronal guidance protein semaphorin 7A (SEMA7A). (ozgene.com)
  • Agomir of miRNA-30d - a potential new therapeutic target for prevention of ischemic cardiomyopathy after myocardial infarction? (escardio.org)
  • The coronary circulation is both culprit and victim of acute myocardial infarction. (omeka.net)
  • However, no-reflow is still a serious complication of reperfused myocardial infarction and carries, independently from infarct size, an unfavourable prognosis. (omeka.net)
  • Myocardial infarction (MI), a clinical manifestation of coronary heart disease, is the leading cause of cardiovascular-related deaths [ 1 ]. (biomedcentral.com)
  • In the inflamed microvasculature, C15 rapidly modulates neutrophil physiology inducing adherent cell detachment from the inflamed endothelium, while reducing neutrophil recruitment and heart damage in a murine myocardial infarction model. (westminster.ac.uk)
  • We showed that NG-R1 administration significantly decreased the myocardial infarction area, alleviated myocardial cell damage and improved cardiac function in MI/R mice . (bvsalud.org)
  • The results suggest that Myr-PKCε- given at reperfusioneffectively reduces infarct size, improves cardiac function and is aputative treatment that could aid in clinical myocardial infarction/organ transplantation patient recovery. (avensonline.org)
  • Myocardial cell death from ischemia-reperfusion (I/R) injury (e.g. myocardial infarction) continues to be a major cause of morbidity and mortality in Western nations [ 1 ]. (avensonline.org)
  • Reperfusion is essential tosalvage ischemic myocardial tissue from infarction. (avensonline.org)
  • The size of the infarct that results from the combination of the ischemic and reperfusion injury is the major determinant of the prognosis of patients who survive the acute myocardial infarction incident [ 3-7 ]. (avensonline.org)
  • The purpose of this study is to determine whether remote ischemic conditioning can reduce cardiac death and hospitalization for heart failure at 12 months in patients presenting with a ST-elevation myocardial infarction and treated by percutaneous coronary intervention. (clinicaltrials.gov)
  • The CONDI2/ERIC-PPCI trial is a randomised controlled clinical trial investigating whether remote ischemic conditioning (RIC) can reduce cardiac death and hospitalization for heart failure at 12 months in 5400 patients presenting with a ST-elevation myocardial infarction (STEMI) and treated by percutaneous coronary intervention (PPCI). (clinicaltrials.gov)
  • Myocardial infarction (MI) is followed by cardiac remodeling involving extensive fibrosis and which can ultimately progress into heart failure. (temple.edu)
  • In numerous studies, treatment with recombinant human annexins and annexin analogue peptides have consistently found positive outcomes in animal models of sepsis, myocardial infarction, and ischemia reperfusion injury. (frontiersin.org)
  • We conclude that, prolongation of acidic conditions during reperfusion by BZ could be responsible for the cardioprotective benefits of reduced infarction and better myocontractile function, through P38MAPK-dependent pathways. (conicet.gov.ar)
  • 13 Recently, our studies prove that hypoxia induction and macrophage migration inhibitory (MIF) modification can strengthen the therapeutic capacity of MSC-derived exosomes on myocardial infarction (MI) through inhibiting apoptosis and promoting angiogenesis. (researchsquare.com)
  • Ischemia/Reperfusion Injury following Acute Myocardial Infarction: A Critical Issue for Clinicians and Forensic Pathologists. (thieme-connect.de)
  • Mounting evidence supports that stem cell therapies may be promising in this field on the basis of potential therapeutic use of stem cells in damaged organs such as the myocardium after heart infarction, stroke, spinal cord injury, retina diseases, and damaged liver [ 2 - 4 ]. (hindawi.com)
  • The goal of the trial was to evaluate treatment with cyclosporine compared with saline in ST-elevation myocardial infarction patients undergoing percutaneous coronary intervention (PCI). (medscape.com)
  • Cyclosporine will be more effective at decreasing the size of myocardial infarction. (medscape.com)
  • These side effects will need to be carefully studied in the ST-elevation myocardial infarction patient population since these patients are already at risk of contrast nephropathy. (medscape.com)
  • Cite this: Effect of Cyclosporine on Reperfusion Injury in Acute Myocardial Infarction (Effect of Cyclosporine on Reperfusion Injury in AMI) - Medscape - Jul 30, 2008. (medscape.com)
  • Background: Adenosine administered as an adjunct to reperfusion can reduce coronary no-reflow and limit myocardial infarct (MI) size in ST-segment elevation myocardial infarction (STEMI) patients. (uea.ac.uk)
  • We calculated pooled relative risks using a fixed-effect meta-analysis assessing the impact of adjunctive adenosine therapy on major clinical endpoint including all-cause mortality, non-fatal myocardial infarction, and heart failure. (uea.ac.uk)
  • Stroke and myocardial infarction are among the most common causes of mortality and disability in the world. (cdc.gov)
  • Variations in the eicosapentaenoic acid-arachidonic acid ratio associated with age in acute myocardial infarction patients undergoing primary percutaneous coronary intervention. (twmu.ac.jp)
  • The gadolinium-based contrast agents used for LGE differentiate viable myocardium from scar on the basis of differences in cell membrane integrity for acute myocardial infarction. (cdc.gov)
  • In chronic myocardial infarction, the scarred tissue enhances much more than normal myocardium due to increases in extracellular volume. (cdc.gov)
  • When combined with a measure of area at risk like T2-weighted images, CMR can determine infarct size, area at risk, and thus estimate myocardial salvage 1-7 days after acute myocardial infarction. (cdc.gov)
  • Her past medical history was significant for peripheral vascular disease (PVD), diabetes, myocardial infarction with percutaneous intervention, and ischemic cardiomyopathy. (hindawi.com)
  • The current review provides an overview of strategies to protect the coronary circulation from acute myocardial ischaemia/reperfusion injury. (omeka.net)
  • Timely reperfusion therapy can effectively reduce myocardial loss and significantly reduce acute mortality in patients with MI [ 2 ]. (biomedcentral.com)
  • Acute lung injury (ALI) is an inflammatory disorder. (biomedcentral.com)
  • Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is severe disorder of lungs with high mortality [ 1 , 2 ]. (biomedcentral.com)
  • A recent study showed that soluble epoxide hydrolase (sEH) plays a prevailing role in the pathogenesis of acute lung injury (ALI) [ 4 ]. (biomedcentral.com)
  • Verapamil, a calcium channel blocker, is known to protect the myocardium against ischemia and reperfusion injury. (ekja.org)
  • Methods: A total of 70 male SD rats were randomly divided into seven equal groups ( n =10): blank control (S group), ischemia/reperfusion injury (C group), DEX preconditioning (DEX group), tertiary butylhydroquinone (tBHQ) control (tBHQ group), combined tBHQ and DEX preconditioning (tBHQ+DEX group), all-trans retinoic acid (ATRA) control (ATRA group), and combined ATRA and DEX preconditioning (ATRA+DEX group). (portlandpress.com)
  • The aim of these experiments was to determine the effects of combining high levels of vitamin E and lipoic acid supplementation on myocardial performance and arrhythmias during in vivo ischemia and reperfusion (I-R). Female Sprague-Dawley rats (4 months old) were randomly assigned to either a control diet group or a vitamin E and lipoic acid supplementation group. (umn.edu)
  • Thirty-two Wistar rats were randomly divided into a CTRL non-treated control group with myocardial I/R injury and three experimental groups of rats treated with 50, 100, or 200 mg/kg of ME for 7 days per os. (ac.rs)
  • Activation of an Efferent Cholinergic Pathway Produces Strong Protection Against Myocardial Ischemia/Reperfusion Injury in Rats: Retraction. (medscape.com)
  • White R, Holdaway BB, Moody JD, Chang Y. Chronic caffeine administration attenuates vascular injury-induced neointimal hyperplasia in rats. (atsu.edu)
  • reported that Semen Cassiae may reduce hepatic injury in rats [ 12 ]. (biomedcentral.com)
  • Methods: We performed an up-to-date search for all RCTs investigating adenosine as an adjunct to reperfusion in STEMI patients. (uea.ac.uk)
  • Conclusion: We find evidence of improved clinical outcome in terms of less heart failure in STEMI patients administered intracoronary adenosine as an adjunct to reperfusion. (uea.ac.uk)
  • However, ischaemia and reperfusion cause damage not only in cardiomyocytes but also in the coronary circulation, including microembolisation of debris and release of soluble factors from the culprit lesion, impairment of endothelial integrity with subsequently increased permeability and oedema formation, platelet activation and leukocyte adherence, erythrocyte stasis, a shift from vasodilation to vasoconstriction, and ultimately structural damage to the capillaries with eventual no-reflow, microvascular obstruction and intramyocardial haemorrhage. (omeka.net)
  • The aim of this review is to show the potential for developing cardioprotective drugs on the basis of endogenous cardioprotection by pre- and postconditioning (i.e., drug applied as trigger or to activate signaling pathways associated with endogenous cardioprotection) and to review the evidence that comorbidities and aging accompanying coronary disease modify responses to ischemia/reperfusion and the cardioprotection conferred by preconditioning and postconditioning. (nih.gov)
  • Quesnelle KM, Bystrom PV and Toledo-Pereyra LH: Molecular responses to ischemia and reperfusion in the liver. (spandidos-publications.com)
  • Ischemic preconditioning of myocardium is a well described adaptive response in which brief exposure to ischemia/reperfusion before sustained ischemia markedly enhances the ability of the heart to withstand a subsequent ischemic insult. (nih.gov)
  • Preconditioning of the myocardium can be induced by several rounds of brief ischemia (i.e. less than 4 min) followed by several rounds of brief reperfusion (i.e. less than 6 min) prior to prolonged ischemia (i.e. 30 min or greater) followed by the final reperfusion period [ 12 ]. (avensonline.org)
  • Damage to the MYOCARDIUM resulting from MYOCARDIAL REPERFUSION (restoration of blood flow to ischemic areas of the HEART . (bvsalud.org)
  • Red blood cell-derived semaphorin 7A promotes thrombo-inflammation in myocardial ischemia-reperfusion injury through platelet GPIb. (ozgene.com)
  • Therapy consists of the restitution of coronary perfusion which is followed by myocardial inflammation. (ozgene.com)
  • Efficient removal of dead cells and timely resolution of inflammation are exactly the keys to the restoration of cardiac function after myocardial ischemia-reperfusion (MI/R) injury [ 6 , 7 , 8 ]. (biomedcentral.com)
  • Inflammation is one of the most crucial mechanism underlying hepatic ischemia‑reperfusion injury (HIRI). (spandidos-publications.com)
  • van Golen RF, Reiniers MJ, Olthof PB, van Gulik TM and Heger M: Sterile inflammation in hepatic ischemia/reperfusion injury: Present concepts and potential therapeutics. (spandidos-publications.com)
  • The ischemic injury underlying these illnesses is complex, involving intricate interplays among many biological functions including energy metabolism, vascular regulation, hemodynamics, oxidative stress, inflammation, platelet activation, and tissue repair that take place in a context- and time-dependent manner. (cdc.gov)
  • Most experimental studies on cardioprotection have been undertaken in animal models, in which ischemia/reperfusion is imposed in the absence of other disease processes. (nih.gov)
  • We hypothesized that inhibition of Drp1 may be effective to reduce MI/R injury in diabetic hearts. (biomedcentral.com)
  • Delivery of Mdivi-1 into diabetic mice markedly inhibited Drp1 translocation to the mitochondria and reduced mitochondrial fission following MI/R. Inhibition of Drp1 in diabetic hearts improved mitochondrial function and cardiac function following MI/R. Moreover, inhibition of Drp1 reduced myocardial infarct size and serum cardiac troponin I and lactate dehydrogenase activities. (biomedcentral.com)
  • Pharmacological inhibition of Drp1 prevents mitochondrial fission and reduces MI/R injury in diabetic mice. (biomedcentral.com)
  • We characterize the effects of inhibition of CA with benzolamide (BZ) during cardiac ischemia-reperfusion (I/R). Langendorff perfused isolated rat hearts were subjected to 30 min of global ischemia and 60 min of reperfusion. (conicet.gov.ar)
  • In summary, we show that Sema7a binds to platelet GPIb and enhances platelet thrombo-inflammatory activity, aggravating post-ischemic myocardial tissue injury. (ozgene.com)
  • Selective intracoronary hypothermia is a novel method aimed at reducing myocardial reperfusion injury, but its presumed protective effects in AMI still await further elucidation. (tue.nl)
  • Many cardioprotective pharmacological agents failed to exert their protective effects in diabetic hearts subjected to myocardial ischemia/reperfusion (MI/R). Identify the molecular basis linking diabetes with MI/R injury is scientifically important and may provide effective therapeutic approaches. (biomedcentral.com)
  • A 24hr I/R study on 13wk old C57B/L6NJ mice showed that injection of mCBSCs and mCBSC-derived exosomes into the ischemic region of an infarct had a protective effect against I/R injury. (temple.edu)
  • Protective Effects of Melanocortins on Short-Term Changes in a Rat Model of Traumatic Brain Injury: Retraction. (medscape.com)
  • Exosomes (Exos) secreted from MSCs have protective against myocardial injury. (researchsquare.com)
  • To investigate the protective effects and potential mechanisms of estrogen modified human bone marrow mesenchymal stem cells (hBMSC) on high glucose (HG)-induced injury of vascular endothelial cells. (magtech.com.cn)
  • Estrogen may promote the secretion of NO, VEGF and IL-8 by activating the Akt/eNOS signaling pathway of hBMSC cells, increase the cell viability and migration ability of HUVECs and inhibit the occurrence of apoptosis, play a protective role against the injury of HUVECs induced by HG condition. (magtech.com.cn)
  • Targeting mitochondrial dynamics by restoring Klf4 might be potentially cardio-protective strategies attenuating I/R injury. (bvsalud.org)
  • We evaluated the myocardial protective effect of verapamil cardioplegia on the hypertrophied left ventricle during CPB. (ekja.org)
  • He has advanced our understanding of the mechanisms responsible for injury to the heart during ischemia and reperfusion, opening the way for developing novel protective strategies in patients with ischemic heart disease. (medicalnews.md)
  • We studied whether serum serotonin was associated with I/R injury assessed by ECG analysis and by analysis of TIMI myocardial perfusion grade (TMP) and myocardial blush grade (MGB). (uni-koeln.de)
  • Cardiac magnetic resonance (CMR) is a noninvasive imaging method that can determine myocardial anatomy, function, perfusion, and viability in a relative short examination. (cdc.gov)
  • Single photon emission computed tomography (SPECT) detects viability by imaging a combination of myocardial metabolism and perfusion. (cdc.gov)
  • Echocardiographic bubble contrast agents represent a relatively pure intravascular perfusion assessment so do not assess myocardial viability or cell membrane integrity per se. (cdc.gov)
  • Combining the natural inflammatory response and reactive oxygen species (ROS) overproduction after reperfusion injury, we developed a platelet-bionic, ROS-responsive RvD1 delivery platform. (biomedcentral.com)
  • The generation of reactive oxygen species (ROS) during myocardial ischemia (I)/reperfusion (R) contributes to postreperfusion cardiac injury. (avensonline.org)
  • In multiple metabolic disorders, maintaining a dynamic balance of mitochondrial number and function is necessary to prevent the overproduction of reactive oxygen species (ROS), which has been proved to be one of the important mechanisms of cardiomyocyte injury due to the mismatching of oxygen consumption and mitochondrial population and finally to heart failure. (dovepress.com)
  • Additionally, the application of brief repetitive episodes of ischemia/reperfusion at the immediate onset of reperfusion, which has been termed "postconditioning," reduces the extent of reperfusion injury. (nih.gov)
  • Mdivi-1 (1.2 mg/kg), a small molecule inhibitor of Drp1 or vehicle was administrated 15 min before the onset of reperfusion. (biomedcentral.com)
  • In control animals (n = 12), 115 ml of saline was infused through left atrium at the onset of reperfusion whereas treated animals (n = 8) received loading dose of MPG (40 mg/kg) infused through left atrium for 1 h followed by maintenance dose (25 mg/kg) for remaining 3 hours. (who.int)
  • Patients with IC have varied presentations that depend on the onset and duration of injury and extent of involvement. (hindawi.com)
  • Drp1 is translocated to mitochondria in models of myocardial I/R, resulting in mitochondrial fission and dysfunction. (biomedcentral.com)
  • Such interventions have been shown to reduce infarct size, attenuate the frequency and severity of reperfusion-induced arrhythmias, and prevent endothelial dysfunction [ 9-13 ]. (avensonline.org)
  • In early studies Bolli established a primary role of oxygen-free radicals in development of reversible heart dysfunction, or "myocardial stunning. (medicalnews.md)
  • We hypothesize that a cell permeable PKCε peptide inhibitor, (N-myristic acid-EAVSLKPT, Myr-PKCε-) given at reperfusion will improve postreperfused cardiac function and attenuate infarct size compared to untreated isolated perfused rat hearts subjected to ischemic reperfusion injury. (avensonline.org)
  • Infarct size (IZ) and myocardial function were assessed, and phosphorylated forms of P38MAPK, Akt and PKCε were evaluated by immunoblotting. (conicet.gov.ar)
  • In these diseases and aging, the pathological processes are associated with fundamental molecular alterations that can potentially affect the development of ischemia/reperfusion injury per se and responses to cardioprotective interventions. (nih.gov)
  • Involvement of protein tyrosine phosphatase 1B in insulin-enhanced vascular injury-induced neointima formation 3. (atsu.edu)
  • Chang Y, Zhuang D, Zhang C, Hassid A. Increase of PTP levels in vascular injury and in cultured aortic smooth muscle cells treated with specific growth factors. (atsu.edu)
  • The HIRI model was established by occluding the branch of the hepatic pedicle to the left and median liver lobes with an atraumatic vascular clamp for 45 min, followed by reperfusion for 24 h. (spandidos-publications.com)
  • Reperfusion takes place when there is spontaneous thrombolysis, THROMBOLYTIC THERAPY , collateral flow from other coronary vascular beds, or reversal of vasospasm. (bvsalud.org)
  • Present study was designed to examine the effectiveness of N-2-mercaptopropionyl glycine (MPG) on oxygen free radical (OFR) mediated reperfusion injury. (who.int)
  • The aims of premedication are to minimize myocardial oxygen demands by reducing heart rate and systemic arterial pressure and to improve myocardial blood flow with vasodilators. (medscape.com)
  • We have observed that hydrogen peroxide (H2O2), the dismutated product of superoxide, is a coronary metabolic dilator and couples myocardial oxygen consumption to coronary blood flow. (omeka.net)
  • METHODS: Loss-of-function and gain-of-function strategies were applied to investigate the role of Klf4 in cardiac I/R injury via genetic ablation or intra-myocardial adenovirus injection. (bvsalud.org)
  • A number of methods are now clinically available for assessing myocardial viability and there is overlap in the pathophysiological mechanisms that enable each of these diagnostic findings ( Figure 1 ). (cdc.gov)
  • Thus, all of the major cardiac imaging methods can be used to determine myocardial viability. (cdc.gov)
  • They were not associated with the severity of coronary artery disease, the outcome of coronary angiography, the extent of I/R injury, or the degree of heart failure. (uni-koeln.de)
  • In the isolated beating porcine heart model of AMI, reperfusion was associated with additional myocardial injury beyond ischemic injury. (tue.nl)
  • Resolvin D1 (RvD1) has been shown to provide effective protection against ischemia-reperfusion injury in multiple vital organs such as the heart, brain, kidney. (biomedcentral.com)
  • However, reperfusion concurrently elicits multiple adverse events, so that a significant proportion of surviving patients eventually head to heart failure. (biomedcentral.com)
  • Objectives: Aortic ischemia and reperfusion periods, which are often associated with infrarenal abdominal aortic cross-clamping and declamping, cause injury in distant organs including the heart. (sdu.edu.tr)
  • Previous studies show that notoginsenoside R1 (NG-R1), a novel saponin isolated from Panax notoginseng , protects kidney , intestine , lung , brain and heart from ischemia-reperfusion injury . (bvsalud.org)
  • These data suggest mat myocardial performance and rhythm disturbances are not affected by vitamin E and lipoic acid supplementation during in vivo ischemia-reperfusion in the rat heart. (umn.edu)
  • Dynamin-related protein 1 (Drp1)-mediated mitochondrial fission plays an important role in MI/R injury under non-diabetic conditions. (biomedcentral.com)
  • As mitochondria have been considered as vital cell organelles in cardiomyocytes due to their pivotal role in ATP production required for myocardial contraction and survival, targeting mitochondrial pathological alterations may be one promising strategy against diabetic ischemic injury [ 7 - 9 ]. (biomedcentral.com)
  • These studies suggest that Drp1-mediated mitochondrial fission plays an important role in myocardial ischemia/reperfusion (MI/R) injury under non-diabetic conditions. (biomedcentral.com)
  • Annexins A1 and A5 improve organ function and reduce mortality in animal sepsis models, inhibit inflammatory processes, reduce inflammatory mediator release, and protect against ischemic injury. (frontiersin.org)
  • Several studies have shown that Ac2‑26, the active N ‑terminal peptide of Annexin A1, could modulate anti‑inflammatory processes and protect the organs from ischemia‑reperfusion injury (IRI). (spandidos-publications.com)
  • Certain medications, chemical injury, collagenous colitis, inflammatory bowel disease, ischemia, and other infectious pathogens can reportedly cause mucosal injury and subsequent pseudomembrane formation. (hindawi.com)
  • After one hour, two hearts were treated with selective intracoronary hypothermia followed by normal reperfusion (cooled hearts). (tue.nl)
  • Outcome measures included mitochondrial morphology, mitochondrial function, myocardial injury, cardiac function and oxidative stress. (biomedcentral.com)
  • Therefore, we hypothesized that GdCl3 may attenuate myocardial injury induced by aortic IR. (sdu.edu.tr)
  • Collectively, NG-R1 alleviates MI/R injury by suppressing the activity of TAK1, subsequently inhibiting JNK/p38 signaling and attenuating cardiomyocyte apoptosis . (bvsalud.org)
  • The necessity for effective pharmacological intervention still exists, despite numerous basic studies firmly establishing that I/R injury can be delayed or even reduced by the introduction of cardioprotective agents or strategies prior to a prolonged ischemic insult (preconditioning) or at the start of reperfusion [ 1,8 ]. (avensonline.org)
  • Notoginsenoside R1 protects against myocardial ischemia/reperfusion injury in mice via suppressing TAK1-JNK/p38 signaling. (bvsalud.org)
  • However, the clinical translational potential of systemic administration of RvD1 in the treatment of ischemia-reperfusion injury is greatly limited due to biological instability and lack of targeting ability. (biomedcentral.com)
  • RATIONAL: Excessive mitochondrial fission is considered key process involved in myocardial ischemia/reperfusion (I/R) injury. (bvsalud.org)
  • This study aims to investigate how Klf4 regulates mitochondrial dynamics and further clarify its underlying mechanism during cardiac I/R injury. (bvsalud.org)
  • Klf4 deficiency upregulated the expression of ROCK1 at transcriptional level, thus increasing S616-DRP1-mediated mitochondrial fission during I/R. Finally, reconstitution of Klf4 inhibited mitochondrial fission, restored mitochondrial function and alleviated I/R injury. (bvsalud.org)
  • CONCLUSION: Our study provides the first evidence that Klf4 deficiency exacerbates myocardial I/R injury through regulating ROCK1 expression at transcriptional level to induce DRP1-mediated mitochondrial fission. (bvsalud.org)
  • In this study we investigated the cardioprotective mechanisms of NG-R1 in myocardial ischemia / reperfusion (MI/R) injury in vivo and in vitro . (bvsalud.org)
  • Activation of alkalinizing transport mechanisms associated with carbonic anhydrases (CA) leads to myocardial intracellular Ca2+ increase. (conicet.gov.ar)
  • We recently reported that Kupffer cell blockage with gadolinium chloride (GdCl3) attenuates lung injury induced by aortic ischemia-reperfusion (IR). (sdu.edu.tr)
  • Xu L, Ge F, Hu Y, Yu Y, Guo K and Miao C: Sevoflurane postconditioning attenuates hepatic ischemia-reperfusion injury by limiting HMGB1/TLR4/NF-kappaB pathway via modulating microRNA-142 in vivo and in vitro. (spandidos-publications.com)
  • Modified Huangqi Chifeng Decoction Attenuates Proteinuria by Reducing Podocyte Injury in a Rat Model of. (ijddc.com)
  • Objective: To explore the role and mechanism of the Kelch sample related protein-1-nuclear factor erythroid-2 related factor 2/antioxidant response element (Keap1-Nrf2/ARE) signaling pathway in protection of dexmedetomidine (DEX) preconditioning against myocardial ischemia/reperfusion injury (MIRI). (portlandpress.com)
  • Importantly, mice injected with miR-17-3p agomir were protected from adverse remodeling after cardiac ischemia/reperfusion injury. (thno.org)
  • MI/R injury was induced in mice by occluding the left anterior descending coronary artery for 30 min followed by 4 h reperfusion . (bvsalud.org)
  • To this end, a total of 72 adult C57BL/6 mice were randomly divided into sham operation (sham), ischemia‑reperfusion (I/R), I/R + Ac2‑26 and Ac2‑26 groups. (spandidos-publications.com)
  • Natural antioxidant can protect against cardiovascular disease - Science Daily, 6/16/12 - 'The enzyme -- glutathione peroxidase, or GPx3 -- is a natural antioxidant that helps protect organisms from oxidant injury and helps the body naturally repair itself. (qualitycounts.com)
  • As such, new drugs that would complement reperfusion by providing neural and cardiovascular protection and by targeting multiple abnormalities in ischemia are receiving increased attention. (cdc.gov)
  • Myocardial performance was analyzed by measuring 1) peak arterial pressure development and 2) the rate of change of pressure development by a catheter placed in the arch of the aorta. (umn.edu)
  • Afterward, hearts were isolated, and cardiodynamic function was assessed via the Langendorff model of global 20 min ischemia and 30 min reperfusion. (ac.rs)
  • We aimed to investigate the cardioprotective effects of ethanolic Melissa officinalis L. extract (ME) in the rat model of myocardial ischemia/reperfusion (I/R) injury. (ac.rs)
  • Treatment with anti-Sema7a antibody protected from myocardial tissue injury. (ozgene.com)
  • The rupture of an epicardial atherosclerotic plaque with superimposed thrombosis causes coronary occlusion, and this occlusion must be removed to induce reperfusion. (omeka.net)
  • Twenty dogs underwent 90 min of left anterior descending (LAD) coronary artery occlusion followed by 4 h of reperfusion. (who.int)
  • Occlusion was maintained for 25 minutes followed by a 10 minute period of reperfusion. (umn.edu)
  • however, reperfusion has the potential to exacerbate lethal tissue injury, a process termed "reperfusion injury. (nih.gov)
  • Therefore, identify the molecular basis linking diabetes with MI/R injury is scientifically important and may provide effective therapeutic approaches. (biomedcentral.com)
  • Despite many efforts to treat these injuries, there is still no complete recovery and complete improvement in patients with ischemic stroke. (shefayekhatam.ir)