AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesInformation ScienceHealth Care
Myocardial Reperfusion InjuryMyocardial ReperfusionReperfusion InjuryIschemic PostconditioningMyocardial InfarctionMyocardiumCreatine KinaseCardioplegic SolutionsMyocardial IschemiaCoronary CirculationPeroxidaseCardiotonic AgentsReperfusionP-SelectinDisease Models, AnimalHemodynamicsHeartRandom AllocationRats, WistarRats, Sprague-DawleyDogsMyocardial ContractionNeutrophilsThrombectomyWounds and InjuriesIschemic Preconditioning, MyocardialSuctionTime FactorsAngioplasty, Balloon, CoronaryElectrocardiographyBrain InjuriesIschemic PreconditioningVentricular Function, LeftPerfusionHeart Arrest, InducedThrombolytic TherapyCoronary VesselsCoronary AngiographyNecrosisIschemiaCreatine Kinase, MB FormMitochondria, HeartMyocytes, CardiacAnterior Wall Myocardial InfarctionCoronary ThrombosisMitochondrial Membrane Transport ProteinsPercutaneous Coronary InterventionAthletic InjuriesTreatment OutcomeMicrocirculationSpinal Cord InjuriesMalondialdehydeAcute Kidney InjuryWarm IschemiaLung InjuryProtective AgentsMice, Inbred C57BLRabbitsImmunoglobulin Fab FragmentsPlatelet Glycoprotein GPIIb-IIIa ComplexSwineEchocardiographyBrain IschemiaApoptosisEndothelium, VascularInjury Severity ScoreNeutrophil InfiltrationOxidative StressL-Lactate DehydrogenaseLiverLeg InjuriesCold IschemiaOrgan PreservationKidneyCytoprotectionOrgan Preservation SolutionsAcute Lung InjurySuperoxide DismutaseAlanine TransaminaseAspartate AminotransferasesMice, KnockoutProspective StudiesEye InjuriesModels, AnimalCoronary DiseaseFree RadicalsInfarction, Middle Cerebral ArteryAntioxidantsNeck InjuriesNitric OxideFree Radical ScavengersMyocardial StunningNeuroprotective AgentsConstrictionStentsPredictive Value of Tests
Myocardial Reperfusion Injury: Damage to the MYOCARDIUM resulting from MYOCARDIAL REPERFUSION (restoration of blood flow to ischemic areas of the HEART.) Reperfusion takes place when there is spontaneous thrombolysis, THROMBOLYTIC THERAPY, collateral flow from other coronary vascular beds, or reversal of vasospasm.Myocardial Reperfusion: Generally, restoration of blood supply to heart tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. Reperfusion can be induced to treat ischemia. Methods include chemical dissolution of an occluding thrombus, administration of vasodilator drugs, angioplasty, catheterization, and artery bypass graft surgery. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing MYOCARDIAL REPERFUSION INJURY.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.Ischemic Postconditioning: The application of repeated, brief periods of vascular occlusion at the onset of REPERFUSION to reduce REPERFUSION INJURY that follows a prolonged ischemic event. The techniques are similar to ISCHEMIC PRECONDITIONING but the time of application is after the ischemic event instead of before.Myocardial Infarction: NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).Myocardium: The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.Creatine Kinase: A transferase that catalyzes formation of PHOSPHOCREATINE from ATP + CREATINE. The reaction stores ATP energy as phosphocreatine. Three cytoplasmic ISOENZYMES have been identified in human tissues: the MM type from SKELETAL MUSCLE, the MB type from myocardial tissue and the BB type from nervous tissue as well as a mitochondrial isoenzyme. Macro-creatine kinase refers to creatine kinase complexed with other serum proteins.Cardioplegic Solutions: Solutions which, upon administration, will temporarily arrest cardiac activity. They are used in the performance of heart surgery.Myocardial Ischemia: A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (CORONARY ARTERY DISEASE), to obstruction by a thrombus (CORONARY THROMBOSIS), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (MYOCARDIAL INFARCTION).Coronary Circulation: The circulation of blood through the CORONARY VESSELS of the HEART.Peroxidase: A hemeprotein from leukocytes. Deficiency of this enzyme leads to a hereditary disorder coupled with disseminated moniliasis. It catalyzes the conversion of a donor and peroxide to an oxidized donor and water. EC 1.11.1.7.Cardiotonic Agents: Agents that have a strengthening effect on the heart or that can increase cardiac output. They may be CARDIAC GLYCOSIDES; SYMPATHOMIMETICS; or other drugs. They are used after MYOCARDIAL INFARCT; CARDIAC SURGICAL PROCEDURES; in SHOCK; or in congestive heart failure (HEART FAILURE).Reperfusion: Restoration of blood supply to tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. It is primarily a procedure for treating infarction or other ischemia, by enabling viable ischemic tissue to recover, thus limiting further necrosis. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing REPERFUSION INJURY.P-Selectin: Cell adhesion molecule and CD antigen that mediates the adhesion of neutrophils and monocytes to activated platelets and endothelial cells.Disease Models, Animal: Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.Hemodynamics: The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.Heart: The hollow, muscular organ that maintains the circulation of the blood.Random Allocation: A process involving chance used in therapeutic trials or other research endeavor for allocating experimental subjects, human or animal, between treatment and control groups, or among treatment groups. It may also apply to experiments on inanimate objects.Rats, Wistar: A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.Rats, Sprague-Dawley: A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.Dogs: The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)Myocardial Contraction: Contractile activity of the MYOCARDIUM.Neutrophils: 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.Thrombectomy: 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.Wounds and Injuries: Damage inflicted on the body as the direct or indirect result of an external force, with or without disruption of structural continuity.Ischemic Preconditioning, Myocardial: Exposure of myocardial tissue to brief, repeated periods of vascular occlusion in order to render the myocardium resistant to the deleterious effects of ISCHEMIA or REPERFUSION. The period of pre-exposure and the number of times the tissue is exposed to ischemia and reperfusion vary, the average being 3 to 5 minutes.Suction: 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.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Angioplasty, Balloon, Coronary: Dilation of an occluded coronary artery (or arteries) by means of a balloon catheter to restore myocardial blood supply.Electrocardiography: Recording of the moment-to-moment electromotive forces of the HEART as projected onto various sites on the body's surface, delineated as a scalar function of time. The recording is monitored by a tracing on slow moving chart paper or by observing it on a cardioscope, which is a CATHODE RAY TUBE DISPLAY.Brain Injuries: Acute and chronic (see also BRAIN INJURIES, CHRONIC) injuries to the brain, including the cerebral hemispheres, CEREBELLUM, and BRAIN STEM. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with DIFFUSE AXONAL INJURY or COMA, POST-TRAUMATIC. Localized injuries may be associated with NEUROBEHAVIORAL MANIFESTATIONS; HEMIPARESIS, or other focal neurologic deficits.Ischemic Preconditioning: A technique in which tissue is rendered resistant to the deleterious effects of prolonged ISCHEMIA and REPERFUSION by prior exposure to brief, repeated periods of vascular occlusion. (Am J Physiol 1995 May;268(5 Pt 2):H2063-7, Abstract)Ventricular Function, Left: The hemodynamic and electrophysiological action of the left HEART VENTRICLE. Its measurement is an important aspect of the clinical evaluation of patients with heart disease to determine the effects of the disease on cardiac performance.Perfusion: Treatment process involving the injection of fluid into an organ or tissue.Heart Arrest, Induced: 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).Thrombolytic Therapy: Use of infusions of FIBRINOLYTIC AGENTS to destroy or dissolve thrombi in blood vessels or bypass grafts.Coronary Vessels: The veins and arteries of the HEART.Coronary Angiography: Radiography of the vascular system of the heart muscle after injection of a contrast medium.Necrosis: The pathological process occurring in cells that are dying from irreparable injuries. It is caused by the progressive, uncontrolled action of degradative ENZYMES, leading to MITOCHONDRIAL SWELLING, nuclear flocculation, and cell lysis. It is distinct it from APOPTOSIS, which is a normal, regulated cellular process.Ischemia: A hypoperfusion of the BLOOD through an organ or tissue caused by a PATHOLOGIC CONSTRICTION or obstruction of its BLOOD VESSELS, or an absence of BLOOD CIRCULATION.Creatine Kinase, MB Form: An isoenzyme of creatine kinase found in the CARDIAC MUSCLE.Mitochondria, Heart: The mitochondria of the myocardium.Myocytes, Cardiac: Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).Anterior Wall Myocardial Infarction: 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.Coronary Thrombosis: Coagulation of blood in any of the CORONARY VESSELS. The presence of a blood clot (THROMBUS) often leads to MYOCARDIAL INFARCTION.Mitochondrial Membrane Transport Proteins: Proteins involved in the transport of specific substances across the membranes of the MITOCHONDRIA.Percutaneous Coronary Intervention: 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.Athletic Injuries: Injuries incurred during participation in competitive or non-competitive sports.Treatment Outcome: Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.Microcirculation: The circulation of the BLOOD through the MICROVASCULAR NETWORK.Spinal Cord Injuries: Penetrating and non-penetrating injuries to the spinal cord resulting from traumatic external forces (e.g., WOUNDS, GUNSHOT; WHIPLASH INJURIES; etc.).Malondialdehyde: The dialdehyde of malonic acid.Acute Kidney Injury: 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.Warm Ischemia: A tissue or organ remaining at physiological temperature during decreased BLOOD perfusion or in the absence of blood supply. During ORGAN TRANSPLANTATION it begins when the organ reaches physiological temperature before the completion of SURGICAL ANASTOMOSIS and ends with reestablishment of the BLOOD CIRCULATION through the tissue.Lung Injury: 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.Protective Agents: 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.Mice, Inbred C57BLRabbits: 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.Immunoglobulin Fab Fragments: 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 Glycoprotein GPIIb-IIIa Complex: 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.Swine: Any of various animals that constitute the family Suidae and comprise stout-bodied, short-legged omnivorous mammals with thick skin, usually covered with coarse bristles, a rather long mobile snout, and small tail. Included are the genera Babyrousa, Phacochoerus (wart hogs), and Sus, the latter containing the domestic pig (see SUS SCROFA).Echocardiography: Ultrasonic recording of the size, motion, and composition of the heart and surrounding tissues. The standard approach is transthoracic.Brain Ischemia: Localized reduction of blood flow to brain tissue due to arterial obstruction or systemic hypoperfusion. This frequently occurs in conjunction with brain hypoxia (HYPOXIA, BRAIN). Prolonged ischemia is associated with BRAIN INFARCTION.Apoptosis: One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.Endothelium, Vascular: Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.Injury Severity Score: 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.Neutrophil Infiltration: 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.Oxidative Stress: A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).L-Lactate Dehydrogenase: A tetrameric enzyme that, along with the coenzyme NAD+, catalyzes the interconversion of LACTATE and PYRUVATE. In vertebrates, genes for three different subunits (LDH-A, LDH-B and LDH-C) exist.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.Leg Injuries: General or unspecified injuries involving the leg.Cold Ischemia: The chilling of a tissue or organ during decreased BLOOD perfusion or in the absence of blood supply. Cold ischemia time during ORGAN TRANSPLANTATION begins when the organ is cooled with a cold perfusion solution after ORGAN PROCUREMENT surgery, and ends after the tissue reaches physiological temperature during implantation procedures.Organ Preservation: 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).Kidney: Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.Cytoprotection: The process by which chemical compounds provide protection to cells against harmful agents.Organ Preservation Solutions: Solutions used to store organs and minimize tissue damage, particularly while awaiting implantation.Acute Lung Injury: 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).Superoxide Dismutase: 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.Alanine Transaminase: 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.Aspartate Aminotransferases: 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.Mice, Knockout: Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.Prospective Studies: Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group.Eye Injuries: Damage or trauma inflicted to the eye by external means. The concept includes both surface injuries and intraocular injuries.Models, Animal: Non-human animals, selected because of specific characteristics, for use in experimental research, teaching, or testing.Coronary Disease: An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels.Free Radicals: 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.Infarction, Middle Cerebral Artery: NECROSIS occurring in the MIDDLE CEREBRAL ARTERY distribution system which brings blood to the entire lateral aspects of each CEREBRAL HEMISPHERE. Clinical signs include impaired cognition; APHASIA; AGRAPHIA; weak and numbness in the face and arms, contralaterally or bilaterally depending on the infarction.Antioxidants: Naturally occurring or synthetic substances that inhibit or retard the oxidation of a substance to which it is added. They counteract the harmful and damaging effects of oxidation in animal tissues.Neck Injuries: General or unspecified injuries to the neck. It includes injuries to the skin, muscles, and other soft tissues of the neck.Nitric Oxide: A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.Free Radical Scavengers: 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.Myocardial Stunning: Prolonged dysfunction of the myocardium after a brief episode of severe ischemia, with gradual return of contractile activity.Neuroprotective Agents: Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids.Constriction: The act of constricting.Stents: Devices that provide support for tubular structures that are being anastomosed or for body cavities during skin grafting.Predictive Value of Tests: 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)

Remote ischaemic preconditioning and postconditioning and the reperfusion injury salvage kinase pathway | HeartRemote ischaemic preconditioning and postconditioning and the reperfusion injury salvage kinase pathway | Heart
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. ...
Effect of Lipoxin A4 on Myocardial Ischemia Reperfusion Injury Following Cardiac Arrest in a Rabbit Model | SpringerLinkEffect of Lipoxin A4 on Myocardial Ischemia Reperfusion Injury Following Cardiac Arrest in a Rabbit Model | SpringerLink
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
1 The cathepsin-L inhibitor CAA0225 protects against myocardial ischaemia-reperfusion injury | Heart1 The cathepsin-L inhibitor CAA0225 protects against myocardial ischaemia-reperfusion injury | Heart
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 ...
Braz J Cardiovasc Surg - Effect of Simulated Geomagnetic Activity on Myocardial Ischemia/Reperfusion Injury in RatsBraz J Cardiovasc Surg - Effect of Simulated Geomagnetic Activity on Myocardial Ischemia/Reperfusion Injury in Rats
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. ...
Preconditioning effects of on myocardial ischemia/reperfusion injury in rats | AVESİSPreconditioning effects of on myocardial ischemia/reperfusion injury in rats | AVESİS
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. ...
Activated platelets contribute importantly to myocardial reperfusion injury<...Activated platelets contribute importantly to myocardial reperfusion 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. ...
MicroRNA 3113-5p is a novel marker for early cardiac ischemia/reperfusion injury | Diagnostic Pathology | Full TextMicroRNA 3113-5p is a novel marker for early cardiac ischemia/reperfusion injury | Diagnostic Pathology | Full Text
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.
Fatty acid analogue accumulation: A marker of myocyte viability in ischemic-reperfused myocardium<...Fatty acid analogue accumulation: A marker of myocyte viability in ischemic-reperfused myocardium<...
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 ...
Critical Role of AT1 Receptor Expression After Ischemia/Reperfusion in Isolated Rat Hearts | Circulation ResearchCritical Role of AT1 Receptor Expression After Ischemia/Reperfusion in Isolated Rat Hearts | Circulation Research
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 ...
Gene transfer of IkappaBalpha limits infarct size in a mouse model of myocardial ischemia-reperfusion injury. | Archivio della...Gene transfer of IkappaBalpha limits infarct size in a mouse model of myocardial ischemia-reperfusion injury. | Archivio della...
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 ...
Figure 5 | Honokiol Ameliorates Myocardial Ischemia/Reperfusion Injury in Type 1 Diabetic Rats by Reducing Oxidative Stress and...Figure 5 | Honokiol Ameliorates Myocardial Ischemia/Reperfusion Injury in Type 1 Diabetic Rats by Reducing Oxidative Stress and...
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
Papers with the keyword Intralipd | Read by QxMDPapers with the keyword Intralipd | Read by QxMD
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 ...
Progression in attenuating myocardial reperfusion injury: An overview<...Progression in attenuating myocardial reperfusion injury: An overview<...
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 - ...
Holdings: Management of Myocardial Reperfusion InjuryHoldings: Management of Myocardial Reperfusion Injury
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 Injury: A Perspective on Lethal Reperfusion Injury | OMICS InternationalAcute Myocardial Injury: A Perspective on Lethal Reperfusion Injury | OMICS International
Acute myocardial infarction contributes significantly to mortality in patients with coronary artery disease. Timely reperfusion of an infarct-related artery within a reas..
Methionine protects from myocardial ischemia/reperfusion injury via down regulation of the inflammatory response and apoptosis ...Methionine protects from myocardial ischemia/reperfusion injury via down regulation of the inflammatory response and apoptosis ...
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 ...
British Library EThOS: The role of T lymphocytes in myocardial ischaemia/reperfusion injuryBritish Library EThOS: The role of T lymphocytes in myocardial ischaemia/reperfusion injury
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 ...
Abstract 027: Therapeutic Potential of a Novel Necrosis Inhibitor in Myocardial Ischemia-Reperfusion Injury | Circulation...Abstract 027: Therapeutic Potential of a Novel Necrosis Inhibitor in Myocardial Ischemia-Reperfusion Injury | Circulation...
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 ...
The alleviation of myocardial ischemia/reperfusion injury by lycopene | AbstractThe alleviation of myocardial ischemia/reperfusion injury by lycopene | Abstract
Myocardial Ischemia/Reperfusion (MI/R) injury is a clinical phenomenon including myocardial structural damage, dysfunction and disorders of metabolism..
Effect of estrogen on global myocardial ischemia-reperfusion injury in female rats - Fingerprint - University of Illinois...Effect of estrogen on global myocardial ischemia-reperfusion injury in female rats - Fingerprint - University of Illinois...
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. ...
Intravenous Administration of Lycopene, a Tomato Extract, Protects against Myocardial Ischemia-Reperfusion Injury. - Semantic...Intravenous Administration of Lycopene, a Tomato Extract, Protects against Myocardial Ischemia-Reperfusion Injury. - Semantic...
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
Promoting effects of IL‑23 on myocardial ischemia and reperfusion are associated with increased expression of IL‑17A and...Promoting effects of IL‑23 on myocardial ischemia and reperfusion are associated with increased expression of IL‑17A and...
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 ...
High mobility group [corrected] box 1 mediates neutrophil recruitment in myocardial ischemia-reperfusion injury through toll...High mobility group [corrected] box 1 mediates neutrophil recruitment in myocardial ischemia-reperfusion injury through toll...
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 …
Cardiac Protection with Targeted Drug Delivery to Ischemic-Reperfused MyocardiumCardiac Protection with Targeted Drug Delivery to Ischemic-Reperfused Myocardium
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Vitexin attenuates myocardial ischemia/reperfusion injury in rats by regulating mitochondrial dysfunction induced by...Vitexin attenuates myocardial ischemia/reperfusion injury in rats by regulating mitochondrial dysfunction induced by...
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...
Extracellular matrix proteomics in cardiac Ischemia/Reperfusion: The Search Is on<...Extracellular matrix proteomics in cardiac Ischemia/Reperfusion: The Search Is on<...
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 - ...
Abstract 17380: Nanoparticles-Mediated Delivery of Pioglitazone Reduces Myocardial Ischemia-Reperfusion Injury by Antagonizing...Abstract 17380: Nanoparticles-Mediated Delivery of Pioglitazone Reduces Myocardial Ischemia-Reperfusion Injury by Antagonizing...
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 ...
Good News for Experimental Concept but Bad News for Clinically Effective Therapy | CirculationGood News for Experimental Concept but Bad News for Clinically Effective Therapy | Circulation
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 ...
Seeing through the murine heart - quantitative 3D assessment of myocardial ischemia/reperfusion injury and responseSeeing through the murine heart - quantitative 3D assessment of myocardial ischemia/reperfusion injury and response
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
Fibrin-Derived Peptide FX06 Reduces Cardiac Reperfusion InjuryFibrin-Derived Peptide FX06 Reduces Cardiac Reperfusion Injury
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 ...
Role of oxygen free radicals in cardiocyte injury in the reperfused rat heart - Folia Histochemica et Cytobiologica. Supplement...Role of oxygen free radicals in cardiocyte injury in the reperfused rat heart - Folia Histochemica et Cytobiologica. Supplement...
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 ...
Bursts of reperfusion arrhythmias occur independently of area at risk size and are the first marker of reperfusion injury -...Bursts of reperfusion arrhythmias occur independently of area at risk size and are the first marker of reperfusion injury -...
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- ...
MicroRNA-125b protects against myocardial ischaemia/reperfusion injury via targeting p53-mediated apoptotic signalling and...MicroRNA-125b protects against myocardial ischaemia/reperfusion injury via targeting p53-mediated apoptotic signalling and...
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].
Hsa-circ-0068566 inhibited the development of myocardial ischemia reperfusion injury by regulating hsa-miR-6322/PARP2 signal...Hsa-circ-0068566 inhibited the development of myocardial ischemia reperfusion injury by regulating hsa-miR-6322/PARP2 signal...
OBJECTIVE: In recent years, studies have shown that noncoding RNA (circRNA) is an important regulatory molecule involved in cell physiology and pathology.
Citations | MBL Life Science -JAPANCitations | MBL Life Science -JAPAN
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 ...
Efficacy of FX06 in the Prevention of Myocardial Reperfusion Injury - Full Text View - ClinicalTrials.govEfficacy of FX06 in the Prevention of Myocardial Reperfusion Injury - Full Text View - ClinicalTrials.gov
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the contacts provided below. For general information, Learn About Clinical Studies. ...
Release of tissue-specific proteins into coronary perfusate as a model for biomarker discovery in myocardial ischemia...Release of tissue-specific proteins into coronary perfusate as a model for biomarker discovery in myocardial ischemia...
TY - JOUR. T1 - Release of tissue-specific proteins into coronary perfusate as a model for biomarker discovery in myocardial ischemia/reperfusion injury. AU - Cordwell, Stuart J.. AU - Edwards, Alistair V G. AU - Liddy, Kiersten A.. AU - Moshkanbaryans, Lia. AU - Solis, Nestor. AU - Parker, Benjamin L.. AU - Yong, Andy S C. AU - Wong, Clement. AU - Kritharides, Leonard. AU - Hambly, Brett D.. AU - White, Melanie Y.. PY - 2012/4/6. Y1 - 2012/4/6. N2 - Diagnosis of acute coronary syndromes is based on protein biomarkers, such as the cardiac troponins (cTnI/cTnT) and creatine kinase (CK-MB) that are released into the circulation. Biomarker discovery is focused on identifying very low abundance tissue-derived analytes from within albumin-rich plasma, in which the wide dynamic range of the native protein complement hinders classical proteomic investigations. We employed an ex vivo rabbit model of myocardial ischemia/reperfusion (I/R) injury using Langendorff buffer perfusion. Nonrecirculating ...
Cardioprotective Effects of Genistin in Rat Myocardial Ischemia-Reperfusion Injury Studies by Regulation of P2X7/NF-κB PathwayCardioprotective Effects of Genistin in Rat Myocardial Ischemia-Reperfusion Injury Studies by Regulation of P2X7/NF-κB Pathway
Evidence-Based Complementary and Alternative Medicine (eCAM) is an international peer-reviewed, Open Access journal that seeks to understand the sources and to encourage rigorous research in this new, yet ancient world of complementary and alternative medicine.
GLP also showed cardioprotective effects iGLP also showed cardioprotective effects i
GLP-1 also showed cardioprotective effects (i.e., infarct size reduction and ejection fraction improvement) in experimental models of myocardial ischemia-reperfusion injury by suppressing caspase-3 activation and preventing apoptosis of cardiomyocytes [[50], [51]]. Of note, such a cardioprotection was previously reported to be mediated by both GLP-1R-dependent and GLP-1R-independent mechanisms [78]. More importantly, GLP-1 has been reported to improve ejection fraction of left ventricle and to prevent its ischemic dysfunction in patients with acute myocardial infarction [79] and coronary artery disease (CAD) [53], respectively. Besides its beneficial effects in CAD, GLP-1 might improve heart failure by increasing glucose uptake and, therefore, left ventricular function, as suggested by both animal [80] and human [[81], [82]] studies. DPP-4 inhibition resulted in similar cardioprotective effects in preclinical models [[83], [84]]. Regarding cerebrovascular function, GLP-1 attenuated cerebral ...
Reperfusion Injury | CTDReperfusion Injury | CTD
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 ...
234658 | Stanford Health Care234658 | Stanford Health Care
3 ,4-Dihydroxyflavonol reduces infarct size in a porcine acute myocardial ischaemia-reperfusion model Congress of the European-Society-of-Cardiology Teramoto, T., Ikeno, F., Lyons, J., Thomas, C. J., May, C. N., Woodman, O. L., Jarrott, B., Yeung, A. C., Fearon, W. F. OXFORD UNIV PRESS. 2010: 493-494 View details for Web of Science ID 000281531903177 ...
Trash and Recycling Archives - Home is Where Our Heart isTrash and Recycling Archives - Home is Where Our Heart is
Is the web dwelling of Arrange-It, your storage and group useful resource, and is proud to offer prospects nice merchandise for organizing their home and simplifying their lives. The mechanical behaviour of living matter is governed not only by an elastic or viscoelastic response to loading on quick time scales up to a number of minutes, but additionally by typically essential progress and remodelling responses on time scales from hours to months.. On this Evaluation we characterise the remodelling processes in atherosclerosis, vascular and myocardial ischaemia-reperfusion damage, and coronary heart failure, and we draw consideration to potential avenues for progressive therapeutic approaches, together with conditioning and metabolic strategies.. NEW TOOLS: There can be an opportunity to select from all kinds of accessible makes and models of economic-grade electric lawn and garden gear, including handheld trimmers, chainsaws, pruners, backpack and handheld blowers and ride-on, stand-on, ...
Cardioprotection by endogenous fibroblast growth factor 2 in cardiac i by Stacey House, Carla Weinheimer et al."Cardioprotection by endogenous fibroblast growth factor 2 in cardiac i" by Stacey House, Carla Weinheimer et al.
House, Stacey; Weinheimer, Carla; Kovacs, Attila; Ornitz, David, "Cardioprotection by endogenous fibroblast growth factor 2 in cardiac ischemia-reperfusion injury in vivo" (2011). Conference Abstracts and Posters. Paper 7. http://digitalcommons.wustl.edu/em_conf/7. ...
Increased myocardial ischemia-reperfusion injury in renal failure involves cardiac adiponectin signal deficiency. | Sigma...Increased myocardial ischemia-reperfusion injury in renal failure involves cardiac adiponectin signal deficiency. | Sigma...
Sigma-Aldrich offers abstracts and full-text articles by [Yanbin Song, Qiujun Yu, Junyi Zhang, Weidong Huang, Yi Liu, Haifeng Pei, Jingyi Liu, Lu Sun, Lu Yang, Congye Li, Yan Li, Fuyang Zhang, Yan Qu, Ling Tao].
Curculigoside attenuates myocardial ischemia‑reperfusion injury by inhibiting the opening of the mitochondrial permeability...Curculigoside attenuates myocardial ischemia‑reperfusion injury by inhibiting the opening of the mitochondrial permeability...
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 ...
Sodium nitroprusside exacerbates myocardial ischemia-reperfusion injury<...Sodium nitroprusside exacerbates myocardial ischemia-reperfusion injury<...
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 ...
miR-17-3p contributes to exercise-induced cardiac growth and protects against myocardial ischemia-reperfusion injurymiR-17-3p contributes to exercise-induced cardiac growth and protects against myocardial ischemia-reperfusion injury
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 ...
Phenserine inhibits neuronal apoptosis following ischemia/reperfusion injury<...Phenserine inhibits neuronal apoptosis following ischemia/reperfusion injury<...
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 ...
SIRT1 protects against myocardial ischemia-reperfusion injury via activating eNOS in diabetic rats | Cardiovascular Diabetology...SIRT1 protects against myocardial ischemia-reperfusion injury via activating eNOS in diabetic rats | Cardiovascular Diabetology...
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 ...
Staff Profile - Faculty of Medical Sciences - Newcastle UniversityStaff Profile - Faculty of Medical Sciences - Newcastle University
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 ...
British Library EThOS: Role of cyclophilins and heat shock proteins in myocardial ischaemia/reperfusion injuryBritish Library EThOS: Role of cyclophilins and heat shock proteins in myocardial ischaemia/reperfusion injury
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 ...
Delayed onset of apoptosis following ischemia/reperfusion in rat liver: Downregulation of BAX gene<...Delayed onset of apoptosis following ischemia/reperfusion in rat liver: Downregulation of BAX gene<...
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 - ...
Cureus | Edematous Bullae: An Atypical Presentation of Reperfusion Injury. A Discussion of Ischemic-reperfusion Injury and...Cureus | Edematous Bullae: An Atypical Presentation of Reperfusion Injury. A Discussion of Ischemic-reperfusion Injury and...
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.
Remote preconditioning, perconditioning, and postconditioning: a comparative study of their cardioprotective properties in rat...Remote preconditioning, perconditioning, and postconditioning: a comparative study of their cardioprotective properties in rat...
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.
GW27-e0640 Aldehyde dehydrogenase-2 reduces chronic neuropathic pain increased susceptibility to ischemia/reperfusion injury in...GW27-e0640 Aldehyde dehydrogenase-2 reduces chronic neuropathic pain increased susceptibility to ischemia/reperfusion injury in...
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) ...
Molecules | Free Full-Text | Clematichinenoside (AR) Attenuates Hypoxia/Reoxygenation-Induced H9c2 Cardiomyocyte Apoptosis via...Molecules | Free Full-Text | Clematichinenoside (AR) Attenuates Hypoxia/Reoxygenation-Induced H9c2 Cardiomyocyte Apoptosis via...
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
The harmful effects of ventricular distention during postischemic reperfusion<...The harmful effects of ventricular distention during postischemic reperfusion<...
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 ...
Insulin and GSK3β-inhibition abrogates the infarct sparing-effect of ischemic postconditioning in ex vivo rat heartsInsulin and GSK3β-inhibition abrogates the infarct sparing-effect of ischemic postconditioning in ex vivo rat hearts
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). ...
3,4-Dihydroxyflavonol reduces infarct size and injury associated with myocardial ischaemia and reperfusion in sheep - RMIT...3',4'-Dihydroxyflavonol reduces infarct size and injury associated with myocardial ischaemia and reperfusion in sheep - RMIT...
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 ...
Potential role of renin-angiotensin system blockade for preventing myocardial ischemia/reperfusion injury and remodeling after...Potential role of renin-angiotensin system blockade for preventing myocardial ischemia/reperfusion injury and remodeling after...
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
IJMS | Free Full-Text | Deficiency of Senescence Marker Protein 30 Exacerbates Cardiac Injury after Ischemia/ReperfusionIJMS | Free Full-Text | Deficiency of Senescence Marker Protein 30 Exacerbates Cardiac Injury after Ischemia/Reperfusion
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 | EGFR Tyrosine Kinase Inhibitors...We've investigated the consequences of hypoxia and myocardial ischemia/reperfusion for the | EGFR Tyrosine Kinase Inhibitors...
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 ...
Impact of a novel cardioprotective agent on the ischaemia-reperfusion- induced Akt kinase activation<...Impact of a novel cardioprotective agent on the ischaemia-reperfusion- induced Akt kinase activation<...
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 ...
Endogenous Mechanisms of Cardioprotection : Cardioprotection - oiEndogenous Mechanisms of Cardioprotection : Cardioprotection - oi
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. ...
S1P 3-mediated cardiac fibrosis in sphingosine kinase 1 transgenic mice involves reactive oxygen species<...S1P 3-mediated cardiac fibrosis in sphingosine kinase 1 transgenic mice involves reactive oxygen species<...
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...Cardiovascular drugs attenuated myocardial resistance against ischaemia-induced and reperfusion-induced injury in a rat model...
Cardiovascular drugs attenuated myocardial resistance against ischaemia-induced and reperfusion-induced injury in a rat model of repetitive occlusion ...
Endothelin receptor mediated Ca(2+) signaling in coronary arteries after experimentally induced ischemia/reperfusion injury in...Endothelin receptor mediated Ca(2+) signaling in coronary arteries after experimentally induced ischemia/reperfusion injury in...
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 ON REDICING ISCHEMIA REPERFUSION INJURY IN SCALETAL MUSCLE - Turkish Journal of Thoracic and Cardiovascular SurgeryTICLOPIDIN ON REDICING ISCHEMIA REPERFUSION INJURY IN SCALETAL MUSCLE - Turkish Journal of Thoracic and Cardiovascular Surgery
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 ...
Novel Small Molecule Inhibitor of C1s Exerts Cardioprotective Effects in Ischemia-Reperfusion Injury in Rabbits | The Journal...Novel Small Molecule Inhibitor of C1s Exerts Cardioprotective Effects in Ischemia-Reperfusion Injury in Rabbits | The Journal...
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, ...
Hydrogen Flush After Cold Storage as a New End-Ischemic Ex Vivo Treatment for Liver Grafts Against Ischemia/Reperfusion Injury<...Hydrogen Flush After Cold Storage as a New End-Ischemic Ex Vivo Treatment for Liver Grafts Against Ischemia/Reperfusion Injury<...
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 ...
Anticoagulant therapy in critical organ ischaemia/reperfusion injury<...Anticoagulant therapy in critical organ ischaemia/reperfusion injury<...
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 Deficiency Causes Increased Infarct Size and Apoptosis in a Mouse Cardiac Ischemia-Reperfusion Model | Arteriosclerosis,...Abcc6 Deficiency Causes Increased Infarct Size and Apoptosis in a Mouse Cardiac Ischemia-Reperfusion Model | Arteriosclerosis,...
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 ...
Cardioprotection by Regular Ethanol Consumption: Potential Mechanisms and Clinical Application | Bentham ScienceCardioprotection by Regular Ethanol Consumption: Potential Mechanisms and Clinical Application | Bentham Science
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 ...
Ischemic Postconditioning Protects Neuronal Death Caused by Cerebral Ischemia and Reperfusion via Attenuating Protein...Ischemic Postconditioning Protects Neuronal Death Caused by Cerebral Ischemia and Reperfusion via Attenuating Protein...
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 ...
Increase in experimental infarct size with digoxin in a canine model of myocardial ischemia-reperfusion injury.Increase in experimental infarct size with digoxin in a canine model of myocardial ischemia-reperfusion injury.
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-
Acute inflammatory reaction after myocardial ischemic injury and reperfusion. Development and use of a neutrophil-specific...Acute inflammatory reaction after myocardial ischemic injury and reperfusion. Development and use of a neutrophil-specific...
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 ...
Papers in the shared collection Cardioprotection reviews | Read by QxMDPapers in the shared collection Cardioprotection reviews | Read by QxMD
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 ...
Effect of HEMADO on Level of CK-MB and LDH Enzymes after Ischemia/Reperfusion Injury in Isolated Rat Heart | BIEffect of HEMADO on Level of CK-MB and LDH Enzymes after Ischemia/Reperfusion Injury in Isolated Rat Heart | BI
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,
Homocysteine Exposure Impairs Myocardial Resistance to Ischaemia Reperfusion and Oxidative Stress | Research UNEHomocysteine Exposure Impairs Myocardial Resistance to Ischaemia Reperfusion and Oxidative Stress | Research UNE
Background/Aims: Hyperhomocysteinaemia is recognised as a strong independent risk factor for developing cardiovascular disease. This study investigated how an acute homocysteine dose affected cardiac performance during ischaemia reperfusion and cardiomyocyte contractility and morphology under normal conditions and during oxidative stress. Methods: Cardiac function was measured in isolated and perfused rat hearts before and after 40 minutes global normothermic ischaemia. Where used, 0.1 mM L-homocysteine was present prior to, and throughout ischaemia, before wash out after 10 minutes reperfusion. Calcium transients under normal conditions and changes in contractile synchronicity during oxidative stress (exposure to 0.2 mM H2O2) were measured in freshly isolated rat cardiomyocytes incubated for 60 minutes ± 0.1 mM L-homocysteine. Results: During ischaemia reperfusion 0.1 mM L-homocysteine significantly reduced the rate pressure product during reperfusion (10,038 ± 749 vs. 5955 ± 567 mmHg bpm, ...
ANALOGS THAT TARGET MITOCHONDRIAL DISEASES - STEALTH BIOTHERAPEUTICS CORPANALOGS THAT TARGET MITOCHONDRIAL DISEASES - STEALTH BIOTHERAPEUTICS CORP
Disclosed are analogs of elamipretide (MTP-131). The compounds are useful for the treatment and prevention of ischemia-reperfusion injury (e.g., cardiac ischemia-reperfusion injury) or myocardial infarction.
Human HGF plasmid DNA therapyHuman HGF plasmid DNA therapy
Biological functions of hydrogen sulfideBiological functions of hydrogen sulfide
Gaseous signaling moleculesGaseous signaling molecules
CD9CD9
Histone deacetylase inhibitorHistone deacetylase inhibitor
Succinic acidSuccinic acid
TrapidilTrapidil
HumaninHumanin
Accelerated idioventricular rhythmAccelerated idioventricular rhythm
TNNI3TNNI3
AGGF1AGGF1
Ischemic preconditioningIschemic preconditioning
CardioprotectionCardioprotection
CYBBCYBB
DeoxyschizandrinDeoxyschizandrin
CyclobuxineCyclobuxine
Jawahar L. MehtaJawahar L. Mehta
Contraction band necrosisContraction band necrosis
Diallyl trisulfideDiallyl trisulfide
CollectinCollectin
Heart nanotechnologyHeart nanotechnology
Adenosine A3 receptorAdenosine A3 receptor
RotigaptideRotigaptide
SulodexideSulodexide
Terminalia arjunaTerminalia arjuna
PerfusionPerfusion
FSTL1FSTL1
DNM1LDNM1L
ThrombosisThrombosis
Salvia miltiorrhizaSalvia miltiorrhiza
Cerebral hypoxiaCerebral hypoxia
Vitamin CVitamin C
تفاوت میان نسخه‌های «فشار خون بالا» - ویکی‌پدیا، دانشنامهٔ آزادتفاوت میان نسخه‌های «فشار خون بالا» - ویکی‌پدیا، دانشنامهٔ آزاد
Acute respiratory distress syndromeAcute respiratory distress syndrome
Euryale ferox - VicipaediaEuryale ferox - Vicipaedia
ThrombusThrombus
MyoglobinMyoglobin
ThrombusThrombus
Medical emergencyMedical emergency
Regeneration (biology)Regeneration (biology)
SOD1SOD1
PienteholaserhoitoPienteholaserhoito
CiclosporinCiclosporin
Emergency medical servicesEmergency medical services
Pulmonary edemaPulmonary edema
ThromboxaneThromboxane
Interleukiin-10 - VikipeediaInterleukiin-10 - Vikipeedia
ThromboxaneThromboxane
Adenozinski A3 receptor - Википедија, слободна енциклопедијаAdenozinski A3 receptor - Википедија, слободна енциклопедија
Emergency departmentEmergency department
NecrosisNecrosis
Heart-type fatty acid binding proteinHeart-type fatty acid binding protein
ENDOGENDOG
F15845F15845
Emergency departmentEmergency department
Ro5-4864Ro5-4864
Emergency medical servicesEmergency medical services
CP-532,903CP-532,903
AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesInformation ScienceHealth Care
Myocardial Reperfusion InjuryMyocardial ReperfusionReperfusion InjuryIschemic PostconditioningMyocardial InfarctionMyocardiumCreatine KinaseCardioplegic SolutionsMyocardial IschemiaCoronary CirculationPeroxidaseCardiotonic AgentsReperfusionP-SelectinDisease Models, AnimalHemodynamicsHeartRandom AllocationRats, WistarRats, Sprague-DawleyDogsMyocardial ContractionNeutrophilsThrombectomyWounds and InjuriesIschemic Preconditioning, MyocardialSuctionTime FactorsAngioplasty, Balloon, CoronaryElectrocardiographyBrain InjuriesIschemic PreconditioningVentricular Function, LeftPerfusionHeart Arrest, InducedThrombolytic TherapyCoronary VesselsCoronary AngiographyNecrosisIschemiaCreatine Kinase, MB FormMitochondria, HeartMyocytes, CardiacAnterior Wall Myocardial InfarctionCoronary ThrombosisMitochondrial Membrane Transport ProteinsPercutaneous Coronary InterventionAthletic InjuriesTreatment OutcomeMicrocirculationSpinal Cord InjuriesMalondialdehydeAcute Kidney InjuryWarm IschemiaLung InjuryProtective AgentsMice, Inbred C57BLRabbitsImmunoglobulin Fab FragmentsPlatelet Glycoprotein GPIIb-IIIa ComplexSwineEchocardiographyBrain IschemiaApoptosisEndothelium, VascularInjury Severity ScoreNeutrophil InfiltrationOxidative StressL-Lactate DehydrogenaseLiverLeg InjuriesCold IschemiaOrgan PreservationKidneyCytoprotectionOrgan Preservation SolutionsAcute Lung InjurySuperoxide DismutaseAlanine TransaminaseAspartate AminotransferasesMice, KnockoutProspective StudiesEye InjuriesModels, AnimalCoronary DiseaseFree RadicalsInfarction, Middle Cerebral ArteryAntioxidantsNeck InjuriesNitric OxideFree Radical ScavengersMyocardial StunningNeuroprotective AgentsConstrictionStentsPredictive Value of Tests
Efficacy of FX06 in the Prevention of Myocardial Reperfusion Injury - Full Text View - ClinicalTrials.govEfficacy of FX06 in the Prevention of Myocardial Reperfusion Injury - Full Text View - ClinicalTrials.gov
Acute Myocardial Injury: A Perspective on Lethal Reperfusion Injury | OMICS InternationalAcute Myocardial Injury: A Perspective on Lethal Reperfusion Injury | OMICS International
Increased myocardial ischemia-reperfusion injury in renal failure involves cardiac adiponectin signal deficiency. | Sigma...Increased myocardial ischemia-reperfusion injury in renal failure involves cardiac adiponectin signal deficiency. | Sigma...
British Library EThOS: The role of T lymphocytes in myocardial ischaemia/reperfusion injuryBritish Library EThOS: The role of T lymphocytes in myocardial ischaemia/reperfusion injury
1 The cathepsin-L inhibitor CAA0225 protects against myocardial ischaemia-reperfusion injury | Heart1 The cathepsin-L inhibitor CAA0225 protects against myocardial ischaemia-reperfusion injury | Heart
Effect of Lipoxin A4 on Myocardial Ischemia Reperfusion Injury Following Cardiac Arrest in a Rabbit Model | SpringerLinkEffect of Lipoxin A4 on Myocardial Ischemia Reperfusion Injury Following Cardiac Arrest in a Rabbit Model | SpringerLink
Vitexin attenuates myocardial ischemia/reperfusion injury in rats by regulating mitochondrial dysfunction induced by...Vitexin attenuates myocardial ischemia/reperfusion injury in rats by regulating mitochondrial dysfunction induced by...
Abstract 027: Therapeutic Potential of a Novel Necrosis Inhibitor in Myocardial Ischemia-Reperfusion Injury | Circulation...Abstract 027: Therapeutic Potential of a Novel Necrosis Inhibitor in Myocardial Ischemia-Reperfusion Injury | Circulation...
The alleviation of myocardial ischemia/reperfusion injury by lycopene | AbstractThe alleviation of myocardial ischemia/reperfusion injury by lycopene | Abstract
Seeing through the murine heart - quantitative 3D assessment of myocardial ischemia/reperfusion injury and responseSeeing through the murine heart - quantitative 3D assessment of myocardial ischemia/reperfusion injury and response
Ischemia-reperfusion myocardial injury]Ischemia-reperfusion myocardial injury]
JCI - Myocardial ischemia-reperfusion injury: a neglected therapeutic targetJCI - Myocardial ischemia-reperfusion injury: a neglected therapeutic target
JCI - Inadequate ubiquitination-proteasome coupling contributes to myocardial ischemia-reperfusion injuryJCI - Inadequate ubiquitination-proteasome coupling contributes to myocardial ischemia-reperfusion injury
Sivelestat Attenuates Myocardial Reperfusion Injury during Brief Low Flow Postischemic InfusionSivelestat Attenuates Myocardial Reperfusion Injury during Brief Low Flow Postischemic Infusion
JCI - Inadequate ubiquitination-proteasome coupling contributes to myocardial ischemia-reperfusion injuryJCI - Inadequate ubiquitination-proteasome coupling contributes to myocardial ischemia-reperfusion injury
Combination of necroptosis and apoptosis inhibition enhances cardioprotection against myocardial ischemia-reperfusion injury |...Combination of necroptosis and apoptosis inhibition enhances cardioprotection against myocardial ischemia-reperfusion injury |...
Protective Effects of L-Malate against Myocardial Ischemia/Reperfusion Injury in RatsProtective Effects of L-Malate against Myocardial Ischemia/Reperfusion Injury in Rats
Pathophysiology of myocardial reperfusion injury: preconditioning, postconditioning, and translational aspects of protective...Pathophysiology of myocardial reperfusion injury: preconditioning, postconditioning, and translational aspects of protective...
Clinical perspectives on reperfusion injury in acute myocardial infarction.Clinical perspectives on reperfusion injury in acute myocardial infarction.
Sulfonylurea receptor 1 subunits of ATP-sensitive potassium channels and myocardial ischemia/reperfusion injury. - PubMed -...Sulfonylurea receptor 1 subunits of ATP-sensitive potassium channels and myocardial ischemia/reperfusion injury. - PubMed -...
Cyclin-dependent kinase 2 signaling regulates myocardial ischemia/reperfusion injuryCyclin-dependent kinase 2 signaling regulates myocardial ischemia/reperfusion injury
Minimizing Reperfusion Injury in Patients With Acute Myocardial Infarction - No Study Results Posted - ClinicalTrials.govMinimizing Reperfusion Injury in Patients With Acute Myocardial Infarction - No Study Results Posted - ClinicalTrials.gov
03 Cancer therapy drug, doxorubicin, exacerbates myocardial ischaemia reperfusion injury | Heart03 Cancer therapy drug, doxorubicin, exacerbates myocardial ischaemia reperfusion injury | Heart
Myocardial Reperfusion Injury Summary Report | CureHunterMyocardial Reperfusion Injury Summary Report | CureHunter
Effects of acute angiotensin II on ischemia reperfusion injury following myocardial infarction.Effects of acute angiotensin II on ischemia reperfusion injury following myocardial infarction.
IJMS | Free Full-Text | Combined Therapy with SS31 and Mitochondria Mitigates Myocardial Ischemia-Reperfusion Injury in RatsIJMS | Free Full-Text | Combined Therapy with SS31 and Mitochondria Mitigates Myocardial Ischemia-Reperfusion Injury in Rats
Frontiers | Ginsenoside Rg1 Ameliorates Rat Myocardial Ischemia-Reperfusion Injury by Modulating Energy Metabolism Pathways |...Frontiers | Ginsenoside Rg1 Ameliorates Rat Myocardial Ischemia-Reperfusion Injury by Modulating Energy Metabolism Pathways |...
Quercetin postconditioning attenuates myocardial ischemia/reperfusion injury in rats through the PI3K/Akt pathwayQuercetin postconditioning attenuates myocardial ischemia/reperfusion injury in rats through the PI3K/Akt pathway
Luteolin Inhibits Ischemia/Reperfusion-Induced Myocardial Injury in Rats via Downregulation of microRNA-208b-3p. | Sigma-AldrichLuteolin Inhibits Ischemia/Reperfusion-Induced Myocardial Injury in Rats via Downregulation of microRNA-208b-3p. | Sigma-Aldrich
Imbalance Between Tissue Inhibitor of Metalloproteinase-4 and Matrix Metalloproteinases During Acute Myocardial Ischemia...Imbalance Between Tissue Inhibitor of Metalloproteinase-4 and Matrix Metalloproteinases During Acute Myocardial Ischemia...
British Library EThOS: Role of cyclophilins and heat shock proteins in myocardial ischaemia/reperfusion injuryBritish Library EThOS: Role of cyclophilins and heat shock proteins in myocardial ischaemia/reperfusion injury
Acetaminophen to Prevent Ischemic Oxidative Reperfusion Injury During Percutaneous Coronary Intervention for Acute Myocardial...Acetaminophen to Prevent Ischemic Oxidative Reperfusion Injury During Percutaneous Coronary Intervention for Acute Myocardial...
Anti-apoptotic role for C1 inhibitor in ischemia/reperfusion-induced myocardial cell injury.Anti-apoptotic role for C1 inhibitor in ischemia/reperfusion-induced myocardial cell injury.
Molecules | Free Full-Text | Asiatic Acid Attenuates Myocardial Ischemia/Reperfusion Injury via Akt/GSK-3β/HIF-1α Signaling in...Molecules | Free Full-Text | Asiatic Acid Attenuates Myocardial Ischemia/Reperfusion Injury via Akt/GSK-3β/HIF-1α Signaling in...
AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesInformation ScienceHealth Care
Myocardial Reperfusion InjuryMyocardial ReperfusionReperfusion InjuryIschemic PostconditioningMyocardial InfarctionMyocardiumCreatine KinaseCardioplegic SolutionsMyocardial IschemiaCoronary CirculationPeroxidaseCardiotonic AgentsReperfusionP-SelectinDisease Models, AnimalHemodynamicsHeartRandom AllocationRats, WistarRats, Sprague-DawleyDogsMyocardial ContractionNeutrophilsThrombectomyWounds and InjuriesIschemic Preconditioning, MyocardialSuctionTime FactorsAngioplasty, Balloon, CoronaryElectrocardiographyBrain InjuriesIschemic PreconditioningVentricular Function, LeftPerfusionHeart Arrest, InducedThrombolytic TherapyCoronary VesselsCoronary AngiographyNecrosisIschemiaCreatine Kinase, MB FormMitochondria, HeartMyocytes, CardiacAnterior Wall Myocardial InfarctionCoronary ThrombosisMitochondrial Membrane Transport ProteinsPercutaneous Coronary InterventionAthletic InjuriesTreatment OutcomeMicrocirculationSpinal Cord InjuriesMalondialdehydeAcute Kidney InjuryWarm IschemiaLung InjuryProtective AgentsMice, Inbred C57BLRabbitsImmunoglobulin Fab FragmentsPlatelet Glycoprotein GPIIb-IIIa ComplexSwineEchocardiographyBrain IschemiaApoptosisEndothelium, VascularInjury Severity ScoreNeutrophil InfiltrationOxidative StressL-Lactate DehydrogenaseLiverLeg InjuriesCold IschemiaOrgan PreservationKidneyCytoprotectionOrgan Preservation SolutionsAcute Lung InjurySuperoxide DismutaseAlanine TransaminaseAspartate AminotransferasesMice, KnockoutProspective StudiesEye InjuriesModels, AnimalCoronary DiseaseFree RadicalsInfarction, Middle Cerebral ArteryAntioxidantsNeck InjuriesNitric OxideFree Radical ScavengersMyocardial StunningNeuroprotective AgentsConstrictionStentsPredictive Value of Tests
InfarctionInfarctRatsApoptosisReduce myocardialMyocardiumPercutaneous coronary intTherapeuticTissueSerumVivoPathologyMiceProtectsClinicalMicrovascular1999SignificantlyExperimentalPathwaysEndothelialPathophysiologicalReactiveCoronary arteryAdiponectinCardiac injuryMyocytesHeart
Infarction7
Infarct10
Rats2
Apoptosis4
Reduce myocardial1
Myocardium1
  • The present study demonstrates that renal dysfunction increases cardiac susceptibility to ischemic-reperfusion injury, which is associated with downregulated APN/AdipoR1/AMPK signaling and increased oxidative/nitrative stress in local myocardium, and provides the first evidence for the protective role of exogenous supplement of gAd on MI/R outcomes in renal failure. (sigmaaldrich.com)
Percutaneous coronary int1
Therapeutic2
Tissue2
  • Perfusate proteins were separated using two-dimensional gel electrophoresis (2-DE) and identified by mass spectrometry (MS), revealing 26 tissue-specific proteins released during reperfusion post-15I. (edu.au)
  • A total of 192 tissue-specific proteins were identified during reperfusion post-60I. (edu.au)
Serum1
Vivo2
Pathology1
Mice3
Protects1
Clinical3
Microvascular1
19991
Significantly1
Experimental1
Pathways2
  • Debate has gone on, and continues regarding the existence of reperfusion injury and the pathways that are solicited. (omicsonline.org)
  • The present study was designed to investigate the specific role of IL‑23 in myocardial I/R injury, and whether the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2‑STAT3) signaling pathway, one of the important downstream signaling pathways of IL‑23, and the IL‑17A downstream pro‑inflammatory cytokine, were involved. (spandidos-publications.com)
Endothelial1
  • Moreover, SN increased myocardial NO metabolites, superoxide, and their cytotoxic reaction product peroxynitrite, upregulated inducible NO synthase expression, and decreased endothelial NOS phosphorylation. (sigmaaldrich.com)
Pathophysiological1
Reactive1
  • During the development of I/R injury, a surge of reactive oxygen and nitrogen species as well as inflammatory cascades bursts and eventually triggers organ damage [ 3 ]. (biomedcentral.com)
Coronary artery1
  • Four weeks later anesthetized animals were subjected to total occlusion (45 minutes) of the left main coronary artery followed by 5 hours of reperfusion. (units.it)
Adiponectin1
Cardiac injury2
Myocytes1
Heart2
  • microRNA 223-3p and microRNA 3113-5p were among the mostly altered microRNAs and were validated to be up-regulated within the early hours of I/R injury in heart tissues. (biomedcentral.com)
  • So far, more than 200 microRNAs have been considered as heart-specific with many of them being identified to release into the circulatory system during ischemic injury. (biomedcentral.com)
Vitexin attenuates myocardial ischemia/reperfusion injury in rats by regulating mitochondrial dysfunction induced by...
Vitexin attenuates myocardial ischemia/reperfusion injury in rats by regulating mitochondrial dysfunction induced by... (medworm.com)
Plus it
Plus it (bmj.com)
Articles by Giuseppe Ambrosio : Journal of Cardiovascular Pharmacology
Articles by Giuseppe Ambrosio : Journal of Cardiovascular Pharmacology (journals.lww.com)
Oridonin | GreenMedInfo | Substance | Natural Medicine | Alternative
Oridonin | GreenMedInfo | Substance | Natural Medicine | Alternative (greenmedinfo.com)
Mangiferin | GreenMedInfo | Substance | Natural Medicine
Mangiferin | GreenMedInfo | Substance | Natural Medicine (greenmedinfo.com)
Crocetin | GreenMedInfo | Substance | Natural Medicine | Alternative
Crocetin | GreenMedInfo | Substance | Natural Medicine | Alternative (greenmedinfo.com)
Combination of necroptosis and apoptosis inhibition enhances cardioprotection against myocardial ischemia-reperfusion injury |...
Combination of necroptosis and apoptosis inhibition enhances cardioprotection against myocardial ischemia-reperfusion injury |... (link.springer.com)
Thrombosis - Wikipedia
Thrombosis - Wikipedia (en.wikipedia.org)
Gynostemma | GreenMedInfo | Substance | Natural Medicine
Gynostemma | GreenMedInfo | Substance | Natural Medicine (greenmedinfo.com)
Hydroxytyrosol | GreenMedInfo | Substance | Natural Medicine
Hydroxytyrosol | GreenMedInfo | Substance | Natural Medicine (greenmedinfo.com)
Cardioprotective | GreenMedInfo | Category | Natural Medicine
Cardioprotective | GreenMedInfo | Category | Natural Medicine (greenmedinfo.com)
When should a CBC count be obtained in suspected myocardial infarction (MI, heart attack), and which conditions should be...
When should a CBC count be obtained in suspected myocardial infarction (MI, heart attack), and which conditions should be... (medscape.com)
What prehospital care is indicated in chest pain and suspected myocardial infarction (MI, heart attack)?
What prehospital care is indicated in chest pain and suspected myocardial infarction (MI, heart attack)? (medscape.com)
What are the criteria for using ECG in the workup of suspected myocardial infarction (MI, heart attack), and how often should...
What are the criteria for using ECG in the workup of suspected myocardial infarction (MI, heart attack), and how often should... (medscape.com)
Which heart exam findings are associated with heart damage in the setting of myocardial infarction (MI, heart attack)?
Which heart exam findings are associated with heart damage in the setting of myocardial infarction (MI, heart attack)? (medscape.com)
Which GI symptoms are associated with myocardial ischemia and myocardial infarction (MI, heart attack)?
Which GI symptoms are associated with myocardial ischemia and myocardial infarction (MI, heart attack)? (medscape.com)
What are the 2015 AHA guidelines for secondary prevention after coronary artery bypass grafting (CABG)?
What are the 2015 AHA guidelines for secondary prevention after coronary artery bypass grafting (CABG)? (medscape.com)
Why is effective communication between EMS personnel and emergency department staff important?
Why is effective communication between EMS personnel and emergency department staff important? (medscape.com)
Allicin | GreenMedInfo | Substance | Natural Medicine | Alternative
Allicin | GreenMedInfo | Substance | Natural Medicine | Alternative (greenmedinfo.com)
Unmasking the Janus face of myoglobin in health and disease | Journal of Experimental Biology
Unmasking the Janus face of myoglobin in health and disease | Journal of Experimental Biology (jeb.biologists.org)
Bacopa | GreenMedInfo | Substance | Natural Medicine | Alternative
Bacopa | GreenMedInfo | Substance | Natural Medicine | Alternative (greenmedinfo.com)
Baicalein | GreenMedInfo | Substance | Natural Medicine | Alternative
Baicalein | GreenMedInfo | Substance | Natural Medicine | Alternative (greenmedinfo.com)
Effect of Remote Ischaemic Conditioning on Clinical Outcomes in STEMI Patients Undergoing PPCI (CONDI2/ERIC-PPCI) - Full Text...
Effect of Remote Ischaemic Conditioning on Clinical Outcomes in STEMI Patients Undergoing PPCI (CONDI2/ERIC-PPCI) - Full Text... (clinicaltrials.gov)