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Reperfusion InjuryMyocardial Reperfusion InjuryMyocardiumMyocytes, CardiacApoptosisMyocardial ReperfusionReperfusionIschemiaMyocardial IschemiaIschemic Preconditioning, MyocardialRats, Sprague-DawleyCardiotonic AgentsMitochondria, HeartIn Situ Nick-End LabelingIschemic PreconditioningHeartCaspase 3Ischemic PostconditioningDisease Models, AnimalMyocardial InfarctionRats, WistarBrain IschemiaWounds and InjuriesTime FactorsPeroxidaseProtective AgentsWarm IschemiaMice, Inbred C57BLNecrosisMalondialdehydeOxidative StressL-Lactate DehydrogenaseCreatine KinaseCytoprotectionBrain InjuriesCold IschemiaMice, KnockoutDecanoic AcidsHydroxy AcidsSignal TransductionPerfusionMyocardial ContractionKidneyAcute Kidney InjuryNeutrophil InfiltrationReactive Oxygen SpeciesHemodynamicsLiverCoronary CirculationRandom AllocationTioproninVentricular Function, LeftSuperoxide DismutaseNitric OxideModels, AnimalAntioxidantsEnzyme InhibitorsBlotting, WesternCells, CulturedOrgan PreservationAspartate AminotransferasesOrgan Preservation SolutionsAlanine TransaminaseCardioplegic SolutionsAthletic InjuriesNeuroprotective AgentsConstrictionSpinal Cord InjuriesHeme Oxygenase-1NeutrophilsMitochondrial Membrane Transport ProteinsVentricular PressureHeart Function TestsFree Radical ScavengersRats, Inbred LewRabbitsHeart Arrest, InducedInfarction, Middle Cerebral ArteryImmunohistochemistryTumor Necrosis Factor-alphaProto-Oncogene Proteins c-aktCell DeathProtein Kinase C-epsilonCell SurvivalCaspasesDogsEnzyme ActivationRNA, MessengerAdenosineFree RadicalsProto-Oncogene Proteins c-bcl-2Nitric Oxide Synthase Type IILung InjuryMyocardial StunningSpinal Cord IschemiaKATP ChannelsLiver DiseasesMice, TransgenicArrhythmias, CardiacLiver CirculationDose-Response Relationship, DrugRecovery of FunctionHydrogen SulfideIschemic Attack, TransientPhosphorylationApoptosis Regulatory ProteinsReceptor, Adenosine A3DiazoxideMicrocirculationLipid PeroxidationIntestinesMitochondriaLiver Transplantationbcl-2-Associated X ProteinHeart VentriclesNitric Oxide SynthaseSwineP-SelectinUp-RegulationHeme Oxygenase (Decyclizing)InflammationCoronary VesselsHSP20 Heat-Shock ProteinsNitric Oxide Synthase Type IIIAdenosine TriphosphateHeart RateBlood PressureAcute Lung InjuryAllopurinolInjury Severity ScoreHindlimbAnoxiaGlycogen Synthase Kinase 3OxygenDNA FragmentationIntercellular Adhesion Molecule-1Membrane Potential, MitochondrialKidney TubulesHypothermia, InducedCytochromes cCalciumEndothelium, VascularLeg InjuriesNF-kappa BBiological MarkersGene Expression RegulationCell HypoxiaCardiac OutputRaffinoseReverse Transcriptase Polymerase Chain ReactionPeroxynitrous AcidKidney Tubular Necrosis, AcuteTroponin ITrimetazidineHydrogen PeroxideCardiovascular AgentsPotassium ChannelsSuperoxidesCatalaseAnalysis of VarianceBrainPrimary Graft DysfunctionBenzophenanthridinesCytokinesTreatment OutcomeCerebral InfarctionXanthine OxidaseLeukocytesHepatocytesPhosphatidylinositol 3-KinasesAdenosine A3 Receptor AgonistsDrugs, Chinese HerbalKupffer CellsToll-Like Receptor 4LungEye InjuriesAnimals, NewbornSarcolemmaGlutathioneMesenteric Artery, SuperiorElectrocardiographyCreatininePhenanthridinesGene ExpressionBlood Urea NitrogenAnesthetics, InhalationPhosphocreatineBrain EdemaPoly(ADP-ribose) PolymerasesNitratesSulfonesIsofluraneLigationOxidantsKidney DiseasesInflammation MediatorsGuanidinesHydroxyl RadicalNeck InjuriesReceptors, Purinergic P1Ventricular Remodeling
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.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.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.Myocytes, Cardiac: Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).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.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: 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.Ischemia: A hypoperfusion of the BLOOD through an organ or tissue caused by a PATHOLOGIC CONSTRICTION or obstruction of its BLOOD VESSELS, or an absence of BLOOD CIRCULATION.Myocardial Ischemia: A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (CORONARY ARTERY DISEASE), to obstruction by a thrombus (CORONARY THROMBOSIS), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (MYOCARDIAL INFARCTION).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.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.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).Mitochondria, Heart: The mitochondria of the myocardium.In Situ Nick-End Labeling: An in situ method for detecting areas of DNA which are nicked during APOPTOSIS. Terminal deoxynucleotidyl transferase is used to add labeled dUTP, in a template-independent manner, to the 3 prime OH ends of either single- or double-stranded DNA. The terminal deoxynucleotidyl transferase nick end labeling, or TUNEL, assay labels apoptosis on a single-cell level, making it more sensitive than agarose gel electrophoresis for analysis of DNA FRAGMENTATION.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)Heart: The hollow, muscular organ that maintains the circulation of the blood.Caspase 3: A short pro-domain caspase that plays an effector role in APOPTOSIS. It is activated by INITIATOR CASPASES such as CASPASE 9. Isoforms of this protein exist due to multiple alternative splicing of its MESSENGER RNA.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.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.Myocardial Infarction: NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).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.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.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.Time Factors: Elements of limited time intervals, contributing to particular results or situations.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.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.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.Mice, Inbred C57BLNecrosis: 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.Malondialdehyde: The dialdehyde of malonic acid.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.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.Cytoprotection: The process by which chemical compounds provide protection to cells against harmful agents.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.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.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.Decanoic Acids: 10-carbon saturated monocarboxylic acids.Hydroxy Acids: Organic compounds containing both the hydroxyl and carboxyl radicals.Signal Transduction: The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.Perfusion: Treatment process involving the injection of fluid into an organ or tissue.Myocardial Contraction: Contractile activity of the MYOCARDIUM.Kidney: Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.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.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.Reactive Oxygen Species: Molecules or ions formed by the incomplete one-electron reduction of oxygen. These reactive oxygen intermediates include SINGLET OXYGEN; SUPEROXIDES; PEROXIDES; HYDROXYL RADICAL; and HYPOCHLOROUS ACID. They contribute to the microbicidal activity of PHAGOCYTES, regulation of signal transduction and gene expression, and the oxidative damage to NUCLEIC ACIDS; PROTEINS; and LIPIDS.Hemodynamics: The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.Coronary Circulation: The circulation of blood through the CORONARY VESSELS of the HEART.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.Tiopronin: Sulfhydryl acylated derivative of GLYCINE.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.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.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.Models, Animal: Non-human animals, selected because of specific characteristics, for use in experimental research, teaching, or testing.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.Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.Blotting, Western: Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.Cells, Cultured: Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.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).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.Organ Preservation Solutions: Solutions used to store organs and minimize tissue damage, particularly while awaiting implantation.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.Cardioplegic Solutions: Solutions which, upon administration, will temporarily arrest cardiac activity. They are used in the performance of heart surgery.Athletic Injuries: Injuries incurred during participation in competitive or non-competitive sports.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.Spinal Cord Injuries: Penetrating and non-penetrating injuries to the spinal cord resulting from traumatic external forces (e.g., WOUNDS, GUNSHOT; WHIPLASH INJURIES; etc.).Heme Oxygenase-1: A ubiquitous stress-responsive enzyme that catalyzes the oxidative cleavage of HEME to yield IRON; CARBON MONOXIDE; and BILIVERDIN.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.Mitochondrial Membrane Transport Proteins: Proteins involved in the transport of specific substances across the membranes of the MITOCHONDRIA.Ventricular Pressure: The pressure within a CARDIAC VENTRICLE. Ventricular pressure waveforms can be measured in the beating heart by catheterization or estimated using imaging techniques (e.g., DOPPLER ECHOCARDIOGRAPHY). The information is useful in evaluating the function of the MYOCARDIUM; CARDIAC VALVES; and PERICARDIUM, particularly with simultaneous measurement of other (e.g., aortic or atrial) pressures.Heart Function Tests: Examinations used to diagnose and treat heart conditions.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.Rats, Inbred LewRabbits: 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.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).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.Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.Tumor Necrosis Factor-alpha: Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.Proto-Oncogene Proteins c-akt: A protein-serine-threonine kinase that is activated by PHOSPHORYLATION in response to GROWTH FACTORS or INSULIN. It plays a major role in cell metabolism, growth, and survival as a core component of SIGNAL TRANSDUCTION. Three isoforms have been described in mammalian cells.Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.Protein Kinase C-epsilon: A protein kinase C subtype that was originally characterized as a CALCIUM-independent, serine-threonine kinase that is activated by PHORBOL ESTERS and DIACYLGLYCEROLS. It is targeted to specific cellular compartments in response to extracellular signals that activate G-PROTEIN-COUPLED RECEPTORS; TYROSINE KINASE RECEPTORS; and intracellular protein tyrosine kinase.Cell Survival: The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.Caspases: A family of intracellular CYSTEINE ENDOPEPTIDASES that play a role in regulating INFLAMMATION and APOPTOSIS. They specifically cleave peptides at a CYSTEINE amino acid that follows an ASPARTIC ACID residue. Caspases are activated by proteolytic cleavage of a precursor form to yield large and small subunits that form the enzyme. Since the cleavage site within precursors matches the specificity of caspases, sequential activation of precursors by activated caspases can occur.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)Enzyme Activation: Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.RNA, Messenger: RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.Adenosine: A nucleoside that is composed of ADENINE and D-RIBOSE. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter.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.Proto-Oncogene Proteins c-bcl-2: Membrane proteins encoded by the BCL-2 GENES and serving as potent inhibitors of cell death by APOPTOSIS. The proteins are found on mitochondrial, microsomal, and NUCLEAR MEMBRANE sites within many cell types. Overexpression of bcl-2 proteins, due to a translocation of the gene, is associated with follicular lymphoma.Nitric Oxide Synthase Type II: A CALCIUM-independent subtype of nitric oxide synthase that may play a role in immune function. It is an inducible enzyme whose expression is transcriptionally regulated by a variety of CYTOKINES.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.Myocardial Stunning: Prolonged dysfunction of the myocardium after a brief episode of severe ischemia, with gradual return of contractile activity.Spinal Cord Ischemia: Reduced blood flow to the spinal cord which is supplied by the anterior spinal artery and the paired posterior spinal arteries. This condition may be associated with ARTERIOSCLEROSIS, trauma, emboli, diseases of the aorta, and other disorders. Prolonged ischemia may lead to INFARCTION of spinal cord tissue.KATP Channels: Heteromultimers of Kir6 channels (the pore portion) and sulfonylurea receptor (the regulatory portion) which affect function of the HEART; PANCREATIC BETA CELLS; and KIDNEY COLLECTING DUCTS. KATP channel blockers include GLIBENCLAMIDE and mitiglinide whereas openers include CROMAKALIM and minoxidil sulfate.Liver Diseases: Pathological processes of the LIVER.Mice, Transgenic: Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.Arrhythmias, Cardiac: Any disturbances of the normal rhythmic beating of the heart or MYOCARDIAL CONTRACTION. Cardiac arrhythmias can be classified by the abnormalities in HEART RATE, disorders of electrical impulse generation, or impulse conduction.Liver Circulation: The circulation of BLOOD through the LIVER.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Recovery of Function: A partial or complete return to the normal or proper physiologic activity of an organ or part following disease or trauma.Hydrogen Sulfide: A flammable, poisonous gas with a characteristic odor of rotten eggs. It is used in the manufacture of chemicals, in metallurgy, and as an analytical reagent. (From Merck Index, 11th ed)Ischemic Attack, Transient: Brief reversible episodes of focal, nonconvulsive ischemic dysfunction of the brain having a duration of less than 24 hours, and usually less than one hour, caused by transient thrombotic or embolic blood vessel occlusion or stenosis. Events may be classified by arterial distribution, temporal pattern, or etiology (e.g., embolic vs. thrombotic). (From Adams et al., Principles of Neurology, 6th ed, pp814-6)Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.Apoptosis Regulatory Proteins: A large group of proteins that control APOPTOSIS. This family of proteins includes many ONCOGENE PROTEINS as well as a wide variety of classes of INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS such as CASPASES.Receptor, Adenosine A3: A subtype of ADENOSINE RECEPTOR that is found expressed in a variety of locations including the BRAIN and endocrine tissues. The receptor is generally considered to be coupled to the GI, INHIBITORY G-PROTEIN which causes down regulation of CYCLIC AMP.Diazoxide: A benzothiadiazine derivative that is a peripheral vasodilator used for hypertensive emergencies. It lacks diuretic effect, apparently because it lacks a sulfonamide group.Microcirculation: The circulation of the BLOOD through the MICROVASCULAR NETWORK.Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor.Intestines: The section of the alimentary canal from the STOMACH to the ANAL CANAL. It includes the LARGE INTESTINE and SMALL INTESTINE.Mitochondria: Semiautonomous, self-reproducing organelles that occur in the cytoplasm of all cells of most, but not all, eukaryotes. Each mitochondrion is surrounded by a double limiting membrane. The inner membrane is highly invaginated, and its projections are called cristae. Mitochondria are the sites of the reactions of oxidative phosphorylation, which result in the formation of ATP. They contain distinctive RIBOSOMES, transfer RNAs (RNA, TRANSFER); AMINO ACYL T RNA SYNTHETASES; and elongation and termination factors. Mitochondria depend upon genes within the nucleus of the cells in which they reside for many essential messenger RNAs (RNA, MESSENGER). Mitochondria are believed to have arisen from aerobic bacteria that established a symbiotic relationship with primitive protoeukaryotes. (King & Stansfield, A Dictionary of Genetics, 4th ed)Liver Transplantation: The transference of a part of or an entire liver from one human or animal to another.bcl-2-Associated X Protein: A member of the Bcl-2 protein family and homologous partner of C-BCL-2 PROTO-ONCOGENE PROTEIN. It regulates the release of CYTOCHROME C and APOPTOSIS INDUCING FACTOR from the MITOCHONDRIA. Several isoforms of BCL2-associated X protein occur due to ALTERNATIVE SPLICING of the mRNA for this protein.Heart Ventricles: The lower right and left chambers of the heart. The right ventricle pumps venous BLOOD into the LUNGS and the left ventricle pumps oxygenated blood into the systemic arterial circulation.Nitric Oxide Synthase: An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.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).P-Selectin: Cell adhesion molecule and CD antigen that mediates the adhesion of neutrophils and monocytes to activated platelets and endothelial cells.Up-Regulation: A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.Heme Oxygenase (Decyclizing): A mixed function oxidase enzyme which during hemoglobin catabolism catalyzes the degradation of heme to ferrous iron, carbon monoxide and biliverdin in the presence of molecular oxygen and reduced NADPH. The enzyme is induced by metals, particularly cobalt. EC 1.14.99.3.Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.Coronary Vessels: The veins and arteries of the HEART.HSP20 Heat-Shock Proteins: A subfamily of small heat-shock proteins that are closely related to ALPHA B-CRYSTALLIN. Hsp20 heat-shock proteins can undergo PHOSPHORYLATION by CYCLIC GMP-DEPENDENT PROTEIN KINASES.Nitric Oxide Synthase Type III: A CALCIUM-dependent, constitutively-expressed form of nitric oxide synthase found primarily in ENDOTHELIAL CELLS.Adenosine Triphosphate: An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter.Heart Rate: The number of times the HEART VENTRICLES contract per unit of time, usually per minute.Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.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).Allopurinol: A XANTHINE OXIDASE inhibitor that decreases URIC ACID production. It also acts as an antimetabolite on some simpler organisms.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.Hindlimb: Either of two extremities of four-footed non-primate land animals. It usually consists of a FEMUR; TIBIA; and FIBULA; tarsals; METATARSALS; and TOES. (From Storer et al., General Zoology, 6th ed, p73)Anoxia: Relatively complete absence of oxygen in one or more tissues.Glycogen Synthase Kinase 3: A glycogen synthase kinase that was originally described as a key enzyme involved in glycogen metabolism. It regulates a diverse array of functions such as CELL DIVISION, microtubule function and APOPTOSIS.Oxygen: An element with atomic symbol O, atomic number 8, and atomic weight [15.99903; 15.99977]. It is the most abundant element on earth and essential for respiration.DNA Fragmentation: Splitting the DNA into shorter pieces by endonucleolytic DNA CLEAVAGE at multiple sites. It includes the internucleosomal DNA fragmentation, which along with chromatin condensation, are considered to be the hallmarks of APOPTOSIS.Intercellular Adhesion Molecule-1: A cell-surface ligand involved in leukocyte adhesion and inflammation. Its production is induced by gamma-interferon and it is required for neutrophil migration into inflamed tissue.Membrane Potential, Mitochondrial: The voltage difference, normally maintained at approximately -180mV, across the INNER MITOCHONDRIAL MEMBRANE, by a net movement of positive charge across the membrane. It is a major component of the PROTON MOTIVE FORCE in MITOCHONDRIA used to drive the synthesis of ATP.Kidney Tubules: Long convoluted tubules in the nephrons. They collect filtrate from blood passing through the KIDNEY GLOMERULUS and process this filtrate into URINE. Each renal tubule consists of a BOWMAN CAPSULE; PROXIMAL KIDNEY TUBULE; LOOP OF HENLE; DISTAL KIDNEY TUBULE; and KIDNEY COLLECTING DUCT leading to the central cavity of the kidney (KIDNEY PELVIS) that connects to the URETER.Hypothermia, Induced: Abnormally low BODY TEMPERATURE that is intentionally induced in warm-blooded animals by artificial means. In humans, mild or moderate hypothermia has been used to reduce tissue damages, particularly after cardiac or spinal cord injuries and during subsequent surgeries.Cytochromes c: Cytochromes of the c type that are found in eukaryotic MITOCHONDRIA. They serve as redox intermediates that accept electrons from MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX III and transfer them to MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX IV.Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.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.Leg Injuries: General or unspecified injuries involving the leg.NF-kappa B: Ubiquitous, inducible, nuclear transcriptional activator that binds to enhancer elements in many different cell types and is activated by pathogenic stimuli. The NF-kappa B complex is a heterodimer composed of two DNA-binding subunits: NF-kappa B1 and relA.Biological Markers: Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.Gene Expression Regulation: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.Cell Hypoxia: A condition of decreased oxygen content at the cellular level.Cardiac Output: The volume of BLOOD passing through the HEART per unit of time. It is usually expressed as liters (volume) per minute so as not to be confused with STROKE VOLUME (volume per beat).Raffinose: A trisaccharide occurring in Australian manna (from Eucalyptus spp, Myrtaceae) and in cottonseed meal.Reverse Transcriptase Polymerase Chain Reaction: A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.Peroxynitrous Acid: A potent oxidant synthesized by the cell during its normal metabolism. Peroxynitrite is formed from the reaction of two free radicals, NITRIC OXIDE and the superoxide anion (SUPEROXIDES).Kidney Tubular Necrosis, Acute: Acute kidney failure resulting from destruction of EPITHELIAL CELLS of the KIDNEY TUBULES. It is commonly attributed to exposure to toxic agents or renal ISCHEMIA following severe TRAUMA.Troponin I: One of the three polypeptide chains that make up the TROPONIN complex. It inhibits F-actin-myosin interactions.Trimetazidine: A vasodilator used in angina of effort or ischemic heart disease.Hydrogen Peroxide: A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials.Cardiovascular Agents: Agents that affect the rate or intensity of cardiac contraction, blood vessel diameter, or blood volume.Potassium Channels: Cell membrane glycoproteins that are selectively permeable to potassium ions. At least eight major groups of K channels exist and they are made up of dozens of different subunits.Superoxides: Highly reactive compounds produced when oxygen is reduced by a single electron. In biological systems, they may be generated during the normal catalytic function of a number of enzymes and during the oxidation of hemoglobin to METHEMOGLOBIN. In living organisms, SUPEROXIDE DISMUTASE protects the cell from the deleterious effects of superoxides.Catalase: An oxidoreductase that catalyzes the conversion of HYDROGEN PEROXIDE to water and oxygen. It is present in many animal cells. A deficiency of this enzyme results in ACATALASIA.Analysis of Variance: A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.Brain: The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.Primary Graft Dysfunction: A form of ischemia-reperfusion injury occurring in the early period following transplantation. Significant pathophysiological changes in MITOCHONDRIA are the main cause of the dysfunction. It is most often seen in the transplanted lung, liver, or kidney and can lead to GRAFT REJECTION.Benzophenanthridines: Compounds of four rings containing a nitrogen. They are biosynthesized from reticuline via rearrangement of scoulerine. They are similar to BENZYLISOQUINOLINES. Members include chelerythrine and sanguinarine.Cytokines: Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.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.Cerebral Infarction: The formation of an area of NECROSIS in the CEREBRUM caused by an insufficiency of arterial or venous blood flow. Infarcts of the cerebrum are generally classified by hemisphere (i.e., left vs. right), lobe (e.g., frontal lobe infarction), arterial distribution (e.g., INFARCTION, ANTERIOR CEREBRAL ARTERY), and etiology (e.g., embolic infarction).Xanthine Oxidase: An iron-molybdenum flavoprotein containing FLAVIN-ADENINE DINUCLEOTIDE that oxidizes hypoxanthine, some other purines and pterins, and aldehydes. Deficiency of the enzyme, an autosomal recessive trait, causes xanthinuria.Leukocytes: White blood cells. These include granular leukocytes (BASOPHILS; EOSINOPHILS; and NEUTROPHILS) as well as non-granular leukocytes (LYMPHOCYTES and MONOCYTES).Hepatocytes: The main structural component of the LIVER. They are specialized EPITHELIAL CELLS that are organized into interconnected plates called lobules.Phosphatidylinositol 3-Kinases: Phosphotransferases that catalyzes the conversion of 1-phosphatidylinositol to 1-phosphatidylinositol 3-phosphate. Many members of this enzyme class are involved in RECEPTOR MEDIATED SIGNAL TRANSDUCTION and regulation of vesicular transport with the cell. Phosphatidylinositol 3-Kinases have been classified both according to their substrate specificity and their mode of action within the cell.Adenosine A3 Receptor Agonists: Drugs that selectively bind to and activate ADENOSINE A3 RECEPTORS.Drugs, Chinese Herbal: Chinese herbal or plant extracts which are used as drugs to treat diseases or promote general well-being. The concept does not include synthesized compounds manufactured in China.Kupffer Cells: Specialized phagocytic cells of the MONONUCLEAR PHAGOCYTE SYSTEM found on the luminal surface of the hepatic sinusoids. They filter bacteria and small foreign proteins out of the blood, and dispose of worn out red blood cells.Toll-Like Receptor 4: A pattern recognition receptor that interacts with LYMPHOCYTE ANTIGEN 96 and LIPOPOLYSACCHARIDES. It mediates cellular responses to GRAM-NEGATIVE BACTERIA.Lung: Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.Eye Injuries: Damage or trauma inflicted to the eye by external means. The concept includes both surface injuries and intraocular injuries.Animals, Newborn: Refers to animals in the period of time just after birth.Sarcolemma: The excitable plasma membrane of a muscle cell. (Glick, Glossary of Biochemistry and Molecular Biology, 1990)Glutathione: A tripeptide with many roles in cells. It conjugates to drugs to make them more soluble for excretion, is a cofactor for some enzymes, is involved in protein disulfide bond rearrangement and reduces peroxides.Mesenteric Artery, Superior: A large vessel supplying the whole length of the small intestine except the superior part of the duodenum. It also supplies the cecum and the ascending part of the colon and about half the transverse part of the colon. It arises from the anterior surface of the aorta below the celiac artery at the level of the first lumbar vertebra.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.CreatininePhenanthridinesGene Expression: The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.Blood Urea Nitrogen: The urea concentration of the blood stated in terms of nitrogen content. Serum (plasma) urea nitrogen is approximately 12% higher than blood urea nitrogen concentration because of the greater protein content of red blood cells. Increases in blood or serum urea nitrogen are referred to as azotemia and may have prerenal, renal, or postrenal causes. (From Saunders Dictionary & Encyclopedia of Laboratory Medicine and Technology, 1984)Anesthetics, Inhalation: Gases or volatile liquids that vary in the rate at which they induce anesthesia; potency; the degree of circulation, respiratory, or neuromuscular depression they produce; and analgesic effects. Inhalation anesthetics have advantages over intravenous agents in that the depth of anesthesia can be changed rapidly by altering the inhaled concentration. Because of their rapid elimination, any postoperative respiratory depression is of relatively short duration. (From AMA Drug Evaluations Annual, 1994, p173)Phosphocreatine: An endogenous substance found mainly in skeletal muscle of vertebrates. It has been tried in the treatment of cardiac disorders and has been added to cardioplegic solutions. (Reynolds JEF(Ed): Martindale: The Extra Pharmacopoeia (electronic version). Micromedex, Inc, Englewood, CO, 1996)Brain Edema: Increased intracellular or extracellular fluid in brain tissue. Cytotoxic brain edema (swelling due to increased intracellular fluid) is indicative of a disturbance in cell metabolism, and is commonly associated with hypoxic or ischemic injuries (see HYPOXIA, BRAIN). An increase in extracellular fluid may be caused by increased brain capillary permeability (vasogenic edema), an osmotic gradient, local blockages in interstitial fluid pathways, or by obstruction of CSF flow (e.g., obstructive HYDROCEPHALUS). (From Childs Nerv Syst 1992 Sep; 8(6):301-6)Poly(ADP-ribose) Polymerases: Enzymes that catalyze the transfer of multiple ADP-RIBOSE groups from nicotinamide-adenine dinucleotide (NAD) onto protein targets, thus building up a linear or branched homopolymer of repeating ADP-ribose units i.e., POLY ADENOSINE DIPHOSPHATE RIBOSE.Nitrates: Inorganic or organic salts and esters of nitric acid. These compounds contain the NO3- radical.SulfonesIsoflurane: A stable, non-explosive inhalation anesthetic, relatively free from significant side effects.Ligation: Application of a ligature to tie a vessel or strangulate a part.Oxidants: Electron-accepting molecules in chemical reactions in which electrons are transferred from one molecule to another (OXIDATION-REDUCTION).Kidney Diseases: Pathological processes of the KIDNEY or its component tissues.Inflammation Mediators: The endogenous compounds that mediate inflammation (AUTACOIDS) and related exogenous compounds including the synthetic prostaglandins (PROSTAGLANDINS, SYNTHETIC).Guanidines: A family of iminourea derivatives. The parent compound has been isolated from mushrooms, corn germ, rice hulls, mussels, earthworms, and turnip juice. Derivatives may have antiviral and antifungal properties.Hydroxyl Radical: The univalent radical OH. Hydroxyl radical is a potent oxidizing agent.Neck Injuries: General or unspecified injuries to the neck. It includes injuries to the skin, muscles, and other soft tissues of the neck.Receptors, Purinergic P1: A class of cell surface receptors that prefer ADENOSINE to other endogenous PURINES. Purinergic P1 receptors are widespread in the body including the cardiovascular, respiratory, immune, and nervous systems. There are at least two pharmacologically distinguishable types (A1 and A2, or Ri and Ra).Ventricular Remodeling: The geometric and structural changes that the HEART VENTRICLES undergo, usually following MYOCARDIAL INFARCTION. It comprises expansion of the infarct and dilatation of the healthy ventricle segments. While most prevalent in the left ventricle, it can also occur in the right ventricle.
AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesDisciplines and OccupationsInformation ScienceHealth Care
Reperfusion InjuryMyocardial Reperfusion InjuryMyocardiumMyocytes, CardiacApoptosisMyocardial ReperfusionReperfusionIschemiaMyocardial IschemiaIschemic Preconditioning, MyocardialRats, Sprague-DawleyCardiotonic AgentsMitochondria, HeartIn Situ Nick-End LabelingIschemic PreconditioningHeartCaspase 3Ischemic PostconditioningDisease Models, AnimalMyocardial InfarctionRats, WistarBrain IschemiaWounds and InjuriesTime FactorsPeroxidaseProtective AgentsWarm IschemiaMice, Inbred C57BLNecrosisMalondialdehydeOxidative StressL-Lactate DehydrogenaseCreatine KinaseCytoprotectionBrain InjuriesCold IschemiaMice, KnockoutDecanoic AcidsHydroxy AcidsSignal TransductionPerfusionMyocardial ContractionKidneyAcute Kidney InjuryNeutrophil InfiltrationReactive Oxygen SpeciesHemodynamicsLiverCoronary CirculationRandom AllocationTioproninVentricular Function, LeftSuperoxide DismutaseNitric OxideModels, AnimalAntioxidantsEnzyme InhibitorsBlotting, WesternCells, CulturedOrgan PreservationAspartate AminotransferasesOrgan Preservation SolutionsAlanine TransaminaseCardioplegic SolutionsAthletic InjuriesNeuroprotective AgentsConstrictionSpinal Cord InjuriesHeme Oxygenase-1NeutrophilsMitochondrial Membrane Transport ProteinsVentricular PressureHeart Function TestsFree Radical ScavengersRats, Inbred LewRabbitsHeart Arrest, InducedInfarction, Middle Cerebral ArteryImmunohistochemistryTumor Necrosis Factor-alphaProto-Oncogene Proteins c-aktCell DeathProtein Kinase C-epsilonCell SurvivalCaspasesDogsEnzyme ActivationRNA, MessengerAdenosineFree RadicalsProto-Oncogene Proteins c-bcl-2Nitric Oxide Synthase Type IILung InjuryMyocardial StunningSpinal Cord IschemiaKATP ChannelsLiver DiseasesMice, TransgenicArrhythmias, CardiacLiver CirculationDose-Response Relationship, DrugRecovery of FunctionHydrogen SulfideIschemic Attack, TransientPhosphorylationApoptosis Regulatory ProteinsReceptor, Adenosine A3DiazoxideMicrocirculationLipid PeroxidationIntestinesMitochondriaLiver Transplantationbcl-2-Associated X ProteinHeart VentriclesNitric Oxide SynthaseSwineP-SelectinUp-RegulationHeme Oxygenase (Decyclizing)InflammationCoronary VesselsHSP20 Heat-Shock ProteinsNitric Oxide Synthase Type IIIAdenosine TriphosphateHeart RateBlood PressureAcute Lung InjuryAllopurinolInjury Severity ScoreHindlimbAnoxiaGlycogen Synthase Kinase 3OxygenDNA FragmentationIntercellular Adhesion Molecule-1Membrane Potential, MitochondrialKidney TubulesHypothermia, InducedCytochromes cCalciumEndothelium, VascularLeg InjuriesNF-kappa BBiological MarkersGene Expression RegulationCell HypoxiaCardiac OutputRaffinoseReverse Transcriptase Polymerase Chain ReactionPeroxynitrous AcidKidney Tubular Necrosis, AcuteTroponin ITrimetazidineHydrogen PeroxideCardiovascular AgentsPotassium ChannelsSuperoxidesCatalaseAnalysis of VarianceBrainPrimary Graft DysfunctionBenzophenanthridinesCytokinesTreatment OutcomeCerebral InfarctionXanthine OxidaseLeukocytesHepatocytesPhosphatidylinositol 3-KinasesAdenosine A3 Receptor AgonistsDrugs, Chinese HerbalKupffer CellsToll-Like Receptor 4LungEye InjuriesAnimals, NewbornSarcolemmaGlutathioneMesenteric Artery, SuperiorElectrocardiographyCreatininePhenanthridinesGene ExpressionBlood Urea NitrogenAnesthetics, InhalationPhosphocreatineBrain EdemaPoly(ADP-ribose) PolymerasesNitratesSulfonesIsofluraneLigationOxidantsKidney DiseasesInflammation MediatorsGuanidinesHydroxyl RadicalNeck InjuriesReceptors, Purinergic P1Ventricular Remodeling
PRKCEPRKCE
JM Downey was the first to introduce the role of PKC in cardioprotection against ischemia-reperfusion injury in 1994,; this ... "Partial replacement of cardiac troponin I with a non-phosphorylatable mutant at serines 43/45 attenuates the contractile ... This kinase has been shown to be involved in many different cellular functions, such as apoptosis, cardioprotection from ... Yang FH, Pyle WG (Mar 2012). "Reduced cardiac CapZ protein protects hearts against acute ischemia-reperfusion injury and ...
ATP-sensitive potassium channelATP-sensitive potassium channel
Cardiac ischemia, as it slows the oxidation of fatty acids, causes an accumulation of acyl-CoA and induces KATP channel opening ... Similarly, 60 minutes of ischemia followed by 24 to 72 hours of reperfusion leads to an increase in kir6.2 transcription in ... "Mitochondrial ATP-sensitive potassium channels inhibit apoptosis induced by oxidative stress in cardiac cells". Circ. Res. 88 ( ... in mice has been shown to increase the basal level of injury compared to wild type mice. This baseline protection is believed ...
Reperfusion injuryReperfusion injury
... also protects against hepatic ischemia/reperfusion injury by attenuating inflammatory signaling and response of oxidative and ... studies published in the Journal of Cardiovascular Pharmacology suggest that Metformin may prevent cardiac reperfusion injury ... Such reactive species may also act indirectly in redox signaling to turn on apoptosis. White blood cells may also bind to the ... Permeability Transition Pore Opening as an Endpoint to Initiate Cell Death and as a Putative Target for Cardioprotection". Cell ...
MitoQMitoQ
Targeting an antioxidant to mitochondria decreases cardiac ischemia-reperfusion injury, Faseb J, 19 (2005) 1088-1095. G.S. ... Mitochondria-targeted antioxidant MitoQ10 improves endothelial function and attenuates cardiac hypertrophy, Hypertension, 54 ( ... cardioprotection by Mito-Q, Biophys J, 96 (2009) 1388-1398. A. Vergeade, P. Mulder, C. Vendeville-Dehaudt, F. Estour, D. Fortin ... to many other aspects of metabolism and cell death in pathology and disease as they regulate programmed cell death or apoptosis ...
Reperfusion injuryReperfusion injury
... or reperfusion insult, sometimes called ischemia-reperfusion injury (IRI) or reoxygenation injury, is the tissue damage caused when blood supply returns to tissue (re- + perfusion) after a period of ischemia or lack of oxygen (anoxia or hypoxia). The absence of oxygen and nutrients from blood during the ischemic period creates a condition in which the restoration of circulation results in inflammation and oxidative damage through the induction of oxidative stress rather than (or along with) restoration of normal function. Reperfusion of ischemic tissues is often associated with microvascular injury, particularly due to increased permeability of capillaries and arterioles that lead to an increase of diffusion and fluid filtration across the tissues. Activated endothelial ...
SOD1SOD1
Most notably, SOD1 is pivotal in reactive oxygen species (ROS) release during oxidative stress by ischemia-reperfusion injury, specifically in the myocardium as part of a heart attack (also known as ischemic heart disease). Ischemic heart disease, which results from an occlusion of one of the major coronary arteries, is currently still the leading cause of morbidity and mortality in western society.[11][12] During ischemia reperfusion, ROS release substantially contribute to the cell damage and death via a direct effect on the cell as well as via apoptotic signals. SOD1 is known to have a capacity to limit the detrimental effects of ROS. As such, SOD1 is important for its cardioprotective effects.[13] In addition, SOD1 has been implicated in cardioprotection against ischemia-reperfusion ...
SulodexideSulodexide
3.0.CO;2-4. PMID 9436179. Lauver DA, Booth EA, White AJ, Poradosu E, Lucchesi BR (2005). "Sulodexide attenuates myocardial ischemia/reperfusion injury and the deposition of C-reactive protein in areas of infarction without affecting hemostasis". J Pharmacol Exp Ther. 312 (2): 794-800. doi:10.1124/jpet.104.075283. PMID 15365091. Achour A, Kacem M, Dibej K, Skhiri H, Bouraoui S, El May M (2005). "One year course of oral sulodexide in the management of diabetic nephropathy". J Nephrol. 18 (5): 568-574. PMID 16299683. Gambaro G, Venturini AP, Noonan DM, et al. (1994). "Treatment with a glycosaminoglycan formulation ameliorates experimental diabetic nephropathy". Kidney Int. 46 (3): 797-806. doi:10.1038/ki.1994.335. PMID 7527876. Škrha J, Perušičová J, Pont'uch P, Okša A, et al. (1997). "Treatment with a glycosaminoglycan formulation ameliorates experimental diabetic nephropathy". Diabetes Res Clin Practice. 38 ...
Ischemia, le encyclopedia libereIschemia, le encyclopedia libere
Ischemia or ischaemia is a restriction in blood supply to tissues, causing a shortage of oxygen that is needed for cellular metabolism (to keep tissue alive).[3] Ischemia is generally caused by problems with blood vessels, with resultant damage to or dysfunction of tissue. It also means local anemia in a given part of a body sometimes resulting from congestion (such as vasoconstriction, thrombosis or embolism). Ischemia comprises not only insufficiency of oxygen, but also reduced availability of nutrients and inadequate removal of metabolic wastes. Ischemia can be partial (poor perfusion) or total. Contents [show] Signs and symptoms[edit] Since oxygen is carried to tissues in the blood, insufficient blood supply causes tissue to become starved of oxygen. In the highly metabolically active tissues of the heart and brain, irreversible damage to tissues can occur in as little as 3-4 minutes at body temperature. The kidneys are also quickly ...
IschemiaIschemia
... or ischaemia is a restriction in blood supply to tissues, causing a shortage of oxygen and needed for cellular metabolism (to keep tissue alive). Ischemia is generally caused by problems with blood vessels, with resultant damage to or dysfunction of tissue. It also means local anemia in a given part of a body sometimes resulting from congestion (such as vasoconstriction, thrombosis or embolism). Ischemia comprises not only insufficiency of oxygen, but also reduced availability of nutrients and inadequate removal of metabolic wastes. Ischemia can be partial (poor perfusion) or total. Play media Since oxygen is carried to tissues in the blood, insufficient blood supply causes tissue to become starved of oxygen. In the highly metabolically active tissues of the heart and brain, irreversible damage to tissues can occur in as little as 3-4 minutes at body temperature. The kidneys are also quickly damaged by loss of blood flow (renal ...
EIF2A - ويكيبيديا، الموسوعة الحرةEIF2A - ويكيبيديا، الموسوعة الحرة
Page AB، Owen CR، Kumar R، Miller JM، Rafols JA، White BC، DeGracia DJ، Krause GS (Jul 2003). "Persistent eIF2alpha(P) is colocalized with cytoplasmic cytochrome c in vulnerable hippocampal neurons after 4 hours of reperfusion following 10-minute complete brain ischemia". Acta Neuropathologica. 106 (1): 8-16. PMID 12687390. doi:10.1007/s00401-003-0693-2. الوسيط ...
InjuryInjury
In 2013, 4.8 million people world-wide died from injuries, up from 4.3 million in 1990.[2] More than 30% of these deaths were transport-related injuries.[2] In 2013, 367,000 children under the age of five died from injuries, down from 766,000 in 1990.[2] Injuries are the cause of 9% of all deaths, and are the sixth-leading cause of death in the world.[3][4]. ...
InjuryInjury
In 2013, 4.8 million people world-wide died from injuries, up from 4.3 million in 1990.[2] More than 30% of these deaths were transport-related injuries.[2] In 2013, 367,000 children under the age of five died from injuries, down from 766,000 in 1990.[2] Injuries are the cause of 9% of all deaths, and are the sixth-leading cause of death in the world.[3][4]. ...
InjuryInjury
In 2013, 4.8 million people world-wide died from injuries, up from 4.3 million in 1990.[2] More than 30% of these deaths were transport-related injuries.[2] In 2013, 367,000 children under the age of five died from injuries, down from 766,000 in 1990.[2] Injuries are the cause of 9% of all deaths, and are the sixth-leading cause of death in the world.[3][4]. ...
Reperfusion injuryReperfusion injury
... or reperfusion insult, sometimes called ischemia-reperfusion injury (IRI) or reoxygenation injury, is the tissue damage caused when blood supply returns to tissue (re- + perfusion) after a period of ischemia or lack of oxygen (anoxia or hypoxia). The absence of oxygen and nutrients from blood during the ischemic period creates a condition in which the restoration of circulation results in inflammation and oxidative damage through the induction of oxidative stress rather than (or along with) restoration of normal function. Reperfusion of ischemic tissues is often associated with microvascular injury, particularly due to increased permeability of capillaries and arterioles that lead to an increase of diffusion and fluid filtration across the tissues. Activated endothelial ...
SulodexideSulodexide
3.0.CO;2-4. PMID 9436179. Lauver DA, Booth EA, White AJ, Poradosu E, Lucchesi BR (2005). "Sulodexide attenuates myocardial ischemia/reperfusion injury and the deposition of C-reactive protein in areas of infarction without affecting hemostasis". J Pharmacol Exp Ther. 312 (2): 794-800. doi:10.1124/jpet.104.075283. PMID 15365091. Achour A, Kacem M, Dibej K, Skhiri H, Bouraoui S, El May M (2005). "One year course of oral sulodexide in the management of diabetic nephropathy". J Nephrol. 18 (5): 568-574. PMID 16299683. Gambaro G, Venturini AP, Noonan DM, et al. (1994). "Treatment with a glycosaminoglycan formulation ameliorates experimental diabetic nephropathy". Kidney Int. 46 (3): 797-806. doi:10.1038/ki.1994.335. PMID 7527876. Škrha J, Perušičová J, Pont'uch P, Okša A, et al. (1997). "Treatment with a glycosaminoglycan formulation ameliorates experimental diabetic nephropathy". Diabetes Res Clin Practice. 38 ...
CardioprotectionCardioprotection
... encompasses several regimens that have shown to preserve function and viability of cardiac muscle cell tissue subjected to ischemic insult or reoxygenation. Cardioprotection includes strategies that are implemented before an ischemic event (preconditioning, PC), during an ischemic event (perconditioning, PerC) and after the event and during reperfusion (postconditioning, PostC). These strategies can be further stratified by performing the intervention locally or remotely, creating classes of conditioning known as remote ischemic PC (RIPC), remote ischemic PostC and remost ischemic PerC. Classical (local) preconditioning has an early phase with an immediate onset lasting 2-3 hours that protects against myocardial infarction. The early phase involves post-translational modification of preexisting proteins, brought about by the activation of G protein-coupled receptors as well as downstream MAPK's and PI3/Akt. These signaling events act on ...
Siôr, Tywysog Denmarc - WicipediaSiôr, Tywysog Denmarc - Wicipedia
Milwr a phriod Anne, brenhines Prydain Fawr oedd Siôr, Tywysog Denmarc (2 Ebrill 1653 - 28 Hydref 1708). Cafodd ei eni yng Nghopenhagen, mab Frederic III, brenin Denmarc. Priododd y tywysoges Anne y 28 Gorffennaf 1683. ...
AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesDisciplines and OccupationsInformation ScienceHealth Care
Reperfusion InjuryMyocardial Reperfusion InjuryMyocardiumMyocytes, CardiacApoptosisMyocardial ReperfusionReperfusionIschemiaMyocardial IschemiaIschemic Preconditioning, MyocardialRats, Sprague-DawleyCardiotonic AgentsMitochondria, HeartIn Situ Nick-End LabelingIschemic PreconditioningHeartCaspase 3Ischemic PostconditioningDisease Models, AnimalMyocardial InfarctionRats, WistarBrain IschemiaWounds and InjuriesTime FactorsPeroxidaseProtective AgentsWarm IschemiaMice, Inbred C57BLNecrosisMalondialdehydeOxidative StressL-Lactate DehydrogenaseCreatine KinaseCytoprotectionBrain InjuriesCold IschemiaMice, KnockoutDecanoic AcidsHydroxy AcidsSignal TransductionPerfusionMyocardial ContractionKidneyAcute Kidney InjuryNeutrophil InfiltrationReactive Oxygen SpeciesHemodynamicsLiverCoronary CirculationRandom AllocationTioproninVentricular Function, LeftSuperoxide DismutaseNitric OxideModels, AnimalAntioxidantsEnzyme InhibitorsBlotting, WesternCells, CulturedOrgan PreservationAspartate AminotransferasesOrgan Preservation SolutionsAlanine TransaminaseCardioplegic SolutionsAthletic InjuriesNeuroprotective AgentsConstrictionSpinal Cord InjuriesHeme Oxygenase-1NeutrophilsMitochondrial Membrane Transport ProteinsVentricular PressureHeart Function TestsFree Radical ScavengersRats, Inbred LewRabbitsHeart Arrest, InducedInfarction, Middle Cerebral ArteryImmunohistochemistryTumor Necrosis Factor-alphaProto-Oncogene Proteins c-aktCell DeathProtein Kinase C-epsilonCell SurvivalCaspasesDogsEnzyme ActivationRNA, MessengerAdenosineFree RadicalsProto-Oncogene Proteins c-bcl-2Nitric Oxide Synthase Type IILung InjuryMyocardial StunningSpinal Cord IschemiaKATP ChannelsLiver DiseasesMice, TransgenicArrhythmias, CardiacLiver CirculationDose-Response Relationship, DrugRecovery of FunctionHydrogen SulfideIschemic Attack, TransientPhosphorylationApoptosis Regulatory ProteinsReceptor, Adenosine A3DiazoxideMicrocirculationLipid PeroxidationIntestinesMitochondriaLiver Transplantationbcl-2-Associated X ProteinHeart VentriclesNitric Oxide SynthaseSwineP-SelectinUp-RegulationHeme Oxygenase (Decyclizing)InflammationCoronary VesselsHSP20 Heat-Shock ProteinsNitric Oxide Synthase Type IIIAdenosine TriphosphateHeart RateBlood PressureAcute Lung InjuryAllopurinolInjury Severity ScoreHindlimbAnoxiaGlycogen Synthase Kinase 3OxygenDNA FragmentationIntercellular Adhesion Molecule-1Membrane Potential, MitochondrialKidney TubulesHypothermia, InducedCytochromes cCalciumEndothelium, VascularLeg InjuriesNF-kappa BBiological MarkersGene Expression RegulationCell HypoxiaCardiac OutputRaffinoseReverse Transcriptase Polymerase Chain ReactionPeroxynitrous AcidKidney Tubular Necrosis, AcuteTroponin ITrimetazidineHydrogen PeroxideCardiovascular AgentsPotassium ChannelsSuperoxidesCatalaseAnalysis of VarianceBrainPrimary Graft DysfunctionBenzophenanthridinesCytokinesTreatment OutcomeCerebral InfarctionXanthine OxidaseLeukocytesHepatocytesPhosphatidylinositol 3-KinasesAdenosine A3 Receptor AgonistsDrugs, Chinese HerbalKupffer CellsToll-Like Receptor 4LungEye InjuriesAnimals, NewbornSarcolemmaGlutathioneMesenteric Artery, SuperiorElectrocardiographyCreatininePhenanthridinesGene ExpressionBlood Urea NitrogenAnesthetics, InhalationPhosphocreatineBrain EdemaPoly(ADP-ribose) PolymerasesNitratesSulfonesIsofluraneLigationOxidantsKidney DiseasesInflammation MediatorsGuanidinesHydroxyl RadicalNeck InjuriesReceptors, Purinergic P1Ventricular Remodeling
Chronic Testosterone Replacement Exerts Cardioprotection against Cardiac Ischemia-Reperfusion Injury by Attenuating...Chronic Testosterone Replacement Exerts Cardioprotection against Cardiac Ischemia-Reperfusion Injury by Attenuating...
Moreover, current understanding on the cardiac effect of testosterone during cardiac ischemia-reperfusion (I/R) periods is ... Testosterone replacement attenuated the impairment of these parameters in ORX rats during I/R injury, but did not show any ... I/R was performed by left anterior descending coronary artery ligation for 30 minutes, followed by a 120-minute reperfusion. LV ... During I/R, arrhythmia scores and the infarct size were greater, and cardiac mitochondrial function was impaired, whereas the ...
journals.plos.org
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
Terminal dUTP nick end-labeling (TUNEL) and caspase-3 activity detection were used to assess apoptosis (21). To examine cardiac ... that confer cardioprotection at the onset of reperfusion after myocardial ischemia provide a promising approach to attenuate ... Ischemic postconditioning attenuates liver warm ischemia-reperfusion injury through Akt-eNOS-NO-HIF pathway. J Biomed Sci 2011 ... Murphy E, Steenbergen C. Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury. Physiol Rev 2008; 88 ...
scielo.br
Cardiovascular Adaptations Induced by Resistance Training in Animal ModelsCardiovascular Adaptations Induced by Resistance Training in Animal Models
... showed that 12 weeks of the RT reduced the infarct size and provides cardioprotection against ischemia-reperfusion injury. ... Resistance training attenuates salt overload-induced cardiac remodeling and diastolic dysfunction in normotensive rats. ... also observed a reduction in apoptosis in the heart of these animals, corroborating the hypothesis that AT1R can activate ... Although, Doustar et al., [45] showed that 4 weeks of RT did not preserve heart remodeling after ischemia-reperfusion injury, ...
medsci.org
Differential temporal inhibition of mitochondrial fission by Mdivi-1 exerts effective cardioprotection in cardiac ischemia...Differential temporal inhibition of mitochondrial fission by Mdivi-1 exerts effective cardioprotection in cardiac ischemia...
For cardiac I/R injury, rats were randomly divided into pre-ischemia, during-ischemia and upon onset of reperfusion group. A ... and decreased cardiac apoptosis, leading to preserved LV function during I/R injury. Mdivi-1 administered during ischemia and ... Taken together, mitochondrial fission inhibition after myocardial ischemic insults still exerts cardioprotection by attenuating ... inhibition of mitochondrial fission by Mdivi-1 exerts effective cardioprotection in cardiac ischemia/reperfusion injury. ...
clinsci.org
JCI - Volume 125, Issue 8JCI - Volume 125, Issue 8
Macrophages (Mø) are integral in ischemia/reperfusion injury-incited (I/R-incited) acute kidney injury (AKI) that leads to ... we determined that CDC-conditioned macrophages attenuated cardiomyocyte apoptosis and reduced infarct size, thereby ... Cardiosphere-derived cells (CDCs) are a stem-like population that is derived ex vivo from cardiac biopsies; they confer both ... Systemic depletion of macrophages with clodronate abolished CDC-mediated cardioprotection. Using both in vitro coculture assays ...
jci.org
Community Academic Profiles - Faculty & Researchers - Stanford MedicineCommunity Academic Profiles - Faculty & Researchers - Stanford Medicine
CpG-ODN, the TLR9 agonist, attenuates myocardial ischemia/reperfusion injury: Involving activation of PI3K/Akt signaling ... CpG-ODN attenuated I/R-induced myocardial apoptosis and prevented I/R-induced decrease in Bcl2 and increase in Bax levels in ... and they received a single dose of CEPO intraperitoneal at the onset of reperfusion. Myocardial infarct size and cardiac ... CEPO-induced cardioprotection appears to be mediated through a PI3K/Akt-dependent mechanism. ...
med.stanford.edu
Publications | Haobo Li, PhDPublications | Haobo Li, PhD
... protects heart against ischemia/reperfusion injury. However, SPostC cardioprotection is lost in diabetes whose cardiac heme ... NAC significantly attenuated I/RI-induced increases in oxidative stress and cardiac apoptosis, prevented postischemic autophagy ... methylation in ischemia-reperfusion injury." Cell Death Dis, 11, Pp. 478.Abstract. Ischemia-reperfusion (I/R) injury is common ... "N-Acetylcysteine Attenuates Diabetic Myocardial Ischemia Reperfusion Injury through Inhibiting Excessive Autophagy." Mediators ...
scholar.harvard.edu
Zhijuan Caos Profile | Stanford ProfilesZhijuan Cao's Profile | Stanford Profiles
CpG-ODN, the TLR9 agonist, attenuates myocardial ischemia/reperfusion injury: Involving activation of PI3K/Akt signaling ... CpG-ODN attenuated I/R-induced myocardial apoptosis and prevented I/R-induced decrease in Bcl2 and increase in Bax levels in ... and they received a single dose of CEPO intraperitoneal at the onset of reperfusion. Myocardial infarct size and cardiac ... CEPO-induced cardioprotection appears to be mediated through a PI3K/Akt-dependent mechanism. ...
profiles.stanford.edu
Medicina | Free Full-Text | Protecting the Heart Against Ischemia/Reperfusion-Induced Necrosis and Apoptosis: the Effect of...Medicina | Free Full-Text | Protecting the Heart Against Ischemia/Reperfusion-Induced Necrosis and Apoptosis: the Effect of...
... may attenuate ischemia/reperfusion injury though the mechanisms of such protection are not clear. Following our previous ... here we investigated whether these anthocyanins can rescue cardiac cells from death by the mechanism involving the reduction of ... The perfusion of hearts with 20-μM Pg3G did not prevent ischemia/reperfusion-induced apoptosis as well as necrosis. Conclusions ... The perfusion of hearts with 20-μM Cy3G prevented ischemia/reperfusion-induced apoptosis of cardiomyocytes: the number of TUNEL ...
mdpi.com
Cardiac Literature, including Myocardial Infarction, arrthymias, tachycardia, and angina sub-cluster 82Cardiac Literature, including Myocardial Infarction, arrthymias, tachycardia, and angina sub-cluster 82
In this study, we investigated the anti-myocardial ischemia and reperfusion (I/R) injury effects of ND01 in vivo and elucidated ... Cardioprotection with 8-O-acetyl shanzhiside methylester on experimental myocardial ischemia injury. ... and must be applied as soon as possible to attenuate the ischemic insult. However reperfusion is responsible for additional ... Shen-Fu injection reduces postresuscitation myocardial dysfunction in a porcine model of cardiac arrest by modulating apoptosis ...
biomedsearch.com
NDNRViagraNDNRViagra
BACKGROUND: Sildenafil, a phosphodiesterase-5 inhibitor, induces cardioprotection against ischemia/reperfusion injury via ... Doxorubicin-treated mice demonstrated increased apoptosis and desmin disruption, which was attenuated in the sildenafil+ ... Phosphodiesterase-5 inhibitor sildenafil preconditions adult cardiac myocytes against necrosis and apoptosis. Essential role of ... The results may have possible therapeutic potential in preventing myocyte cell death following ischemia/reperfusion. ...
denvernaturopathic.com
Frontiers | Intracoronary Levosimendan during Ischemia Prevents Myocardial Apoptosis | PhysiologyFrontiers | Intracoronary Levosimendan during Ischemia Prevents Myocardial Apoptosis | Physiology
Apoptosis was induced after ischemia-reperfusion in all groups (pre L-IV 0.002±0.004 % vs. post L-IV 0.020±0.017 % p=0.02, pre ... Apoptosis was induced after ischemia-reperfusion in all groups (pre L-IV 0.002±0.004 % vs. post L-IV 0.020±0.017 % p=0.02, pre ... cardioplegic ischemia under cardiopulmonary bypass and 240 minutes of reperfusion. L-IV group received intravenous infusion of ... cardioplegic ischemia under cardiopulmonary bypass and 240 minutes of reperfusion. L-IV group received intravenous infusion of ...
frontiersin.org
Involvement of Na+/K+-ATPase in hydrogen peroxide-induced hypertrophy in cardiac myocytes. - Semantic ScholarInvolvement of Na+/K+-ATPase in hydrogen peroxide-induced hypertrophy in cardiac myocytes. - Semantic Scholar
This resulted in a steady increase in intracellular ROS in cultured cardiac myocytes for at least 12 h. Such sustained, but not ... leading to the activation of hypertrophic pathways in cardiac myocytes. ... was required for ouabain-induced hypertrophy in cultured cardiac myocytes. In the present study we assessed whether long-term ... Cardiac Na / K-ATPase in ischemia-reperfusion injury and cardioprotection. *Qiming Duan ...
semanticscholar.org
Cardioprotective effects of GHRH agonists - University of MiamiCardioprotective effects of GHRH agonists - University of Miami
GHRH cardioprotection was demonstrated in isolated rat hearts subjected to ischemia-reperfusion injury, while in our work, ... but markedly attenuated the degree of cardiac functional decline and remodeling after injury. In contrast, GH administration ... To quantify apoptosis of cardiac cells, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining ... myocardial ischemia, myocardial fibrosis, cardiac weakness, cardiac failure and cardiac inefficiency, especially where heart ...
freepatentsonline.com
Susceptibility to myocardial ischemia reperfusion injury at early stage of type 1 diabetes in rats | Cardiovascular Diabetology...Susceptibility to myocardial ischemia reperfusion injury at early stage of type 1 diabetes in rats | Cardiovascular Diabetology...
... apoptosis assessed by TUNEL staining and cardiac caspase-3 protein expression before and after myocardial ischemia reperfusion ... Postconditioning attenuates myocardial ischemia-reperfusion injury by inhibiting events in the early minutes of reperfusion. ... Przyklenk K, Maynard M, Greiner DL, Whittaker P: Cardioprotection with postconditioning: loss of efficacy in murine models of ... Ischemia reperfusion injuryDiabetes mellitusInfarct size. Background. Despite of the current optimal therapy, the mortality and ...
cardiab.biomedcentral.com
IJERPH | Free Full-Text | Cellular and Mitochondrial Effects of Alcohol Consumption | HTMLIJERPH | Free Full-Text | Cellular and Mitochondrial Effects of Alcohol Consumption | HTML
... preconditioning against ischemic injury [87], reduced ischemia-reperfusion injury and infarction [88], attenuated hypertrophic ... Hajnoczky, G; Buzas, CJ; Pacher, P; Hoek, JB; Rubin, E. Alcohol and mitochondria in cardiac apoptosis: Mechanisms and ... Penumathsa, SV; Maulik, N. Resveratrol: A promising agent in promoting cardioprotection against coronary heart disease. Can. J ... Attenuation of ischemia/reperfusion injury in rats by the anti-inflammatory action of resveratrol. Arzneimittelforschung 2006, ...
mdpi.com
Frontiers | Targeting GPCRs Against Cardiotoxicity Induced by Anticancer Treatments | Cardiovascular MedicineFrontiers | Targeting GPCRs Against Cardiotoxicity Induced by Anticancer Treatments | Cardiovascular Medicine
Cardiotoxicity induced by anti-cancer treatments compromise vasospastic and thromboembolic ischemia, dysrhythmia, hypertension ... myocarditis, and cardiac dysfunction that can result in heart failure. Importantly, none of the strategies to prevent ... However, both conventional and new anticancer treatments induce cardiac adverse effects, which remain a critical issue in ... Cardiotoxicity induced by anti-cancer drugs comprise vasospastic and thromboembolic ischemia, dysrhythmia, hypertension, ...
frontiersin.org
Chemical and Pharmaceutical BulletinChemical and Pharmaceutical Bulletin
Role of Vitamin C in Cardioprotection of Ischemia/Reperfusion Injury by Activation of Mitochondrial KATP Channel ... Post-treatment with VC significantly decreased I/R-induced injury, attenuated apoptosis, and maintained the functional ... in primary neonatal rat cardiac myocytes. We used the mitochondrial permeability transition pore (mPTP) opener lonidamine (LND ... How to provide effective prevention and treatment of myocardial ischemia/reperfusion (I/R) injury and study of the mechanism ...
jstage.jst.go.jp
Physiological and Pharmacological Roles of FGF21 in Cardiovascular DiseasesPhysiological and Pharmacological Roles of FGF21 in Cardiovascular Diseases
The mechanistic study revealed that FGF21-induced protection against ischemia-reperfusion injury in cardiac cells mainly ... attenuated ischemia-reperfusion induced damage in H9c2 cells characterized by inhibition of oxidative stress and apoptosis [62 ... administration of exogenous FGF21 induced significant cardioprotection and restored cardiac function following global ischemia ... 3. FGF21 and Myocardial Ischemia. Myocardial ischemia, a disorder causing cardiomyocytes injury and myocardial infarction and ...
hindawi.com
Nerve Growth Factor Protects the Ischemic Heart via Attenuation of the Endoplasmic Reticulum Stress Induced Apoptosis by...Nerve Growth Factor Protects the Ischemic Heart via Attenuation of the Endoplasmic Reticulum Stress Induced Apoptosis by...
However, when ischemia/reperfusion injury is predicable, such as cardiac arrest during cardiopulmonary bypass, whether ... thus a role of PI3K/Akt pathway in mediating the cardioprotection of NGF on ischemia induced myocardial apoptosis is confirmed ... Nerve growth factor attenuates 2-deoxy-d-glucose-triggered endoplasmic reticulum stress-mediated apoptosis via enhanced ... Cardiac enzymes and cardiac troponin I (cTnI) were assayed before ischemia and at the end of reperfusion. Myocardial apoptosis ...
medsci.org
Journal-related Activities and Other Special Activities at the 2012 American Society of Anesthesiologists Annual Meeting |...Journal-related Activities and Other Special Activities at the 2012 American Society of Anesthesiologists Annual Meeting |...
... to myocardial ischemia-reperfusion injury and resulting left ventricular dysfunction by mediating cardiac myocyte apoptosis. ... TRIF-deficient mice also had attenuated myocardial infarction and apoptosis after 45 min of ischemia and 4 h of reperfusion. ... These results suggest caveolin-3 is not required for intralipid cardioprotection.. "Functional Neural Connectivity of the ... "TRIF Signaling Contributes to Myocardial Ischemia-Reperfusion Injury by Mediating Cardiomyocyte Apoptosis" by Chan Chen, M.D., ...
anesthesiology.pubs.asahq.org
Astragaloside IV alleviates myocardial ischemia-reperfusion injury in rats through regulating PI3K/AKT/GSK-3β signaling pathwaysAstragaloside IV alleviates myocardial ischemia-reperfusion injury in rats through regulating PI3K/AKT/GSK-3β signaling pathways
It can improve the cardiac function and reduce cardiac myocyte apoptosis20. As-IV, the main active ingredient of Astragalus ... HIF-Ια signaling activation by post-ischemia treatment with astragaloside IV attenuates myocardial ischemia-reperfusion injury ... Astragaloside IV from Astragalus membranaceus shows cardioprotection during myocardial ischemia in vivo and in vitro. Planta ... Quercetin postconditioning attenuates myocardial ischemia/reperfusion injury in rats through the PI3K/Akt pathway. Braz J Med ...
scielo.br
Metformin Prevents Progression of Heart Failure in Dogs | CirculationMetformin Prevents Progression of Heart Failure in Dogs | Circulation
... activation or NO production attenuates myocardial ischemia/reperfusion injury in the ischemic model7-9 and prevents cardiac ... also has been reported to protect cardiomyocytes against apoptosis and to attenuate myocardial ischemia/reperfusion injury in ... Metformin is known to activate AMPK, which mediates potent cardioprotection against ischemia/reperfusion injury. AMPK also is ... Indeed, AICAR also has been reported to reduce myocardial ischemia/reperfusion injury in humans and animals.25,26 What ...
circ.ahajournals.org
Effects of propofol on ischemia-induced ventricular arrhythmias and mitochondrial ATP-sensitive potassium channels.Effects of propofol on ischemia-induced ventricular arrhythmias and mitochondrial ATP-sensitive potassium channels.
Kobayashi I,Kokita N,Namiki A. Propofol attenuates ischaemia-reperfusion injury in the rat heart in vivoEur J AnaesthesiolYear ... Phosphorylation of GSK-3β mediates intralipid-induced cardioprotection against ischemia/reperfusion injuryAnesthesiologyYear: ... Myocardial Ischemia / complications*, drug therapy, metabolism. Myocytes, Cardiac / drug effects, metabolism. Propofol / ... Previous Document: Migfilin sensitizes cisplatin-induced apoptosis in human glioma cells in vitro.. Next Document: Luteolin ...
biomedsearch.com
Sang Ging Ong | Stanford Medicine ProfilesSang Ging Ong | Stanford Medicine Profiles
... novel therapeutic targets for protecting the heart against acute ischemia-reperfusion injury (IRI) are required to attenuate ... The cardiac neural crest cells (cNCCs) and the second heart field (SHF) play key roles in development of the cardiac outflow ... Hypoxia-inducible factor as a therapeutic target for cardioprotection PHARMACOLOGY & THERAPEUTICS Ong, S., Hausenloy, D. J. ... regulation of apoptosis, and energy production) may play more important roles than their pro-fusion effects. In this review ...
med.stanford.edu
AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesDisciplines and OccupationsInformation ScienceHealth Care
Reperfusion InjuryMyocardial Reperfusion InjuryMyocardiumMyocytes, CardiacApoptosisMyocardial ReperfusionReperfusionIschemiaMyocardial IschemiaIschemic Preconditioning, MyocardialRats, Sprague-DawleyCardiotonic AgentsMitochondria, HeartIn Situ Nick-End LabelingIschemic PreconditioningHeartCaspase 3Ischemic PostconditioningDisease Models, AnimalMyocardial InfarctionRats, WistarBrain IschemiaWounds and InjuriesTime FactorsPeroxidaseProtective AgentsWarm IschemiaMice, Inbred C57BLNecrosisMalondialdehydeOxidative StressL-Lactate DehydrogenaseCreatine KinaseCytoprotectionBrain InjuriesCold IschemiaMice, KnockoutDecanoic AcidsHydroxy AcidsSignal TransductionPerfusionMyocardial ContractionKidneyAcute Kidney InjuryNeutrophil InfiltrationReactive Oxygen SpeciesHemodynamicsLiverCoronary CirculationRandom AllocationTioproninVentricular Function, LeftSuperoxide DismutaseNitric OxideModels, AnimalAntioxidantsEnzyme InhibitorsBlotting, WesternCells, CulturedOrgan PreservationAspartate AminotransferasesOrgan Preservation SolutionsAlanine TransaminaseCardioplegic SolutionsAthletic InjuriesNeuroprotective AgentsConstrictionSpinal Cord InjuriesHeme Oxygenase-1NeutrophilsMitochondrial Membrane Transport ProteinsVentricular PressureHeart Function TestsFree Radical ScavengersRats, Inbred LewRabbitsHeart Arrest, InducedInfarction, Middle Cerebral ArteryImmunohistochemistryTumor Necrosis Factor-alphaProto-Oncogene Proteins c-aktCell DeathProtein Kinase C-epsilonCell SurvivalCaspasesDogsEnzyme ActivationRNA, MessengerAdenosineFree RadicalsProto-Oncogene Proteins c-bcl-2Nitric Oxide Synthase Type IILung InjuryMyocardial StunningSpinal Cord IschemiaKATP ChannelsLiver DiseasesMice, TransgenicArrhythmias, CardiacLiver CirculationDose-Response Relationship, DrugRecovery of FunctionHydrogen SulfideIschemic Attack, TransientPhosphorylationApoptosis Regulatory ProteinsReceptor, Adenosine A3DiazoxideMicrocirculationLipid PeroxidationIntestinesMitochondriaLiver Transplantationbcl-2-Associated X ProteinHeart VentriclesNitric Oxide SynthaseSwineP-SelectinUp-RegulationHeme Oxygenase (Decyclizing)InflammationCoronary VesselsHSP20 Heat-Shock ProteinsNitric Oxide Synthase Type IIIAdenosine TriphosphateHeart RateBlood PressureAcute Lung InjuryAllopurinolInjury Severity ScoreHindlimbAnoxiaGlycogen Synthase Kinase 3OxygenDNA FragmentationIntercellular Adhesion Molecule-1Membrane Potential, MitochondrialKidney TubulesHypothermia, InducedCytochromes cCalciumEndothelium, VascularLeg InjuriesNF-kappa BBiological MarkersGene Expression RegulationCell HypoxiaCardiac OutputRaffinoseReverse Transcriptase Polymerase Chain ReactionPeroxynitrous AcidKidney Tubular Necrosis, AcuteTroponin ITrimetazidineHydrogen PeroxideCardiovascular AgentsPotassium ChannelsSuperoxidesCatalaseAnalysis of VarianceBrainPrimary Graft DysfunctionBenzophenanthridinesCytokinesTreatment OutcomeCerebral InfarctionXanthine OxidaseLeukocytesHepatocytesPhosphatidylinositol 3-KinasesAdenosine A3 Receptor AgonistsDrugs, Chinese HerbalKupffer CellsToll-Like Receptor 4LungEye InjuriesAnimals, NewbornSarcolemmaGlutathioneMesenteric Artery, SuperiorElectrocardiographyCreatininePhenanthridinesGene ExpressionBlood Urea NitrogenAnesthetics, InhalationPhosphocreatineBrain EdemaPoly(ADP-ribose) PolymerasesNitratesSulfonesIsofluraneLigationOxidantsKidney DiseasesInflammation MediatorsGuanidinesHydroxyl RadicalNeck InjuriesReceptors, Purinergic P1Ventricular Remodeling
DysfunctionOxidativeLeft ventricularProtection against ischemia-reperfusion injuryCell apoptosisInhibitionPathwayEndothelialInduceOnsetPostischemicFibrosisOrgan protection against ischemia-reperfusionMechanismsClinicalMethodsInflammationModel of Myocardial InfarctionReoxygenationMiceInhibits myocardialCardiovascularFunctionMorbidity and mortaVentricularTime of reperfusionVivoProtectiveMinutes of reperfusionMyocardial salvageCellularImpairmentRecovery of PC-induced cardioprotectionInhibitorArrhythmiasProtectsAcute myocardialPI3KPathwaysNecrosis
Dysfunction23
Oxidative27
Left ventricular4
Protection against ischemia-reperfusion injury3
Cell apoptosis6
  • Phosphatidylinositol-3 kinase/serine-threonine protein kinase (PI3K/AKT) and glycogen synthase kinase-3β (GSK-3β) are important signal transduction pathways in cells, which play important biological roles in cell apoptosis, survival and proliferation 17 . (scielo.br)
  • While the latter has demonstrated potential to protect against cell apoptosis, the proposed mechanism of action of aspalathin is linked to its capacity to enhance the expression of nuclear factor (erythroid-derived 2)-like 2 ( Nrf2 ) expression, an intracellular antioxidant response element. (biomedcentral.com)
  • comment on the paper 'Dynamics of serum-induced endothelial cell apoptosis in patients with myocardial Infarction' by Forteza et al. (wiley.com)
  • Qian J, Fang D, Lu H, Cao Y, Zhang J, Ding R, Li L, Huo J (2018) Tanshinone IIA promotes IL2-mediated SW480 colorectal cancer cell apoptosis by triggering INF2-related mitochondrial fission and activating the Mst1-Hippo pathway. (springer.com)
  • Moreover, in in vitro studies, NBP significantly increased the viability of H9c2 cells in a dose-dependent manner, reduced cell apoptosis, protected mitochondrial functions, elevated the cellular ATP levels, and promoted H 2 O 2 -induced mitochondrial biogenesis in H9c2 cardiomyoblasts. (biomedcentral.com)
  • In hearts with MI, BDNF/TrkB relieved myocardial ischemic injury and suppressed myocardial cell apoptosis via the regulation of transient receptor potential canonical (TRPC) 3/6 channels, thus suggesting a new underlying therapy for MI [ 6 ]. (aging-us.com)
Inhibition8
Pathway21
Endothelial5
Induce7
Onset10
Postischemic2
Fibrosis7
Organ protection against ischemia-reperfusion1
Mechanisms13
Clinical6
Methods2
Inflammation2
Model of Myocardial Infarction2
Reoxygenation2
Mice14
Inhibits myocardial2
Cardiovascular9
Function15
Morbidity and morta4
Ventricular5
Time of reperfusion1
Vivo8
Protective8
Minutes of reperfusion1
Myocardial salvage2
Cellular5
Impairment3
Recovery of PC-induced cardioprotection2
Inhibitor4
  • Sprague-Dawley rats were treated with BBR in the absence or presence of the SIRT1 inhibitor sirtinol (Stnl) and then subjected to MI/R injury. (paperity.org)
  • Here coadministration of insulin with the tyrosine kinase inhibitor lavendustin A, the phosphatidylinositol3-kinase (PI3-kinase) inhibitor wortmannin, and mTOR/p70s6 kinase inhibitor rapamycin abolished cardioprotection. (ahajournals.org)
  • The knockdown of H19 and 3-MA (an autophagy inhibitor) protected against h/R-induced apoptosis, cell damage, the expression of cleaved caspase-3 and cleaved caspase-9, the release of cytochrome c (Cyt c ). (conicyt.cl)
  • The cyclin-dependent kinase inhibitor p57 Kip 2 is involved in cell cycle control, differentiation, stress signaling and apoptosis. (biomedcentral.com)
Arrhythmias3
Protects3
Acute myocardial6
PI3K2
Pathways7
  • Joint use of APN and IPo synergistically attenuated myocardial IR injury by activating STAT3 via distinct signaling pathways. (harvard.edu)
  • 4,5 These heart failure-associated alterations in the cardiac ECM are likely regulated, in part, by the cardiac fibroblast through both stretch-sensitive signaling pathways and by neuroendocrine effectors such as angiotensin II and transforming growth factor (TGF)β. (ahajournals.org)
  • Debate has gone on, and continues regarding the existence of reperfusion injury and the pathways that are solicited. (omicsonline.org)
  • Myocardial cell signaling pathways and apoptotic markers were assessed at various time points (0 to 24 hours) following reperfusion. (elsevier.com)
  • However, the role of cardiac leptin signaling in mediating the cardiomyopathy associated with increased body weight is unclear, in particular, whether it develops subsequently to cardiac leptin resistance or overactivation of hypertrophic signaling pathways via elevated leptin levels. (biomedcentral.com)
  • We attempted to investigate whether Caveolin-3 showed beneficial effects in DM patient post-MI injury through the cAMP/PKA and BDNF/TrkB signaling pathways. (aging-us.com)
  • In conclusion, ADRB2 agonist promoted the activity of the BDNF/TrkB and cAMP/PKA signaling pathways, mitigating the HG-aggravated H/R injuries in H9C2 cells. (aging-us.com)
Necrosis3