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.
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.
Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).
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.
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.
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.
The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.
A 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).
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.
The hollow, muscular organ that maintains the circulation of the blood.
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.
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)
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.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
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.
Contractile activity of the MYOCARDIUM.
NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).
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).
Elements of limited time intervals, contributing to particular results or situations.
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.
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.
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.
Damage inflicted on the body as the direct or indirect result of an external force, with or without disruption of structural continuity.
The mitochondria of the myocardium.
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
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.
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.
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.
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.
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).
The dialdehyde of malonic acid.
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.
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.
Treatment process involving the injection of fluid into an organ or tissue.
The circulation of blood through the CORONARY VESSELS of the HEART.
The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.
The chilling of a tissue or organ during decreased BLOOD perfusion or in the absence of blood supply. Cold ischemia time during ORGAN TRANSPLANTATION begins when the organ is cooled with a cold perfusion solution after ORGAN PROCUREMENT surgery, and ends after the tissue reaches physiological temperature during implantation procedures.
The 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)
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.
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.
Refers to animals in the period of time just after birth.
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.
Enlargement of the HEART, usually indicated by a cardiothoracic ratio above 0.50. Heart enlargement may involve the right, the left, or both HEART VENTRICLES or HEART ATRIA. Cardiomegaly is a nonspecific symptom seen in patients with chronic systolic heart failure (HEART FAILURE) or several forms of CARDIOMYOPATHIES.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
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.
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.
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.
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.
The process by which chemical compounds provide protection to cells against harmful agents.
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.
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.
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.
Non-human animals, selected because of specific characteristics, for use in experimental research, teaching, or testing.
Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids.
The diffusion or accumulation of neutrophils in tissues or cells in response to a wide variety of substances released at the sites of inflammatory reactions.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
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.
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
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)
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.
The act of constricting.
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.
Mature contractile cells, commonly known as myocytes, that form one of three kinds of muscle. The three types of muscle cells are skeletal (MUSCLE FIBERS, SKELETAL), cardiac (MYOCYTES, CARDIAC), and smooth (MYOCYTES, SMOOTH MUSCLE). They are derived from embryonic (precursor) muscle cells called MYOBLASTS.
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.
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).
Sulfhydryl acylated derivative of GLYCINE.
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.
Solutions which, upon administration, will temporarily arrest cardiac activity. They are used in the performance of heart surgery.
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).
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).
Prolonged dysfunction of the myocardium after a brief episode of severe ischemia, with gradual return of contractile activity.
An electrogenic ion exchange protein that maintains a steady level of calcium by removing an amount of calcium equal to that which enters the cells. It is widely distributed in most excitable membranes, including the brain and heart.
Enzymes of the transferase class that catalyze the conversion of L-aspartate and 2-ketoglutarate to oxaloacetate and L-glutamate. EC
Solutions used to store organs and minimize tissue damage, particularly while awaiting implantation.
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.
The excitable plasma membrane of a muscle cell. (Glick, Glossary of Biochemistry and Molecular Biology, 1990)
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
An enzyme that catalyzes the conversion of L-alanine and 2-oxoglutarate to pyruvate and L-glutamate. (From Enzyme Nomenclature, 1992) EC
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.
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.
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.
10-carbon saturated monocarboxylic acids.
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.
Organic compounds containing both the hydroxyl and carboxyl radicals.
The circulation of the BLOOD through the MICROVASCULAR NETWORK.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.
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.
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.
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.
Injuries incurred during participation in competitive or non-competitive sports.
The relationship between the dose of an administered drug and the response of the organism to the drug.
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.
Examinations used to diagnose and treat heart conditions.
The hemodynamic and electrophysiological action of the HEART VENTRICLES.
The veins and arteries of the HEART.
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.
Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.
Penetrating and non-penetrating injuries to the spinal cord resulting from traumatic external forces (e.g., WOUNDS, GUNSHOT; WHIPLASH INJURIES; etc.).
The number of times the HEART VENTRICLES contract per unit of time, usually per minute.
An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.
The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.
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.
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.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
One of the three polypeptide chains that make up the TROPONIN complex. It inhibits F-actin-myosin interactions.
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.
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.
Long-lasting voltage-gated CALCIUM CHANNELS found in both excitable and nonexcitable tissue. They are responsible for normal myocardial and vascular smooth muscle contractility. Five subunits (alpha-1, alpha-2, beta, gamma, and delta) make up the L-type channel. The alpha-1 subunit is the binding site for calcium-based antagonists. Dihydropyridine-based calcium antagonists are used as markers for these binding sites.
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).
Proteins involved in the transport of specific substances across the membranes of the MITOCHONDRIA.
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.
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.
The section of the alimentary canal from the STOMACH to the ANAL CANAL. It includes the LARGE INTESTINE and SMALL INTESTINE.
Relatively complete absence of oxygen in one or more tissues.
A ubiquitous stress-responsive enzyme that catalyzes the oxidative cleavage of HEME to yield IRON; CARBON MONOXIDE; and BILIVERDIN.
The circulation of BLOOD through the LIVER.
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)
A partial or complete return to the normal or proper physiologic activity of an organ or part following disease or trauma.
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.
A condition of decreased oxygen content at the cellular level.
Theoretical representations that simulate the behavior or activity of the cardiovascular system, processes, or phenomena; includes the use of mathematical equations, computers and other electronic equipment.
Pathological processes of the LIVER.
A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.
Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor.
Cell adhesion molecule and CD antigen that mediates the adhesion of neutrophils and monocytes to activated platelets and endothelial cells.
A XANTHINE OXIDASE inhibitor that decreases URIC ACID production. It also acts as an antimetabolite on some simpler organisms.
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.
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.
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.
A network of tubules and sacs in the cytoplasm of SKELETAL MUSCLE FIBERS that assist with muscle contraction and relaxation by releasing and storing calcium ions.
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).
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.
A subfamily of the Muridae consisting of several genera including Gerbillus, Rhombomys, Tatera, Meriones, and Psammomys.
Signal transduction mechanisms whereby calcium mobilization (from outside the cell or from intracellular storage pools) to the cytoplasm is triggered by external stimuli. Calcium signals are often seen to propagate as waves, oscillations, spikes, sparks, or puffs. The calcium acts as an intracellular messenger by activating calcium-responsive proteins.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
An electrophysiologic technique for studying cells, cell membranes, and occasionally isolated organelles. All patch-clamp methods rely on a very high-resistance seal between a micropipette and a membrane; the seal is usually attained by gentle suction. The four most common variants include on-cell patch, inside-out patch, outside-out patch, and whole-cell clamp. Patch-clamp methods are commonly used to voltage clamp, that is control the voltage across the membrane and measure current flow, but current-clamp methods, in which the current is controlled and the voltage is measured, are also used.
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.
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.
Surgery performed on the heart.
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.
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.
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.
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.
The transference of a part of or an entire liver from one human or animal to another.
The circulation of blood through the BLOOD VESSELS of the BRAIN.
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.
The voltage differences across a membrane. For cellular membranes they are computed by subtracting the voltage measured outside the membrane from the voltage measured inside the membrane. They result from differences of inside versus outside concentration of potassium, sodium, chloride, and other ions across cells' or ORGANELLES membranes. For excitable cells, the resting membrane potentials range between -30 and -100 millivolts. Physical, chemical, or electrical stimuli can make a membrane potential more negative (hyperpolarization), or less negative (depolarization).
A 21-amino acid peptide produced in a variety of tissues including endothelial and vascular smooth-muscle cells, neurons and astrocytes in the central nervous system, and endometrial cells. It acts as a modulator of vasomotor tone, cell proliferation, and hormone production. (N Eng J Med 1995;333(6):356-63)
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.
A CALCIUM-dependent, constitutively-expressed form of nitric oxide synthase found primarily in ENDOTHELIAL CELLS.
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.
The quantity of volume or surface area of CELLS.
Abrupt changes in the membrane potential that sweep along the CELL MEMBRANE of excitable cells in response to excitation stimuli.
Agents used for the treatment or prevention of cardiac arrhythmias. They may affect the polarization-repolarization phase of the action potential, its excitability or refractoriness, or impulse conduction or membrane responsiveness within cardiac fibers. Anti-arrhythmia agents are often classed into four main groups according to their mechanism of action: sodium channel blockade, beta-adrenergic blockade, repolarization prolongation, or calcium channel blockade.
A group of diseases in which the dominant feature is the involvement of the CARDIAC MUSCLE itself. Cardiomyopathies are classified according to their predominant pathophysiological features (DILATED CARDIOMYOPATHY; HYPERTROPHIC CARDIOMYOPATHY; RESTRICTIVE CARDIOMYOPATHY) or their etiological/pathological factors (CARDIOMYOPATHY, ALCOHOLIC; ENDOCARDIAL FIBROELASTOSIS).
Pathological conditions involving the HEART including its structural and functional abnormalities.
A heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (VENTRICULAR DYSFUNCTION), or a sudden overload beyond its capacity. Chronic heart failure is more common than acute heart failure which results from sudden insult to cardiac function, such as MYOCARDIAL INFARCTION.
Devices for the compression of a blood vessel by application around an extremity to control the circulation and prevent the flow of blood to or from the distal area. (From Dorland, 28th ed)
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.
Unexpected rapid natural death due to cardiovascular collapse within one hour of initial symptoms. It is usually caused by the worsening of existing heart diseases. The sudden onset of symptoms, such as CHEST PAIN and CARDIAC ARRHYTHMIAS, particularly VENTRICULAR TACHYCARDIA, can lead to the loss of consciousness and cardiac arrest followed by biological death. (from Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 7th ed., 2005)
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
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.
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)
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.
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.
The protein constituents of muscle, the major ones being ACTINS and MYOSINS. More than a dozen accessory proteins exist including TROPONIN; TROPOMYOSIN; and DYSTROPHIN.
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)
The chambers of the heart, to which the BLOOD returns from the circulation.
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.
An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels.
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
Use of infusions of FIBRINOLYTIC AGENTS to destroy or dissolve thrombi in blood vessels or bypass grafts.
A trisaccharide occurring in Australian manna (from Eucalyptus spp, Myrtaceae) and in cottonseed meal.
The repeating contractile units of the MYOFIBRIL, delimited by Z bands along its length.
Ultrasonic recording of the size, motion, and composition of the heart and surrounding tissues. The standard approach is transthoracic.
Cessation of heart beat or MYOCARDIAL CONTRACTION. If it is treated within a few minutes, heart arrest can be reversed in most cases to normal cardiac rhythm and effective circulation.
Drugs that selectively bind to and activate beta-adrenergic receptors.
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)
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).
White blood cells. These include granular leukocytes (BASOPHILS; EOSINOPHILS; and NEUTROPHILS) as well as non-granular leukocytes (LYMPHOCYTES and MONOCYTES).
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.
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.
Drugs used to cause dilation of the blood vessels.
Electron-accepting molecules in chemical reactions in which electrons are transferred from one molecule to another (OXIDATION-REDUCTION).
A vasodilator used in angina of effort or ischemic heart disease.
An serine-threonine protein kinase that requires the presence of physiological concentrations of CALCIUM and membrane PHOSPHOLIPIDS. The additional presence of DIACYLGLYCEROLS markedly increases its sensitivity to both calcium and phospholipids. The sensitivity of the enzyme can also be increased by PHORBOL ESTERS and it is believed that protein kinase C is the receptor protein of tumor-promoting phorbol esters.
The rate at which oxygen is used by a tissue; microliters of oxygen STPD used per milligram of tissue per hour; the rate at which oxygen enters the blood from alveolar gas, equal in the steady state to the consumption of oxygen by tissue metabolism throughout the body. (Stedman, 25th ed, p346)
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.
A light microscopic technique in which only a small spot is illuminated and observed at a time. An image is constructed through point-by-point scanning of the field in this manner. Light sources may be conventional or laser, and fluorescence or transmitted observations are possible.
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)
The transference of a heart from one human or animal to another.
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.
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).
One of the three polypeptide chains that make up the TROPONIN complex. It is a cardiac-specific protein that binds to TROPOMYOSIN. It is released from damaged or injured heart muscle cells (MYOCYTES, CARDIAC). Defects in the gene encoding troponin T result in FAMILIAL HYPERTROPHIC CARDIOMYOPATHY.
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.
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.
"Transient Receptor Potential Ankyrin 1 Activation within the Cardiac Myocyte Limits Ischemia-reperfusion Injury in Rodents". ... It has protective effects on cardiac tissue, and is used for research into the function of the TRPA1 receptor. JT-010 PF- ...
... helps to prevent cardiac dysfunction after ischemia-reperfusion injuries. Mitochondrial ROS production and oxidative mtDNA ... in addition to structural abnormalities in cardiac mitochondria and myocytes, suggesting GPX1 may play an important role in ... protecting cardiac mitochondria from reoxygenation damage in vivo. In GPX1 (-/-) mice, oxidant formation is increased, ...
Perrelli MG, Pagliaro P, Penna C (June 2011). "Ischemia/reperfusion injury and cardioprotective mechanisms: Role of ... These changes impair mitochondrial energy production and drive cardiac myocyte apoptosis. Intralipid (5mL/kg) provided five ... "reperfusion injury". The mitochondrial permeability transition pore (mPTP) is normally closed during ischemia, but calcium ... protects the heart against ischemia-reperfusion injury more efficiently than cyclosporine-A". Anesthesiology. 117 (4): 836-46. ...
Yang FH, Pyle WG (March 2012). "Reduced cardiac CapZ protein protects hearts against acute ischemia-reperfusion injury and ... A function of CapZβ in transducing protein kinase C signaling in cardiac myocytes was illuminated by a study in skinned cardiac ... A later study showed that partial reduction of CapZβ was cardioprotective during ischemia-reperfusion injury, concomitant with ... "Integration of cardiac proteome biology and medicine by a specialized knowledgebase". Circulation Research. 113 (9): 1043-53. ...
PKCδ has been implicated in depressing cardiac function and cell death after ischemia-reperfusion injury as well as promoting ... channel reduces ischemic injury in rat cardiac myocytes by activating mitochondrial K(Ca) channel". J Pharmacol Sci. 108 (1): ... protects the heart against ischemia-reperfusion injury". Pflügers Arch. 457 (5): 979-988. doi:10.1007/s00424-008-0583-5. PMID ... have been reported to have cardio-protective effects after ischemic-reperfusion injury. There were reductions in mitochondrial ...
Prevents Spontaneous Ventricular Arrhythmias and Reduces Infarct Size During Myocardial Ischemia/Reperfusion Injury in Open- ... increases gap junction intercellular communication in cardiac myocytes and HeLa cells expressing connexin 43. British Journal ... It is a peptide analog that has been shown to increase gap junction intercellular conductance in cardiac muscle cells. Gap ... This allows for a smoother conduction to pass through the myocytes to propagate a synchronous contraction. This has been shown ...
TSPO ligands are used as a therapy after ischemia reperfusion injury to preserve the action potentials in cardiac tissue and ... to regulate heart rate and contractile force by its interaction with voltage-dependent calcium channels in cardiac myocytes. ... Expression of TSPO is also linked to inflammatory responses that occur after ischemia-reperfusion injury, following hemorrhagic ... and often occurs because of inflammation caused by ischemia reperfusion injury. Coxsackievirus B3 (CVB3) causes immune cells ...
... unique to cardiac myocytes and thought to arise in reperfusion from hypercontraction, which results in sarcolemmal rupture. It ... "Reperfusion injury as a therapeutic challenge in patients with acute myocardial infarction". Heart Fail Rev. 12 (3-4): 207-16. ... which is in excess due to ischemia. a calcium-independent mechanism, as seen in rigor mortis - activation of the contractile ... that span the short axis of the myocyte. They can be thought of extra thick striae, typical of cardiac muscle and striated ...
"Induction of apoptosis and Fas receptor/Fas ligand expression by ischemia/reperfusion in cardiac myocytes requires serine 727 ... inhibition of p38 mitogen-activated protein kinase antagonizes cardiac injury and cell death following ischemia-reperfusion in ... Inhibition of p38 MAPK activity confers cardioprotection against ischemia reperfusion injury in heart However, some reports ... protein kinase decreases cardiomyocyte apoptosis and improves cardiac function after myocardial ischemia and reperfusion". ...
... or during cell injury (such as ischemia-reperfusion injury during heart attacks and strokes) or during developments and ... most notably as part of the mitochondrial death pathway and cardiac myocyte apoptosis signaling. Programmed cell death is a ... In addition, VDAC3 has been implicated in cardioprotection against ischemia-reperfusion injury, such as during ischemic ... "Past and present course of cardioprotection against ischemia-reperfusion injury". Journal of Applied Physiology. 103 (6): 2129- ...
... or during cell injury (such as ischemia-reperfusion injury during heart attacks and strokes) or during developments and ... most notably as part of the mitochondrial death pathway and cardiac myocyte apoptosis signaling. Programmed cell death is a ... Most notably, Enodnuclease G is pivotal during oxidative stress by ischemia-reperfusion injury, specifically in the myocardium ... During ischemia reperfusion, ROS release substantially contribute to the cell damage and death via a direct effect on the cell ...
Polyketal nanoparticles have also been used in the infarcted mouse heart to prevent ischemia-reperfusion injury caused by ... Nox2 and NADPH oxidase combine to act as a major source of cardiac superoxide production, which in excess can lead to myocyte ... dismutase encapsulated in polyketal microparticles to rat myocardium and protection from myocardial ischemia-reperfusion injury ... SOD1-enacapsulated polyketal nanoparticles are able to scavenge reperfusion-injury induced ROS. Furthermore, this treatment ...
... or during cell injury (such as ischemia-reperfusion injury during heart attacks and strokes) or during developments and ... most notably as part of the mitochondrial death pathway and cardiac myocyte apoptosis signaling. Programmed cell death is a ... Most notably, SOD2 is pivotal in reactive oxygen species (ROS) release during oxidative stress by ischemia-reperfusion injury, ... In addition, SOD2 has been implicated in cardioprotection against ischemia-reperfusion injury, such as during ischemic ...
Transfection of cardiac myocytes with human HGF reduces ischemic reperfusion injury after MI. The benefits of HGF therapy ... after induced MI or ischemia. Transfection with HGF plasmids in damaged cardiac tissue also promotes angiogenesis (increased ... After MI, the myocardium suffers from reperfusion injury which leads to death of cardiomyocytes and detrimental remodelling of ... Yellon, D. M.; Hausenloy, D. J. (2007). "Myocardial Reperfusion Injury". New England Journal of Medicine. 357 (11): 1121-1135. ...
Sustained protection by acadesine against ischemia- and reperfusion-induced injury. Studies in the transplanted rat heart. ... In cardiac myocytes, acadesine is phosphorylated to AICAR to activate AMPK without changing the levels of the nucleotides. ... AICAR has been used clinically to treat and protect against cardiac ischemic injury. The drug was first used in the 1980s as a ... A brief period of coronary arterial occlusion followed by reperfusion prior to prolonged ischemia is known as preconditioning. ...
... manifests in ischemia (blood flow restriction to tissue) and reperfusion injury (damage occurring after ischemia when blood ... CsA (cyclosporin A) has been shown to decrease cardiac hypertrophy by affecting cardiac myocytes in many ways. CsA binds to ... clinical study in Europe to determine its ability to ameliorate neuronal cellular damage and reperfusion injury (phase III) in ... Decreasing intramitochondrial Ca2+ allows for reversal of cardiac hypertrophy caused in the original cardiac response. ...
"Roles of the nitric oxide signaling pathway in cardiac ischemic preconditioning against myocardial ischemia-reperfusion injury ... The delayed rectifier potassium ion current is largely responsible for the repolarization of ventricular cardiac myocytes by ... A major topic of research is the impact of hydrogen sulfide on reducing myocardial ischemia-reperfusion injury. Reperfusion ... Reperfusion triggers an inflammatory response and often results in oxidative damage. H2S decreases injury through many ...
The elevated serum aldosterone predisposes to arrhythmias triggered in a coronary artery ligation ischemia/reperfusion injury ... in human cardiac myocytes). similarly, KCNE3 was recently found to inhibit Kv4.2, and it is thought that this regulation ... Mazhari R, Nuss HB, Armoundas AA, Winslow RL, Marbán E (Apr 2002). "Ectopic expression of KCNE3 accelerates cardiac ... "MiRP1 forms IKr potassium channels with HERG and is associated with cardiac arrhythmia". Cell. 97 (2): 175-87. doi:10.1016/ ...
In ischemia, the major damage to the cardiac myocyte, due to hypoxia, is seen following the reperfusion of blood. High ... "Intracellular sodium accumulation during ischemia as the substrate for reperfusion injury". Circulation Research. 84 (12): 1401 ... F15845 is a cardiac drug proposed to have beneficial effects for the treatment of angina pectoris, arrhythmias and ischemia by ... In the cardiac myocyte, the persistent sodium current corresponds to the delayed inactivation of the major sodium channel ...
... of myocytes around the area of injury, which is not enough to restore function of cardiac muscle. However, this may be an ... "MRL mice fail to heal the heart in response to ischemia-reperfusion injury". Wound Repair and Regeneration. 13 (2): 205-8. doi: ... Cardiac myocyte renewal has been found to occur in normal adult humans, and at a higher rate in adults following acute heart ... MRL mice show the same amount of cardiac injury and scar formation as normal mice after a heart attack. However, recent studies ...
Yang FH, Pyle WG (Mar 2012). "Reduced cardiac CapZ protein protects hearts against acute ischemia-reperfusion injury and ... Huang X, Walker JW (Apr 2004). "Myofilament anchoring of protein kinase C-epsilon in cardiac myocytes". Journal of Cell Science ... JM Downey was the first to introduce the role of PKC in cardioprotection against ischemia-reperfusion injury in 1994,; this ... a role in cardioprotection from ischaemia and reperfusion injury". Cardiovascular Research. 88 (1): 83-92. doi:10.1093/cvr/ ...
"MRL mice fail to heal the heart in response to ischemia-reperfusion injury". Wound Repair and Regeneration. 13 (2): 205-8. doi: ... of myocytes around the area of injury, which is not enough to restore function of cardiac muscle. However, this may be an ... MRL mice show the same amount of cardiac injury and scar formation as normal mice after a heart attack.[84] However, recent ... "Evidence that human cardiac myocytes divide after myocardial infarction". The New England Journal of Medicine. 344 (23): 1750-7 ...
... ischemia followed by 24 to 72 hours of reperfusion leads to an increase in kir6.2 transcription in left ventricle rat myocytes ... Cardiac ischemia, as it slows the oxidation of fatty acids, causes an accumulation of acyl-CoA and induces KATP channel opening ... in mice has been shown to increase the basal level of injury compared to wild type mice. This baseline protection is believed ... Cardiac ischemia, while not always immediately lethal, often leads to delayed cardiomyocyte death by necrosis, causing ...
"Involvement of GADD153 and cardiac ankyrin repeat protein in cardiac ischemia-reperfusion injury". Experimental & Molecular ... adrenergic activation of the cardiac ankyrin repeat protein gene in cardiac myocytes". Gene. 297 (1-2): 1-9. doi:10.1016/s0378- ... Decreased expression of CARP in cardiac cells within the ischemic region was detected in a rat model of ischemic injury, and ... CARP, also known as Cardiac adriamycin-responsive protein or Cardiac ankyrin repeat protein is a protein that in humans is ...
... pressure overload and prevented myocardial ischemia/reperfusion injury in a mouse or pig model of ischemia/reperfusion. Muscle- ... "Cardiac myocyte follistatin-like 1 functions to attenuate hypertrophy following pressure overload". Proceedings of the National ... derived Fstl1 modulates vascular remodelling in response to injury. FSTL1 has been shown to have a pronounced ability as a ... "Therapeutic impact of follistatin-like 1 on myocardial ischemic injury in preclinical models". Circulation. 126 (14): 1728-38. ...
Heart-type Fatty Acid-Binding Protein (H-FABP) is a small cytoplasmic protein (15 kDa) released from cardiac myocytes following ... "Release of fatty acid-binding protein from isolated rat heart subjected to ischemia and reperfusion or to the calcium paradox ... The diagnostic potential of the biomarker H-FABP for heart injury was discovered in 1988 by Professor Jan Glatz (Maastricht, ... "Cloning and characterization of a novel cardiac-specific kinase that interacts specifically with cardiac troponin I". Journal ...
1999). "Cardiac myocytes rendered ischemia resistant by expressing the human adenosine A1 or A3 receptor". FASEB J. 12 (15): ... In a mouse model of infarction the A3 selective agonist CP-532,903 protected against myocardial ischemia and reperfusion injury ... "Cl-IB-MECA Reduces Ischemia/Reperfusion Injury in Mice by Activating the A3 Adenosine Receptor". The Journal of Pharmacology ... "The A3 adenosine receptor agonist CP-532,903 protects against myocardial ischemia/reperfusion injury via the sarcolemmal ATP ...
Ischemia-reperfusion injury of the appendicular musculoskeletal system. References[edit]. .mw-parser-output .reflist{font-size: ... myoglobin is not specific for the death of cardiac myocytes, and levels can be elevated in renal disease as well as damage to ... Chung MJ, Brown DL (July 2018). "Diagnosis of acute myocardial infarction.". In Brown DL (ed.). Cardiac Intensive Care-E-Book. ... Myoglobin is a sensitive marker for muscle injury, making it a potential marker for heart attack in patients with chest pain.[ ...
Both 4 h ischemia and ischemia followed by 24 h reperfusion caused a significant increase in lysophosphatidylcholine ... When these myocytes were pretreated with urocortin, the ischemia-induced increase in lysophosphatidylcholine concentration was ... Moreover, co-incubation of cardiac myocytes with urocortin, or the specific phospholipase A2 inhibitor bromoenol lactone, ... reduces the cytotoxicity produced by lysophosphatidylcholine or ischemia/reperfusion. Similarly, in the intact heart ex vivo we ...
... against myocardial ischemia-reperfusion (I-R) injury through suppression of autophagy. Murine myocardial cells that had ... Knockdown of miR-30a with a miR-30a inhibitor could reverse the anti-autophagy effect of Sal B against I-R injury. Furthermore ... These data suggest that miR-30a is involved in Sal B-mediated cardioprotection against I-R injury through the PI3K/Akt ... Urocortin inhibits Beclin1-mediated autophagic cell death in cardiac myocytes exposed to ischaemia/reperfusion injury. J Mol ...
7 compounds were then selected and tested in neonatal rat cardiac myocytes subjected to simulated I/R injury. Six compounds ... 7 compounds were then selected and tested in neonatal rat cardiac myocytes subjected to simulated I/R injury. Six compounds ... A) Isolated neonatal rat cardiac myocytes were subjected to 4 h of simulated ischemia followed by 2 h of simulated reperfusion ... M) Cell viability experiments in isolated neonatal cadiac myocytes subjected to simulated ischemia/reperfusion injury. (N) ...
The pH paradox in ischemia-reperfusion injury to cardiac myocytes. EXS. 1996;76:99-114.. View this article via: PubMed Google ... Inhibiting mitochondrial permeability transition pore opening at reperfusion protects against ischaemia-reperfusion injury. ... Myocardial ischemia-reperfusion injury: a neglected therapeutic target. Derek J. Hausenloy and Derek M. Yellon The Hatter ... Pathophysiology of myocardial reperfusion injury. After the onset of acute myocardial ischemia in patients with STEMI, timely ...
2006) Enhancing macroautophagy protects against ischemia/reperfusion injury in cardiac myocytes. J Biol Chem 281:29776-29787. ...
This brief review provides an overview of these pathways and interconnected cardiac repair mechanisms. ... Oxidative and nitrosative stress are primary contributors to the loss of myocardial tissue in insults ranging from ischemia/ ... reperfusion injury from coronary artery disease and heart transplantation to sepsis-induced myocardial dysfunction and drug- ... Oxidative and nitrosative stress are primary contributors to the loss of myocardial tissue in insults ranging from ischemia/ ...
... injury to the heart is accompanied by the upregulation and posttranslational modification of a number of proteins normally ... Blocking Cdk2 activity reduces apoptosis in cultured cardiac myocytes. Genetic or pharmacological inhibition of Cdk2 activity ... Cyclin-dependent kinase 2 signaling regulates myocardial ischemia/reperfusion injury J Mol Cell Cardiol. 2008 Nov;45(5):610-6. ... Ischemia/reperfusion (I/R) injury to the heart is accompanied by the upregulation and posttranslational modification of a ...
Abcc6-Deficient Mice Have Enhanced Cardiac Myocyte Apoptosis Following Ischemia Reperfusion Injury, But No Change in Cardiac ... We aimed to determine the effects of Abcc6 deficiency in a mouse model of cardiac ischemia-reperfusion (I/R) injury, using the ... B6-Abcc6-KO Mice Have Larger Infarcts Following Cardiac Ischemia Reperfusion Injury Compared With Controls. To determine the ... We tested the role of Abcc6 in response to cardiac ischemia-reperfusion (I/R) injury. ...
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. ... In the present study we assessed whether long-term exposure of myocytes to nontoxic ROS stress alone is sufficient to induce ... was required for ouabain-induced hypertrophy in cultured cardiac myocytes. ...
NFκB Activation Prevents Ischemia/Reperfusion Injury in Cardiac Myocytes Kenneth C. Klein, OMS II; Ryan R. Kahl, BA; Bethany ... The pathophysiology of ischemia-reperfusion (IR) injury is complex and involves the interplay of both proapoptotic and ... HL-1 cells were treated with NFκB inhibitors during reperfusion or during both ischemia and reperfusion. ... depletion in murine HL-1 cardiac myocytes, cells were subjected to 2 hours of simulated ischemia followed by 0.5 4 hours of ...
Increasing O-GlcNAc is protective against IR injury. Experimental cellular and animal models, and also human studies, have ... In this review we discuss how the principal mechanisms underlying tissue protection against IR injury and the associated ... O-GlcNAcylation seems to be an inherent adaptive cytoprotective response to IR injury that is activated by mechanical ... IR injury) associated with ischemic heart disease contributes significantly to morbidity and mortality. O-linked β-N- ...
The Long Noncoding RNA Hotair Regulates Oxidative Stress and Cardiac Myocyte Apoptosis during Ischemia-Reperfusion Injury. ... Revision of serum ALT upper limits of normal facilitates assessment of mild liver injury in obese children with non-alcoholic ... Deficiencies Result in Surrogate Pathways of Complement Activation in Novel Polygenic Lupus-like Models of Kidney Injury. ...
Role of Antioxidants in Hypoxia-Reoxygenation Injury in the Heart and in Cardiac Myocytes.- 19. The Role of Lipid Peroxidation ... The Role of Oxygen Free Radicals during the Course of Myocardial Ischemia/Reperfusion Injury: An Analysis and Critique.- 9. The ... Anthracycline-Enhanced Cardiac Oxygen Radical Metabolism.- 22. Contributions of Leukocytes to Vascular Injury and Thrombosis. ... Alterations of Glutathione Status during Myocardial Ischemia and Reperfusion.- 11. Alterations in Membrane Phospholipids, ...
Pretreatment with QSYQ protected against I/R-induced myocardial structural injury and improved cardiac hemodynamics, as ... on myocardial ischemia/reperfusion (I/R) injury through antioxidative stress and mitochondrial protection.Methods and results: ... and reperfusion (120 minutes). Cardiac functions were evaluated by echocardiogram and hemodynamics. Myocardial mitochondria ... Sprague Dawley rats were pretreated with QSYQ or saline for 7 days and subjected to ischemia (30 minutes occlusion of the left ...
... hormone-releasing hormone promotes survival of cardiac myocytes in vitro and protects against ischaemia-reperfusion injury in ... Our study suggests the possibility of therapeutic use of GHRH analogs for accelerating wound healing after traumatic injury, ... cardiac repair during myocardial infraction, and others (2, 9, 14-16). These findings, in combination with the well-documented ... Recent evidence also demonstrates that this neuropeptide can induce cardiac repair after myocardial infarction, by mechanisms ...
"S-Adenosylmethionine attenuates bile duct early warm ischemia reperfusion injury after rat liver transplantation, Molecular ... Rapid activation of neutral sphingomyelinase by hypoxia-reoxygenation of cardiac myocytes. Hernandez, O.M.; Discher, D.J.; ... Liver ischemia/reperfusion injury: processes in inflammatory networks-a review. Abu-Amara, M.; Yang, S.Y.; Tapuria, N.; Fuller ... S-Adenosylmethionine attenuates bile duct early warm ischemia reperfusion injury after rat liver transplantation. Tang, Yong; ...
Tumor necrosis factor alpha-induced apoptosis in cardiac myocytes: involvement of the sphingolipid signaling cascade in cardiac ... Attenuation of Ischemia/Reperfusion Injury in Rats by a Caspase Inhibitor. Hiroyuki Yaoita, Kazuei Ogawa, Kazuhira Maehara, ... Attenuation of Ischemia/Reperfusion Injury in Rats by a Caspase Inhibitor. Hiroyuki Yaoita, Kazuei Ogawa, Kazuhira Maehara and ... Attenuation of Ischemia/Reperfusion Injury in Rats by a Caspase Inhibitor. Hiroyuki Yaoita, Kazuei Ogawa, Kazuhira Maehara and ...
Enhancing macroautophagy protects against ischemia/reperfusion injury in cardiac myocytes. J Biol Chem. 2006;281 (40):29776- ... Enhancing macroautophagy protects against ischemia/reperfusion injury in cardiac myocytes. J Biol Chem 281:29776-29787, 2006. ... Sulfaphenazole protects heart against ischemia-reperfusion injury and cardiac dysfunction by overexpression of iNOS leading to ... 8. Chen M, Won D J, Krajewski S, and Gottlieb R A. Calpain and mitochondria in ischemia/reperfusion injury. J Biol Chem 277: ...
"Transient Receptor Potential Ankyrin 1 Activation within the Cardiac Myocyte Limits Ischemia-reperfusion Injury in Rodents". ... It has protective effects on cardiac tissue, and is used for research into the function of the TRPA1 receptor. JT-010 PF- ...
... a re-evaluation of the role of p53 in ischemia-reperfusion injury might be warranted. Stretch of cardiac myocytes has also been ... During ischemia-reperfusion in rodents and humans, 5% to 30% of cardiac myocytes in the area at risk undergo apoptosis within ... Fas pathway is a critical mediator of cardiac myocyte death and MI during ischemia-reperfusion in vivo. Am J Physiol Heart Circ ... These data suggest that cardiac myocyte apoptosis plays a critical role in the pathogenesis of ischemia-reperfusion injury. ...
Cardiac Myocyte-Specific Expression of Inducible Nitric Oxide Synthase Protects Against Ischemia/Reperfusion Injury by ... Transgenic ecSOD was localized to the sarcolemma and, notably, the cytoplasm of cardiac myocytes. Ischemia/reperfusion injury ... Halothane reduces reperfusion injury after regional ischaemia in the rabbit heart in vivo. British journal of anaesthesia ... Effect of sevoflurane preconditioning on ischaemia/reperfusion injury in the rat kidney in vivo. European journal of ...
... reperfusion) to the ischemic myocardium after an acute myocardial infarction is critical to the survival of non damaged .. ... Murphy E, Steenbergen C (2008) Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury. Physiol Rev 88 ... Ischemic reperfusion is a major cause of myocyte loss in the heart. Significant loss of cardiac myocytes after ischemia and ... non-ischemic myocytes from a phenomenon called "reperfusion injury". The term reperfusion injury describes a number of events ...
Primary cardiac myocytes exposed to ischemia reperfusion injury (IRI) and IPost were used as the experimental model. The ... and the generation of reactive oxygen species in primary cardiac myocytes exposed to IRI. Mechanistically, we found that Hes1- ... 25211226 - New redox-related arrows in the arsenal of cardiac disease treatment.. 3687356 - Experience with an automatic ... 1644086 - Prevalence of silent myocardial ischaemia during exercise stress testing. its relation .... ...
Q. B. Wu, H. T. Li, Y. Wu et al., "Protective effects of muscone on ischemia-reperfusion injury in cardiac myocytes," Journal ... It has cardiac effects and weak anti-inflammatory activity, may also cause excitation of the respiratory and central nerve ...
Ischemia/reperfusion (I/R) injury induces irreversible oxidative stress damage to the cardiac myocytes. Many studies have ... Propofol alleviates DNA damage induced by oxygen glucose deprivation and reperfusion via FoxO1 nuclear translocation in H9c2 ... revealed that propofol alleviates the important organelle-mediated injury from oxidative stress in vitro. However, it remains ...
Higenamine protects ischemia/reperfusion induced cardiac injury and myocyte apoptosis through activation of β2-AR/PI3K/AKT ... it can protect against myocyte apoptosis in ischemia/reperfusion injury [7], collagen-induced arthritis, and spinal cord injury ... Kosuge, T.; Yokota, M. Studies on cardiac principle of aconite root. Chem. Pharm. Bull. 1976, 24, 176-178. [Google Scholar] [ ... promotes M2 macrophage activation and reduces Hmgb1 production through HO-1 induction in a murine model of spinal cord injury. ...
Delivery of the Fstl1 gene to mice protected the heart from ischemia/reperfusion injury and reduced cardiac myocyte death, ... kinase enhances ischemia/reoxygenation-induced apoptosis in cultured cardiac myocytes and exaggerates reperfusion injury in ... A number of lines of evidence suggest that Fstl1 is secreted from cardiac myocytes. Cardiac myocyte cultures display ... Ischemia/reperfusion injury was performed 5 days after adenoviral injection. C, Quantification of infarction size of each ...
ISCHEMIA-REPERFUSION INJURY; MITRAL-VALVE REPAIR; HEART-FAILURE; ERYTHROID-DIFFERENTIATION; ENDOTHELIAL-CELLS; CARDIAC MYOCYTES ... The effect of heme on cardiac function was assessed in vitro, on primary cardiomyocytes and H9c2 myoblast cell line, and in ... Scavenging heme, Hx counteracts cardiac heme toxicity and preserves left ventricular function. Our data generate the rationale ... Intriguingly, Hx rescued contraction defects of heme-treated cardiomyocytes and preserved cardiac function in hemolytic mice. ...
During kidney transplantation ischemia reperfusion injury (IRI) occurs, which is a risk factor for acute kidney injury, delayed ... These grafts are associated with an increased sensitivity to IRI and decreased graft outcome due to prolonged ischemia and ... during or after ischemia. This review evaluates the different experimental strategies that have been investigated to prevent or ... Haematopoietic stem cells do not transdifferentiate into cardiac myocytes in myocardial infarcts. Nature. 2004;428(6983):664-8. ...
... , Ying Zhang, Hong Li, Qin Zhang, Xiao- ... Ischemia and reperfusion injury is a primary cause of cardiac failure, morbidity, and mortality after cardiac operations or ... Heart failure, ischemia/reperfusion injury and cardiac troponin. Adv Exp Med Biol 2007; 592: 191-200. ... and then induce cardiac myocytes damage in primary cultured neonatal rat cardiac myocytes. Astragaloside IV treatment could ...
  • Acute occlusion of the coronary artery in the STEMI patient subjects the myocardium supplied by that vessel to acute myocardial ischemia, thereby demarcating the area at risk (AAR) of potential MI, should the acute coronary occlusion be sustained or permanent. (
  • 6 The ATP depletion caused by ischemic hypoxia leads to production of the reactive oxygen species (ROS) during reperfusion, which exaggerates myocardium and endothelial cell injury. (
  • Background: The prompt restoration of blood flow (reperfusion) to the ischemic myocardium after an acute myocardial infarction is critical to the survival of non damaged heart tissue. (
  • As opposed to reducing the exposure of cardiomyocytes to injurious stimuli, apoptosis of these cells is attenuated through modulation of the caspase-related proapoptotic process, and this may allow ischemic myocardium to survive even after receiving significant injury. (
  • Numerous studies have studied the effect of halogenated agents on the myocardium, highlighting the beneficial cardiac effect of the pharmacological mechanism (preconditioning and postconditioning) when employed before and after ischemia in patients with ischemic heart disease. (
  • In 1986, Murry et al developed the first animal model to reveal a cardioprotective effect through ischemic preconditioning (PreC) with the performance of small episodes of sublethal ischemia, which subsequently decreased the amount of affected myocardium during prolonged interruptions in coronary flow, unlike the situation in those animals in which this maneuver was not performed. (
  • Both MI/R injury and diabetes mellitus elevated myocardium HDACs activity. (
  • In theory, quicker restoration of blood supply to the ischemic myocardium should reduce the extent of myocardial injury. (
  • However, inhibition of GRK2 activity with the peptide GRK2 inhibitor, ARKct, was cardioprotective, and resulted in less cell death and increased AKT signaling, with more viable myocardium and improved post-ischemic cardiac function. (
  • This study revealed that when the GRK2 protein is absent from heart cells, there is limited damage to the myocardium after ischemic injury, including decreased cell death. (
  • The results of these studies show that inhibiting GRK2 is a viable therapeutic approach that reduces acute ischemia injury to the myocardium, and is a strategy to limit acute myocardial ischemia. (
  • Buja LM, Burton KP, Hagler HK, Willerson JT (1983) Quantitative x-ray microanalysis of the elemental composition of individual myocytes in hypoxic rabbit myocardium. (
  • Many children undergoing cardiac surgery in the first year of life exhibit varying degrees of cyanotic heart disease where the myocardium is chronically perfused with hypoxic blood. (
  • Understanding the mechanisms by which cyanotic congenital heart disease modifies the myocardium and how that modification impacts on protective mechanics during ischemia may provide insight into developing treatments for limiting myocardial damage during surgery. (
  • Several studies indicated that Que, when given before ischemia (preconditioning), protects the myocardium from I/R injury through its antioxidant and anti-inflammatory activities ( 12 , 13 ). (
  • Postischemic reperfusion can result in further damage to the myocardium through an acute inflammatory response mediated by cytokines, neutrophils, macrophages, and reactive oxygen species. (
  • Moreover, ROS may also activate signal transducer and activator of transcription (STAT) 3 during I/R, which has been demonstrated to protect the myocardium from ischemia and oxidative stress through the upregulation of cardioprotective genes and the modulation of mitochondrial respiration ( 11 , 12 ). (
  • Cardiac myocyte size in the non-infarcted left ventricular myocardium was also increased following myocardial infarction. (
  • Cardioplegia arrest induces apoptotic signal cascades in endothelial cells and cardiac myocytes in the human myocardium [11, 12]. (
  • The timely restoration of blood flow to the ischemic myocardium (reperfusion) became the standard treatment for these patients. (
  • Increased expression of nerve growth factor (NGF) has been found in the myocardium suffered from ischemia and reperfusion (I/R). The pro-survival activity of NGF on ischemic heart has been supposed to be mediated by phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway. (
  • Unfortunately, restoring blood flow to the ischemic myocardium can also induce injury. (
  • All three NOS isoforms have been shown to be present in human myocardium 4 and may be activated in response to hypoxia or ischaemia. (
  • Intravenous injections of Hph1-PLCδ1 in rats with I/R-injured myocardium caused significant reductions in infarct size and apoptosis and also improved systolic and diastolic cardiac functioning. (
  • These data suggest that miR-30a is involved in Sal B-mediated cardioprotection against I-R injury through the PI3K/Akt signaling pathway. (
  • 18 ]. also reported that inhibition of the PI3K/Akt signaling pathway could abolish the effects of B-type natriuretic peptide on myocardial ischemia-reperfusion (I-R) injury. (
  • High fructose causes cardiac hypertrophy via mitochondrial signaling pathway. (
  • Conclusion- These data identify Abcc6 as a novel modulator of cardiac myocyte survival after I/R. This cardioprotective mechanism may involve inhibition of the BMP signaling pathway, which modulates apoptosis. (
  • Collectively, these findings demonstrate that within the heart GHRH-agonists can activate cardiac repair following MI, suggesting the existence of a potential signaling pathway based on GHRH in the heart. (
  • Male Sprague-Dawley rats were randomly allocated to 5 groups (20 animals/group): sham, I/R, Que postconditioning, Que+LY294002 [a phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway inhibitor], and LY294002+I/R. I/R was produced by 30-min coronary occlusion followed by 2-h reperfusion. (
  • Several studies have indicated that the PI3K/Akt signaling pathway plays a key role in cardiac protection against I/R injury ( 16 , 17 ). (
  • Furthermore, inhibition of the NLRP3 signaling pathway has been shown to protect against myocardial ischemic injury induced by coronary artery ligation ( 11 ). (
  • In summary, ICS II reduces hypoxic injury in H9c2 cells via the miR‑7‑5p/BTG2 axis and activation of the PI3K/Akt signaling pathway. (
  • Oxidative and nitrosative stress are primary contributors to the loss of myocardial tissue in insults ranging from ischemia/reperfusion injury from coronary artery disease and heart transplantation to sepsis-induced myocardial dysfunction and drug-induced myocardial damage. (
  • 7. Cardiac Defense Mechanisms against Oxidative Damage: The Role of Superoxide Dismutase and Glutathione-Related Enzymes. (
  • Pretreatment with QSYQ protected against I/R-induced myocardial structural injury and improved cardiac hemodynamics, as demonstrated by normalized serum creatine kinase and suppressed oxidative stress. (
  • Pretreatment of QSYQ in Sprague Dawley rats improves ventricular function and energy metabolism and reduces oxidative stress via ameliorating multiple mitochondrial dysfunctions during I/R injury. (
  • 4 Reperfusion causes cell damage and cell death mostly by initiating a localized oxidative burst and regional inflammatory response. (
  • Because diverse pathological factors, such as inflammation, oxidative stress, and apoptosis, contribute to the pathological mechanism underlying myocardial I/R (MI/R) injury, 9 - 13 most research efforts have been focused on interference with production of peroxide, 14 expression of adhesion molecules, 15 release of inflammatory factors, 16 , 17 and apoptosis of cardiac myocytes. (
  • We show that heme-mediated oxidative stress perturbs cardiac Ca2+ homeostasis and promotes contractile dysfunction. (
  • Ischemia/reperfusion (I/R) injury induces irreversible oxidative stress damage to the cardiac myocytes. (
  • Many studies have revealed that propofol alleviates the important organelle-mediated injury from oxidative stress in vitro. (
  • Ischemia reperfusion (I/R) injury is a common event following myocardial infarction (MI) resulting in excessive oxidative stress, calcium overload, inflammation, and cardiomyocyte death. (
  • Mitochondrial ROS production and oxidative mtDNA damage is increased during reoxygenation in the GPX1 knockout mice, in addition to structural abnormalities in cardiac mitochondria and myocytes, suggesting GPX1 may play an important role in protecting cardiac mitochondria from reoxygenation damage in vivo. (
  • Many cardiovascular diseases involve an increase in oxidative stress to the heart and blood vessels, including ischemic heart disease, reperfusion injury, heart failure and shock. (
  • Our long-term objective is to develop and test specific pharmacological treatments to protect the heart from oxidative stress injury (e.g. matrix metalloproteinase or nitric oxide synthase inhibitors, superoxide or peroxynitrite scavengers). (
  • During myocardial oxidative stress, the generation of ROS is enhanced and the defense mechanisms of myocytes are altered. (
  • The following aspects are covered: oxidative stress, mitochondrial dysfunction and pathophysiological mechanisms of atherosclerosis, precipitation of MI, sources of ROS in cardiac myocytes, effects of ROS in the heart, and ischemia and reperfusion injuries and their mechanisms. (
  • Oxidative stress serves important roles in cardiac injury during the process of ischemia/reperfusion (I/R). Y‑box protein 1 (YB1), a member of the highly conserved Y‑box protein family, is closely associated with inflammation and stress responses by regulating gene transcription, RNA splicing and mRNA translation. (
  • However, the roles of YB1 in oxidative stress‑induced myocardial‑I/R (M‑I/R) injury are unknown. (
  • Myocardial ischemia/reperfusion (MI/R) causes loss of cardiomyocytes via oxidative stress-induced cardiomyocyte apoptosis. (
  • Taxifolin treatment remarkably improved the cardiac function, regulated oxidative stress and attenuated apoptosis. (
  • In view of the unclear etiologies of AF and a potential role of oxidative stress, the present study examined cardiac reactive oxygen species production and NADPH oxidase (NOX) expression in AF patients. (
  • Considering the current opioid epidemic, I am currently focusing on the effect of chronic opioid exposure on endothelial and cardiac function. (
  • We have reported that physiological cardiac hypertrophy in Akt transgenic mice is dependent on vascular endothelial growth factor secretion and the coupling of coronary angiogenesis with myocyte growth. (
  • During ischemia and reperfusion, ROS can be produced by both endothelial cells and circulating phagocytes. (
  • Recent study has shown that apoptosis of coronary endothelial cells, which peaked at 1 h of reperfusion, precedes cardiac myocyte apoptosis in ischemia-reperfusion injury. (
  • 2 This suggests that reperfusion induces the release of soluble proapoptotic mediators from endothelial cells that promote myocyte apoptosis. (
  • Experimental studies with experimental rodent models and cultures (cardiac myocytes, endothelial cells) indicate that moderate alcohol exposure can promote anti-inflammatory processes involving adenosine receptors, protein kinase C (PKC), nitric oxide synthase, heat shock proteins, and others which could underlie cardioprotection. (
  • Neutrophil expression of CD18, malondialdehyde, inhibitor-kappa B alpha, myocardial infarction, endothelial expression of intercellular adhesion molecule 1, apoptosis-related proteins, and histological and ultrastructural evidence of myocardial damage were assessed after reperfusion. (
  • Treatment with HNG significantly increased phosphorylation of AMPK and phosphorylation of endothelial nitric oxide synthase in the heart and attenuated Bcl-2-associated X protein and B-cell lymphoma-2 levels following myocardial ischemia and reperfusion. (
  • Conclusion-: These data show that HNG provides cardioprotection in a mouse model of myocardial ischemia and reperfusion potentially through activation of AMPK-endothelial nitric oxide synthase-mediated signaling and regulation of apoptotic factors. (
  • Involvement of Na+/K+-ATPase in hydrogen peroxide-induced hypertrophy in cardiac myocytes. (
  • We have shown that increased production of reactive oxygen species (ROS) was required for ouabain-induced hypertrophy in cultured cardiac myocytes. (
  • In the present study we assessed whether long-term exposure of myocytes to nontoxic ROS stress alone is sufficient to induce hypertrophy. (
  • Redox sensitive signaling pathways in cardiac remodeling, hypertrophy and failure. (
  • Intracellular reactive oxygen species mediate the linkage of Na+/K+-ATPase to hypertrophy and its marker genes in cardiac myocytes. (
  • 1 Work from a number of laboratories has shown that cardiac-specific overexpression of modified forms of Akt1 or Akt3 will have different effects on heart phenotype ranging from mild hypertrophy and increased cardiac function to extensive hypertrophy associated with interstitial fibrosis and contractile dysfunction. (
  • Previously, we constructed a cardiac-specific inducible Akt1 transgenic mouse system that produces a physiological form of hypertrophy after short-term induction and a pathological form of hypertrophy after long-term induction. (
  • Specifically, the fetal gene program is predominant in a variety of pathophysiologic conditions including hypoxia, ischemia, hypertrophy, and atrophy. (
  • This is in line with the observations that inhibition of HDACs in cardiac myocytes silences fetal gene activation, attenuates cardiac hypertrophy, and prevents cardiac remodeling [ 16 , 17 ]. (
  • HCM is a disease characterized by myocardial hypertrophy, myocyte and myofibrillar disarray, as well as an increased risk of sudden death. (
  • In the present study, we aimed to investigate the function of miR-24 in cardiac hypertrophy by establishing a transverse aortic constriction (TAC) rat model, and miR-24 overexpressing in neonatal rat cardiac myocytes (NRCMs). (
  • Connexin expression is affected by age and gender as well as several pathophysiological alterations such as hypertension, hypertrophy, diabetes, hypercholesterolemia, ischemia, post-myocardial infarction remodeling or heart failure, and post-translationally connexins are modified by phosphorylation/de-phosphorylation and nitros(yl)ation which can modulate channel activity. (
  • Studies also indicate that TRPV1 is involved in the pathogenesis of cardiac hypertrophy and that TRPV2 channels participate in the pathogenesis of dilated cardiomyopathy. (
  • It is essential to restore coronary flow to the ischemic region (reperfusion), but if no additional measures are taken, reperfusion causes the production of reactive oxygen species (ROS), which can lead to substantial tissue death (reperfusion injury) [ 1 ]. (
  • Moreover, Hes1 inhibited the opening of mitochondrial permeability transition pore (mPTP) and the generation of reactive oxygen species in primary cardiac myocytes exposed to IRI. (
  • The formation of reactive oxygen species (superoxide and peroxynitrite) during early reperfusion, measured by electron spin resonance spectroscopy, was similar in nondiabetic WT and TG hearts, but it was significantly higher in diabetic TG hearts. (
  • Thus, providing additional endogenous NO is sufficient to protect nondiabetic hearts against ischemia-induced injury, but for a similar protection in diabetic hearts, effective scavenging of reactive oxygen species is also important. (
  • We have discovered that some of these reactive oxygen species mediate their damaging effects through activation of an enzyme called matrix metalloproteinase-2 (MMP-2) within the cardiac myocyte. (
  • Ischemia/reperfusion (I/R) injury in cardiomyocytes is related to excess reactive oxygen species (ROS) generation and can be modulated by nitric oxide (NO). We have previously shown that grape seed proanthocyanidin extract (GSPE), a naturally occurring antioxidant, decreased ROS and may potentially stimulate NO production. (
  • A further explanation for the dichotomous effects of NO may lie in its complex interaction with reactive oxygen species, which is particularly pertinent in the context of ischaemia-reperfusion. (
  • Thus, superoxide may be an important rate limiting factor determining the protective versus toxic effects of NO. 10 Although the interaction of NO with reactive oxygen species is very complex, this simple hypothesis may explain why, even though the majority of animal studies have shown cytoprotective effects 11-14 of NO against ischaemia-reperfusion injury, others have shown cytotoxicity. (
  • To elucidate the association between myocardial ischemia and inflammation, and to develop effective protective drugs, a rat model of myocardial ischemia was induced using isoproterenol (ISO) and an inflammation model in H9C2 cells was induced with lipopolysaccharide + adenosine triphosphate. (
  • We evaluated the effects of a potent analog of HN (HNG) in an in vivo murine model of myocardial ischemia and reperfusion. (
  • Urocortin protects cardiac myocytes from ischemia/reperfusion injury by attenuating calcium-insensitive phospholipase A2 gene expression. (
  • Sprague Dawley rats were pretreated with QSYQ or saline for 7 days and subjected to ischemia (30 minutes occlusion of the left anterior descending coronary artery) and reperfusion (120 minutes). (
  • Methods and Results -Sprague-Dawley rats were subjected to a 30-minute coronary occlusion followed by a 24-hour reperfusion. (
  • Diabetic rats were subjected to 45 min of ischemia, followed by 3 h of reperfusion. (
  • Growth hormone alone or combined with metoprolol preserves cardiac function after myocardial infarction in rats", Eur J Heart Fail, (2001) 3:651-660. (
  • Growth Hormone Attenuates Early Left Ventricular Remodeling and Improves Cardiac Function in Rats With Large Myocardial Infarction", J Am Coll/Cardio, (Apr. (
  • Growth Hormone Releasing Hormone (GHRH) Agonist Improves Cardiac Performance in the Chronic Model of Myocardial Infarction (MI) in Rats", Best of AHA Specialty Conferences Poster Session: BCVS 2010, Chicago, Illinois, Nov. 15, 2010 (Abstract). (
  • The results demonstrated that treatment with Sal B markedly alleviated the acute myocardial ischemic injury induced by hypodermic injection of ISO in rats. (
  • Interestingly, propofol, when applied at a clinically achievable high dose primarily during ischemia and the early phase of reperfusion followed by a relatively low dose during reperfusion, seems able to provide better cardiac protection against ischemia injury in hearts from middle-aged rats than from young rats. (
  • This study is aimed at investigating the effects of procyanidin on cardiomyocyte apoptosis of myocardial ischemia/reperfusion (I/R) injury in rats. (
  • Cardiotonic pills, a compound Chinese medicine, protects ischemia-reperfusion-induced microcirculatory disturbance and myocardial damage in rats. (
  • Male Sprague-Dawley rats were subjected to left coronary anterior descending branch occlusion for 30 min followed by reperfusion with or without pretreatment with CP (0.1, 0.4, or 0.8 g/kg). (
  • Cardiotonic pills, a compound Chinese medicine, protects ischemia-reperfusion-induced microcirculatory disturbance and myocardial damage in rats[J]. AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY,2010,298(4):H1166-H1176. (
  • Cardiac vanilloid receptor 1-expressing afferent nerves and their role in the cardiogenic sympathetic reflex in rats. (
  • Similarly, in the intact heart ex vivo we found that cardiac damage measured by infarct size was significantly increased when lysophoshatidylcholine was applied during ischemia, compared with ischemia alone, and that pre-treatment with both urocortin and bromoenol lactone reversed the increase in infarct size. (
  • Genetic or pharmacological inhibition of Cdk2 activity in vivo during I/R injury led to a 36% reduction in infarct size (IFS), when compared to control mice, associated with a reduction in apoptotic myocytes. (
  • 1 In coronary artery disease, the most effective therapy to reduce ischemic myocardial injury and infarct size is efficient myocardial reperfusion and early sustained restoration of blood flow (reperfusion) through the occluded coronary artery. (
  • 7 Animal studies have suggested that reperfusion injury is responsible for up to 50% of the final infarct size. (
  • In a rat model for myocardial reperfusion injury, infarct size and the appearance of presumed apoptotic cardiomyocytes were assessed in two groups that were or were not administered this protease inhibitor. (
  • At the end of reperfusion, myocardial infarct size and biochemical changes were compared. (
  • Inhibition of p38, c-Jun NH 2 -terminal kinases (JNK) and/or extracellular signal-regulated kinases (ERK) 1 and 2 (all three of which are MAPKs, namely MAPK 8, 3 and 1, respectively), may protect the heart from I/R injury by reducing cardiomyocyte death and infarct size, in addition to attenuating left ventricular function impairment, as demonstrated in M-I/R models ( 7 - 10 ). (
  • Intramyocardial injection of mimic-miR322 significantly diminished cardiac apoptosis (as determined by expression levels of active caspase 3 by Western blot analysis and immunostaining for TUNEL) and reduced infarct size by about 40%, in association with reduced FBXW7 and increased active Notch 1 levels in the ischemic hearts. (
  • In hearts isolated from wild type (WT) mice subjected to 30 minutes global I/R, LPI (10 μmol L −1 ) administered via the coronary circulation increased infarct size when applied prior to ischemia onset, but not when given at the time of reperfusion. (
  • The effects of CHD are usually attributable to the detrimental effects of acute myocardial ischemia-reperfusion injury (IRI). (
  • Engler RL, Dahlgren MD, Morris DD, Peterson MA, Schmid-Schonbein GW, Role of leukocytes in response to acute myocardial ischemia and reflow in dogs. (
  • Mitochondrial dysfunction plays a central role in mediating myocardial cell death by ischemia/reperfusion (IR). (
  • postulated that the LV protection by Mdivi-1 in cardiac I/R could be due to an improvement in mitochondrial dysfunction through attenuating excessive mitochondrial fission which then reduces apoptotic myocytes. (
  • GPX1 helps to prevent cardiac dysfunction after ischemia-reperfusion injuries. (
  • In acute myocardial infarction (AMI), two distinct types of damage occur to the heart: ischemic injury and reperfusion injury, which lead to mitochondrial dysfunction in heart cells. (
  • In other instances, as in the setting of hypertension or myocardial infarction, cardiac remodeling is maladaptive, predisposing to arrhythmia and contractile dysfunction. (
  • The reperfusion of ischemic tissues is often associated with microvascular dysfunction. (
  • Myocardial Ca 2+ overload induced by ischemia/reperfusion (I/R) is a major element of myocardial dysfunction in heart failure. (
  • Specifically we are interested in the roles of nitric oxide, superoxide and peroxynitrite in both cardiac and vascular injury relating to the activation of the immune system as well as in myocardial ischemia and reperfusion injury. (
  • The sources of ROS in cardiac myocytes could be mitochondrial electron transport chain, nitric oxide synthase (NOS), NADPH oxidase, xanthine oxidase, and lipoxygenase/cyclooxygenase and the auto-oxidation of various substances, particularly catecholamines. (
  • In this review we discuss how the principal mechanisms underlying tissue protection against IR injury and the associated immediate elevation of O-GlcNAc may involve attenuation of calcium overload, attenuation of mitochondrial permeability transition pore opening, reduction of endoplasmic reticulum stress, modification of inflammatory and heat shock responses, and interference with established cardioprotective pathways. (
  • To investigate the potential cardioprotective effects of QiShenYiQi Pill ® (QSYQ) on myocardial ischemia/reperfusion (I/R) injury through antioxidative stress and mitochondrial protection. (
  • Myocardial mitochondria were obtained to evaluate changes in mitochondrial structure and function, immediately after 120 minutes reperfusion. (
  • Hypoxia-inducible pro-death protein BNIP3 (BCL-2/adenovirus E1B 19-kDa interacting protein 3), provokes mitochondrial permeabilization causing cardiomyocyte death in ischemia-reperfusion injury. (
  • Suppression of HDACs activity triggered protective effects against MI/R and H/R injury under hyperglycemia conditions through Akt-modulated mitochondrial apoptotic pathways via Foxo3a/Bim. (
  • Importantly, however, it remains obscure whether the delay of mPTP opening is the direct consequence of modulation in the putative mPTP components by GSK-3 inhibition or secondary to reduction in mitochondrial injury. (
  • Mitochondrial homeostasis including their dynamics are imbalanced in cardiac I/R injury in favor of increased mitochondrial fission. (
  • Inhibition of mitochondrial fission prior to I/R injury is protective and improves cardiac function following MI. (
  • 2018) 132 , 1669-1683] examined the effect of inhibiting mitochondrial fission using the mitochondrial division inhibitor (Mdivi-1) at different time points, pre-ischemia, during-ischemia, and upon onset of reperfusion, in a rat cardiac I/R model. (
  • The findings showed the greatest cardiac function improvement with pre-ischemia treatment along with decreased mitochondrial fragmentation and increased mitochondrial function. (
  • Their findings provide new insights into future treatment of patients suffering acute MI which could consider targetting the excessive mitochondrial fission during cardiac ischemia or at onset of reperfusion. (
  • Energy stress, such as ischemia, induces mitochondrial damage and death in the heart. (
  • In conclusion, these findings indicated that Sal B exerted protective effects against myocardial ischemic injury by promoting mitophagy and maintaining mitochondrial function. (
  • Hence, TAX has a cardioprotective effect against I/R injury by modulating mitochondrial apoptosis pathway. (
  • Thus, we propose that mitochondrial GRK2 plays a detrimental role in cardiac glucose oxidation post-injury. (
  • These results suggest that Hph1-PLCδ1 may manifest as a promising cardioprotective drug due to its inhibition of the mitochondrial apoptotic pathway in cells suffering from I/R injury. (
  • There is evidence of early cardiac disease in PXE individuals deficient for ABCC6 12 , 13 and population studies have identified the common Arg1141X mutation as associated with coronary artery disease in a Dutch population. (
  • Although early reperfusion is essential for myocardial salvage, it induces reperfusion injury, which reduces the benefits of myocardial reperfusion ( 1 , 2 ). (
  • 1 Therefore, it might be hypothesized that this type of injury could be attenuated if a portion of the injured myocardial cells could be rescued from an apoptotic death. (
  • Whereas, both JI-38 and GH augmented levels of cardiac precursor cell proliferation, only JI-38 increased anti-apoptotic gene expression. (
  • After 2 h of reperfusion, apoptotic cardiac myocytes assumed a more homogeneous distribution around the vessels. (
  • Myocardial cell signaling pathways and apoptotic markers were assessed at various time points (0 to 24 hours) following reperfusion. (
  • This brief review provides an overview of these pathways and interconnected cardiac repair mechanisms. (
  • 11. Alterations in Membrane Phospholipids, Mechanisms of Free Radical Damage and Antioxidant Protection during Myocardial Ischemia and Reperfusion. (
  • Recent evidence also demonstrates that this neuropeptide can induce cardiac repair after myocardial infarction, by mechanisms involving a direct action on the cardiomyocytes ( 15 , 16 ). (
  • To identify factors with novel therapeutic applications in cardiac diseases, we focused on the identification of factors secreted from Akt1-activated cells that have cardioprotective effects through autocrine/paracrine mechanisms. (
  • 8 To elucidate the mechanisms by which Akt signaling regulates cardiac phenotype, we performed an Affymetrix microarray analysis on transgenic mouse hearts at different time points after Akt induction to identify differentially regulated transcripts. (
  • Over the last 30 years, our knowledge of the cardiac effects of various anesthetic drugs employed for patients undergoing heart surgery has helped us understand that the selection of hypnotic drug in the intraoperative and postoperative periods can (in addition to ensuring these patients' sedation) serve as cardioprotective therapy through various mechanisms. (
  • The purpose of this chapter is to discuss the potential mechanisms by which neutrophil-mediated inflammatory injury may complicate myocardial infarction. (
  • Rather, our goal is to describe mechanisms of reaction to injury and to present evidence suggesting that this secondary reaction might extend and complicate cardiac injury associated with ischemia. (
  • Hearse DJ, Bolli R. Reperfusion-induced injury: Manifestations, mechanisms and clinical relevance. (
  • The overall objective of my research program is to understand the mechanisms by which adaptation of the heart to chronic hypoxia increases resistance to subsequent ischemia. (
  • The current study investigated whether Que postconditioning has any protective effects on myocardial ischemia/reperfusion (I/R) injury in vivo and its potential cardioprotective mechanisms. (
  • Autophagy is activated by ischemia and nutrient starvation in the heart through Sirt1-FoxO- and adenosine monophosphate (AMP)-activated protein kinase (AMPK)-dependent mechanisms, respectively. (
  • Although several studies have been performed, the molecular mechanisms underlying myocardial ischemic injury remain unclear ( 3 , 4 ). (
  • Ischemia also causes alterations in the defense mechanisms against ROS. (
  • Among the mechanisms activated by cardiac stress and contributing to these remodeling events, recent work has pointed to cardiomyocyte autophagy as a major element. (
  • Therefore, understanding the underlying mechanisms of cardiac I/R injury is necessary for the development of novel therapeutic strategies for the prevention and treatment of this pathology. (
  • This study aimed to evaluate its effect and potential mechanisms on myocardial ischemia/reperfusion (I/R) injury. (
  • These data suggest that Cdk2 signaling pathways are critical regulators of cardiac I/R injury in vivo and support a cardioprotective role for Rb. (
  • Several pathways have been identified, including attenuation of NFκB activation and reduced expression of TNFα, IL-1, intracellular adhesion molecules, eNOS, the hypercontraction reduction that follows reperfusion, and antiapoptotic activating kinases (Akt, ERK1/2). (
  • Erythropoietin activates protein kinase signaling pathways and can increase resistance to cerebral ischemia. (
  • Longstanding evidence has linked the stimulation of lysosomal pathways to pathologic cardiac remodeling and a number of cardiac diseases, including heart failure and ischemia. (
  • The goal of the present study was to determine signaling pathways related to increased myocardial ZmRacD and to what extent hearts with increased ZmRacD proteins are susceptible to I/R injury. (
  • A number of new therapeutic strategies currently under investigation for preventing myocardial reperfusion injury have the potential to improve clinical outcomes in patients with acute MI treated with PPCI. (
  • IRI typically arises in patients presenting with an acute ST-segment elevation myocardial infarction (STEMI), in whom the most effective therapeutic intervention for reducing acute myocardial ischemic injury and limiting the size of myocardial infarction (MI) is timely and effective myocardial reperfusion using either thrombolytic therapy or primary percutaneous coronary intervention (PPCI). (
  • In this respect, myocardial reperfusion injury remains a neglected therapeutic target for cardioprotection in PPCI patients. (
  • 8 Thus, myocardial protection against I/R injury becomes a primary goal of therapeutic intervention. (
  • Here, we evaluated whether free heme directly affects cardiac function, and tested the therapeutic potential of replenishing serum Hx for increasing serum heme buffering capacity. (
  • We hypothesize that the electron transfer Complex I may be a part of the pore and may be regulated by Complex I. We have developed a cell-permeable therapeutic protein that can protect the heart against ischemia/reperfusion injury, and we plan to test its usefulness in additional model systems. (
  • Mesenchymal stem cells (MSCs) have therapeutic potential for the repair of myocardial injury. (
  • Myocardial ischemia reperfusion injury and cardioprotection in the presence of sensory neuropathy: therapeutic options , BRITISH JOURNAL OF PHARMACOLOGY 177: (23) pp. 5336-5356. (
  • These data identify FBXW7 as a direct target of miR322 and suggest that miR322 could have potential therapeutic application for cardioprotection against ischemia/reperfusion-induced injury. (
  • Therefore, the current review will focus on the importance of connexin 43 for irreversible injury of heart and brain tissues following ischemia/reperfusion and will highlight the importance of connexin 43 as an emerging therapeutic target in cardio- and neuroprotection. (
  • These data suggest that in the context of GSPE stimulation, Akt may help activate eNOS, leading to protective levels of NO. GSPE offers an alternative approach to therapeutic cardioprotection against I/R injury and may offer unique opportunities to improve cardiovascular health by enhancing NO production and increasing Akt-eNOS signaling. (
  • We have used Affymetrix gene chip technology to look for changes in gene expression caused by a 24 h exposure of rat primary neonatal cardiac myocytes to the cardioprotective agent urocortin. (
  • This study was designed to ascertain if miR-30a is involved in the cardioprotective actions of salvianolic acid B (Sal B) against myocardial ischemia-reperfusion (I-R) injury through suppression of autophagy. (
  • Conclusion: Platelet gel is cardioprotective to non- ischemic reperfused cardiac tissue after acute myocardial infarction and reperfusion. (
  • 1 The cardioprotective and antiapoptotic properties of Akt have been documented in cultured cardiac myocytes 2 and in myocardial ischemia/reperfusion and heart failure models. (
  • Astragaloside IV treatment could inhibit the PKCβ/Egr-1 pathway and protect against hypoxia/ reoxygenation-induced cardiac myocytes death, which contributes to improve our knowledge of mechanism in the cardioprotective function of Astragaloside IV. (
  • Many chemicals such as erythropoietin ( 4 ), adenosine (5), and hydrogen sulfide ( 6 ) are known to be cardioprotective when given at the onset of reperfusion, but none has been widely used. (
  • ENGLISH ABSTRACT: Introduction: The cardioprotective actions of the hormone melatonin against myocardial ischaemiareperfusion injury (IRI) are well-established. (
  • In fact, a number of compounds, including sevoflurane, cilostazol and selenium, have been demonstrated to have cardioprotective effects and to alleviate M-I/R injury by activating STAT3 signaling ( 13 - 15 ). (
  • We are investigating novel compounds that protect the heart from ischemia/reperfusion injury, even when given after ischemia, at the time of reperfusion. (
  • HNG or vehicle was administered IP 1 hour prior or at the time of reperfusion. (
  • However, the process of reperfusion can itself induce cardiomyocyte death, known as myocardial reperfusion injury, for which there is still no effective therapy. (
  • However, the myocardial reperfusion process can also induce further myocardial cell death, a phenomenon known as myocardial ischemia/reperfusion (I/R) injury. (
  • In the present study, we confirmed that hypoxia/reoxygenation could increase PKCβ and Egr-1 expression, and then induce cardiac myocytes damage in primary cultured neonatal rat cardiac myocytes. (
  • In patients with MI, the treatment of choice for reducing acute myocardial ischemic injury and limiting MI size is timely and effective myocardial reperfusion using either thombolytic therapy or primary percutaneous coronary intervention (PPCI). (
  • Methods and Results- To determine the role of Abcc6 in cardioprotection, we induced ischemic injury in mice in vivo by occluding the left anterior descending artery (30 minutes) followed by reperfusion (48 hours). (
  • Rossen RD, Swain JL, Michael LH, Weakley S, Giannini E, Entman ML. Selective accumulation of the first component of complement and leukocytes in ischemic canine heart muscle: A possible initiator of an extra myocardial mechanism of ischemic injury. (
  • Ischemic injury to the heart causes various types of cardiomyocyte death such as necrosis, apoptosis, or autophagy. (
  • These studies suggested that SIRT1-mediated mitophagy is a negative regulator of NLRP3 inflammasome activation ( 13 ) and could significantly protect against myocardial ischemic injury ( 14 ). (
  • However, whether salvianolic acid B (Sal B) could alleviate myocardial ischemic injury by promoting SIRT1-mediated mitophagy remains unclear. (
  • The purpose of this study was to investigate how reduced ASMase expression impacts retinal ischemic injury. (
  • Our results demonstrate that reducing ASMase expression provides partial protection from ischemic injury. (
  • 4 - 11 However, the roles of these molecules in retinal ischemic injury are unknown. (
  • NOS inhibition worsened reperfusion function in diabetic hearts. (
  • Recently, selective inhibition of classes I and II HDACs with an inhibitor, trichostatin A (TSA), showed protective effects against MI/R injury [ 15 ]. (
  • Furthermore, HDACs inhibition was recently reported to improve myocardial function and prevent cardiac remodeling in diabetic mice [ 18 ]. (
  • However, an important question remains: How does GSK-3 inhibition achieve cardioprotection against ischemia? (
  • Inhibition of GRK2 is protective against acute cardiac stres. (
  • PHILADELPHIA) Inhibition of a protein known to contribute to heart failure also appears to be protective of the heart in more acute cardiac stress injury, namely ischemia reperfusion, according to two studies conducted at the Center for Translational Medicine at Thomas Jefferson University. (
  • NF2 promotes I/R injury through the activation of Mst1 and inhibition of Yap, thereby regulating Hippo signaling in the adult heart. (
  • We are interested in Bid, a BH3-only protein that is proteolytically activated during ischemia/reperfusion and targets the mitochondria to initiate apoptosis. (
  • Mitophagy mediated through the Ulk1/Rab9/Rip1/Drp1 pathway protected the heart against ischemia by maintaining healthy mitochondria. (
  • therefore, the maintenance of a pool of healthy mitochondria is essential for sustaining normal cardiac performance. (
  • In addition to its role in down-regulating activated GPCRs, GRK2 also localizes to mitochondria both basally and post-IR injury, where it regulates cellular metabolism. (
  • We previously showed that phosphorylation of GRK2 at Ser670 is essential for the translocation of GRK2 to the mitochondria of cardiomyocytes post-IR injury in vitro and that this localization promotes cell death. (
  • When these myocytes were pretreated with urocortin, the ischemia-induced increase in lysophosphatidylcholine concentration was significantly lowered. (
  • MiR-30a is a member of the miR-30 family, which was identified significantly altered miRNAs in mice cardiac tissue with a model of myocardial I/R compared with normal cardiac tissue in our previous study. (
  • TUNEL positive nuclei and caspase-3 activity were augmented by 92% and 36%, respectively, following injury in the CRb(L/L) mice demonstrating that loss of Rb in the heart significantly exacerbates I/R injury. (
  • Ischemia reperfusion injury (IR injury) associated with ischemic heart disease contributes significantly to morbidity and mortality. (
  • Implementation of reperfusion modalities, including percutaneous coronary intervention and thrombolytic therapy, has significantly improved mortality and morbidity over the last 20 years [ 3 , 4 ]. (
  • Exposed under hypoxia/reoxygenation condition, the primary cultured neonatal rat cardiac myocytes viability was reduced significantly. (
  • During storage of the transplant, the temperature is reduced to approximately 4 °C. During this cold ischemia period, metabolism is significantly reduced which allows for prolonged preservation of the organ until transplantation. (
  • These approaches were also associated with significantly reduced plasma concentrations of cardiac troponin I, a sensitive marker for myocardial cellular damage. (
  • YB1 knockdown through transfection of small interfering RNA significantly aggravated cardiac cell apoptosis. (
  • Finally, YB1 knockdown, mediated by a lentivirus carrying YB1 targeted short hairpin RNA, significantly decreased left ventricle percentage fractional shortening and ejection fraction values, while increasing the infarct sizes in a rat model of M‑I/R injury. (
  • Moreover, miR322 levels were significantly reduced in the heart at 24 h after MI/R injury. (
  • NGF pretreatment significantly improved the recovery of post-ischemia cardiac hemodynamics. (
  • In ASMase +/− mice, retinal ischemia did not significantly alter ASMase activity, and the rise in ceramide levels were significantly reduced compared to levels in retinas from wild-type mice. (
  • Following 20-min global ischemia and 45-min reperfusion, postischemic cardiac contractile function and heart rate were significantly reduced in TG hearts compared with WT hearts. (
  • Importantly, acute regional myocardial I/R (30-min ischemia and 24-h reperfusion) caused significantly larger MI in TG mice compared with WT mice. (
  • The involvement of NO in cardiovascular biology has contributed significantly to our understanding of complex disease states including atherosclerosis, systemic and pulmonary hypertension, endotoxic shock, pre-eclampsia, 1 cardiomyopathy, 2 and cardiac allograft rejection. (
  • Myocardial ischemia activates Cdk2, resulting in the phosphorylation and inactivation of Rb. (
  • The activity of GSK-3β is decreased by ischemia because of phosphorylation of serine 9 through a phosphatidylinositol 3-kinase-dependent mechanism. (
  • These results demonstrated for the first time (to the best of our knowledge) that YB1 may protect cardiac myocytes against H2O2 or M‑I/R‑induced injury by binding to PIAS3 mRNA and resulting in the phosphorylation of STAT3. (
  • Attempts to reduce the extent of myocardial reperfusion injury have included lowering the risk posed by certain injurious factors and potentiating various aspects of cardioprotection relating to ischemic duration, 1 oxygen free radicals, 2 3 proinflammatory cytokines, 4 5 and preconditioning. (
  • Growth hormone-releasing hormone promotes survival of cardiac myocytes in vitro and protects against ischaemia-reperfusion injury in rat heart", Cardiovasc Res, (Mar. 17, 2009) 83:303-312. (
  • 15. Acute Effects of Antioxidants on in Vivo Models of Experimental Myocardial Ischemia and Infarction. (
  • Background -Z-Val-Ala-Asp(OMe)-CH 2 F (ZVAD-fmk), a tripeptide inhibitor of the caspase interleukin-1β-converting enzyme family of cysteine proteases, may reduce myocardial reperfusion injury in vivo by attenuating cardiomyocyte apoptosis within the ischemic area at risk. (
  • 6 In the present study, we investigated whether ZVAD-fmk lowers the extent of experimental myocardial reperfusion injury in vivo by attenuating cardiomyocyte apoptosis. (
  • The effect of heme on cardiac function was assessed in vitro, on primary cardiomyocytes and H9c2 myoblast cell line, and in vivo, in Hx(-/-) mice and in genetic and acquired mouse models of intravascular hemolysis. (
  • However, it is unclear whether Que postconditioning has a protective effect against myocardial I/R injury in vivo . (
  • In the present study, Que postconditioning was used as an adjuvant to attenuate myocardial I/R injury in an in vivo rat model. (
  • Recently erythropoietin has been observed to increase resistance of the heart to regional ischemia in vivo. (
  • In vivo, the serum levels of creatine kinase isoenzyme MB, glutamic oxaloacetic transaminase and IL‑1β, the cardiac function and the mRNA expression levels of NLR family pyrin domain‑containing 3 (NLRP3) inflammasome components were evaluated using ELISAs, an electrocardiogram, hematoxylin and eosin staining and reverse transcription‑quantitative PCR, respectively. (
  • However, these assays are based on cardiomyoblast cell lines or primary neonatal and adult cardiac myocytes [1] and thus have major limitations, including a low proliferation capacity, uncontrolled stress during cell isolation, low throughput, and poor predictability of the assays towards in vivo efficacy [2]. (
  • Additionally, it is not know the implications of those cellular effects on the in vivo cardiac electrophysiology profile. (
  • In vitro reversible myocardial I/R for postischemic cardiac function and in vivo regional myocardial I/R for MI were performed. (
  • Coronary blood flow, vascular diameter, velocity of red blood cells, and albumin leakage were evaluated in vivo after reperfusion. (
  • Mice deficient for NF2 in cardiomyocytes, NF2 cardiomyocyte-specific knockout (CKO), were protected against global I/R ex vivo and showed improved cardiac functional recovery. (
  • Moreover, NF2 cardiomyocyte-specific knockout mice were protected against I/R injury in vivo and showed the upregulation of Yap target gene expression. (
  • To confirm that Rb was the critical target in Cdk2-mediated I/R injury, we determined the consequences of I/R injury in cardiac-specific Rb-deficient mice (CRb(L/L)). IFS was increased 140% in CRb(L/L) mice compared to CRb+/+ controls. (
  • The spectrum of PXE has been noted in Abcc6 -deficient mice, including dystrophic cardiac calcification. (
  • There were no differences in cardiac calcification following I/R, but increased cardiac apoptosis was noted in Abcc6 -deficient mice. (
  • Consistent with this finding, BMP4 and BMP9 were increased and activin receptor-like kinase-2 and endoglin were downregulated in cardiac extracts from Abcc6 -deficient mice versus controls. (
  • Intriguingly, Hx rescued contraction defects of heme-treated cardiomyocytes and preserved cardiac function in hemolytic mice. (
  • Using mice overexpressing eNOS (transgenic genotype) and wild-type control mice with normal enzyme levels, we investigated the role of NO in diabetic cardiomyopathy in normoxic hearts and in hearts subjected to ischemia-reperfusion. (
  • In wild-type mice, ischemia produced a significant increase in retinal ASMase activity and ceramide levels. (
  • The exacerbation of tissue injury by LPI was not seen in hearts from GPR55 −/− mice or in the presence of Y-27632, confirming that injury is mediated via the GPR55/ROCK/p38 MAPK pathway. (
  • Methods and results-: Male C57BL6/J mice (8 to 10 week old) were subjected to 45 minutes of left coronary artery occlusion followed by a 24-hour reperfusion. (
  • Lefer, David J. / Acute humanin therapy attenuates myocardial ischemia and reperfusion injury in mice . (
  • Here, we showed that mice with a S670A knock-in mutation in endogenous GRK2 showed reduced cardiomyocyte death and better cardiac function post-IR injury. (
  • Background- The Akt protein kinase is an important mediator of cardiac myocyte growth and survival. (
  • Here we report that the activation of JNK by reoxygenation correlates with myocyte survival. (
  • Activation of autophagy during ischemia is essential for cell survival and maintenance of cardiac function. (
  • 1 In fact, animal research has since demonstrated that PQQ participates in a range of biological functions with apparent survival benefits, and that PQQ supplementation may also provide benefits related to cognitive, energy metabolism, immune and antioxidant functions, as well as help protect against cardiac ischemic events. (
  • The receptor for GHRH was detectable on myocytes supporting direct activation of cardiac signal transduction. (
  • Activation of growth hormone releasing hormone (GHRH) receptor stimulates cardiac reverse remodeling after myocardial infarction (MI)", Proc Natl Acad Sci USA, (Dec. 27, 2011), 109(2):559-563. (
  • Exposure of isolated cardiac myocytes to chronic hypoxia followed by reoxygenation results in the early activation of c-Jun N-terminal kinase (JNK) and death by apoptosis of approx. (
  • Although JNK activation has been described in a number of models of ischaemia/reperfusion, the contribution of JNK activation to cell fate has not been established. (
  • Activation of autophagy during reperfusion could be either protective or detrimental, depending on the experimental model. (
  • In addition, it has been reported that the occurrence of myocardial ischemia is often accompanied by severe inflammatory response ( 5 ) and activation of the NLR family pyrin domain-containing 3 (NLRP3) inflammasome ( 6 ). (
  • An overload of ROS may trigger the activation of mitogen-activated protein kinase (MAPK) signaling and aggravate lethal cellular processes, particularly during I/R injury. (
  • This study was aimed to investigate whether NGF induced heart protection against I/R injury includes a mechanism of attenuation of ER stress-induced myocardial apoptosis by activation of PI3K/Akt pathway. (
  • In this study we explored whether activation of the Rho kinase/ROCK/p38 MAPK pathway is responsible for LPI-induced extension of I/R injury. (
  • The knockout of the TRPV1 gene promotes increased tolerance of the isolated perfused heart to the impact of ischemia/reperfusion (I/R). However, activation of TRPV1 increases the resistance of the heart to I/R due to calcitonin gene-related peptide (CGRP) release from afferent nerve endings. (
  • It has also been documented that the activation of TRPV4 negatively affects the stability of cardiomyocytes to the H/R. The blockade of TRPV4 can be considered as a new approach to the prevention of I/R injury of the heart. (
  • The hearts were exposed to global ischemia for 30 min and reperfused for 60 min. (
  • The role of erythropoietin in conferring immediate cardioprotection in the setting of cardiac surgery in children, where the heart is subjected to global ischemia, is unknown. (
  • Hearts in I/R group were perfused with KHB for a 75-min of equilibration period followed by 30 min of global ischemia and 120 min of KHB reperfusion. (
  • Hearts in the NGF group accepted 45 min of euilibration perfusion and 30 min of NGF pretreatment (with a final concentration of 100 ng/ml in the KHB) before 30 min of global ischemia and 120 min of reperfusion. (
  • Knockdown of miR-30a with a miR-30a inhibitor could reverse the anti-autophagy effect of Sal B against I-R injury. (
  • In mouse hearts [ 11 ] and isolated rabbit hearts [ 12 ], autophagy can be induced by ischemia and enhanced further by reperfusion. (
  • Is autophagy part of the injury process or a repair response? (
  • Here, we show that mitophagy during myocardial ischemia was mediated predominantly through autophagy characterized by Rab9-associated autophagosomes, rather than the well-characterized form of autophagy that is dependent on the autophagy-related 7 (Atg) conjugation system and LC3. (
  • Knockin of Rab9 (S179A) abolished mitophagy and exacerbated the injury in response to myocardial ischemia, without affecting conventional autophagy. (
  • As an adaptive response mechanism, autophagy affords the cell the ability to avert the cytotoxic effects of damaged organelles and aggregated proteins during cellular stress, such as nutrient deprivation or ischemia. (
  • Is Autophagy in Response to Ischemia and Reperfusion Protective or Detrimental for the Heart? (
  • Autophagy is active in the heart at baseline and further stimulated under stress conditions including starvation, ischemia/reperfusion, and heart failure. (
  • Autophagy is strongly activated in the heart during reperfusion after ischemia. (
  • Astragaloside IV exerts beneficial effects on hypoxia/reoxygenation-induced cardiomyocyte injury. (
  • This study was designed to investigate the role of PKCβ/Egr-1 pathway in the protective effect of Astragaloside IV on hypoxia/reoxygenation injury. (
  • Recent researches suggest that ischemia/reperfusion- or hypoxia/reoxygenation-induced myocardial injury might be partly mediated by Egr-1 [ 11 - 13 ]. (
  • 2015) Doxycycline attenuates renal injury in a swine model of neonatal hypoxia-reoxygenation. (
  • To investigate its role, PLCδ1 was fused to Hph1, a cell-permeable protein transduction domain (PTD), and treated into rat neonatal cardiomyocytes and rat hearts under respective hypoxia-reoxygenation (H/R) and ischemia-reperfusion conditions. (
  • Based on the MMP-2 inhibitory tests using gelatin zymography, 7 compounds were then selected and tested in neonatal rat cardiac myocytes subjected to simulated I/R injury. (
  • It has protective effects on cardiac tissue, and is used for research into the function of the TRPA1 receptor. (
  • 3,4 Furthermore, phosphatidylinositol 3-kinase (PI3K)-Akt signaling plays important roles in cardiac tissue growth. (
  • Reperfusion injury occurs when ischaemic tissue is reperfused. (
  • Aikawa E, Whittaker P, Farber M, Mendelson K, Padera RF, Aikawa M, Schoen FJ (2006) Human semilunar cardiac valve remodeling by activated cells from fetus to adult: implications for postnatal adaptation, pathology, and tissue engineering. (
  • Nowadays, tissue injury induced by I/R is a major factor, which often cause death. (
  • At that time, they estimated that only "25% or less" of patients treated by thrombolysis had an optimal reperfusion, defined as a rapid, complete, and sustained coronary recanalization with adequate myocardial tissue perfusion. (
  • abstract = "The phospholipid l-α-lysophosphatidylinositol (LPI), an endogenous ligand for GPR55, is elevated in patients with acute coronary syndrome, and a GPR55 antagonist cannabidiol (CBD) reduces experimental ischemia/reperfusion (I/R) injury. (
  • Mdivi-1 given during ischemia and at onset of reperfusion also improved cardiac function, but to a lesser extent than pre-ischemia intervention. (
  • Ischemic postconditioning, defined as brief periods of ischemia and reperfusion (I/R) at the onset of reperfusion, has been shown to protect against lethal reperfusion injury in many species including humans ( 3 ). (
  • Increasing O-GlcNAc is protective against IR injury. (
  • Transfection of myocytes with JNK pathway interfering plasmid vectors or infection with adenoviral vectors support the hypothesis that JNK is protective. (
  • 14 ) reported a protective role for Que, when administered during reperfusion (postconditioning), in an isolated rat heart model. (
  • Here, we investigated the protective role of PLCδ1 against myocardial I/R injury through the regulation of Ca 2+ homeostasis. (
  • Ischemia/reperfusion (I/R) injury to the heart is accompanied by the upregulation and posttranslational modification of a number of proteins normally involved in regulating cell cycle progression. (
  • Many of the causal genes for inherited hypertrophic cardiomyopathy (HCM) encode for proteins involved in the proper function of the cardiac sarcomere. (
  • Some proteins, including heat-shock proteins, are overexpressed in conditions of ischemia/reperfusion and can protect from cardiac injury. (
  • Endoplasmic reticulum (ER) stress, which is activated initially as a defensive response to eliminate the accumulated unfolded proteins, has shown a critical involvement in the ischemia induced myocardial apoptosis. (
  • The lack of ATP during ischemia ceases function of the 3Na + -2K + ATPase, thereby exacerbating the intracellular Na + overload. (
  • As highly metabolic cells, cardiomyocytes maintain a high cellular store of phosphocreatine and adenosine triphosphate (ATP), which is required for continuous cardiac function. (
  • Our objective was to investigate the role of autologous platelet rich plasma or platelet gel prepared using nanosecond pulsed electric fields (nsPEFs) in improving left ventricular mechanical function after ischemic reperfusion. (
  • 5-8 In addition, overexpression of nuclear localization of a nuclear-targeted form of nonactivated Akt1 increases contractile function and protects myocytes from apoptosis. (
  • 8 Furthermore, it has been reported that the injection of Akt-transduced mesenchymal stem cells into infarcted rat hearts leads to an improvement in cardiac function that results from the release of paracrine factors from these cells rather than through their limited ability to fuse with or differentiate into myocytes. (
  • Scavenging heme, Hx counteracts cardiac heme toxicity and preserves left ventricular function. (
  • Four weeks after diabetes induction with streptozotocin (blood glucose ∼29 mM), isolated isovolumic heart function and cellular NO metabolites in response to brief normothermic ischemia-reperfusion were determined. (
  • Similarly, the transgene also improved reperfusion systolic and diastolic function in nondiabetic but not in diabetic hearts. (
  • During kidney transplantation ischemia reperfusion injury (IRI) occurs, which is a risk factor for acute kidney injury, delayed graft function and acute and chronic rejection. (
  • We propose that in failing heart muscle at a certain point the fetal gene program is no longer sufficient to support cardiac structure and function. (
  • In contrast, GH administration markedly elevated body weight, heart weight, circulating GH and IGF-I, but did not offset the decline in cardiac structure and function. (
  • It plays an adaptive role in the heart at baseline, thereby maintaining cardiac structure and function and inhibiting age-related cardiac abnormalities. (
  • Miller catheter was used to evaluate cardiac function. (
  • Effect of hypercholesterolemia on myocardial function, ischemia-reperfusion injury and cardioprotection by preconditioning, postconditioning and remote conditioning , BRITISH JOURNAL OF PHARMACOLOGY 174: (12) pp. 1555-1569. (
  • miR322, orthologous to human miR-424, was identified as an ischemia-induced angiogenic miRNA, but its cellular source and function in the setting of acute MI/R remains largely unknown. (
  • The improvement of NGF on recovery of cardiac function and alleviation of myocardial injury were completely abolished by K252a or LY294002. (
  • However, limited data are available regarding the mechanism of action of CP on myocardial function during ischemia-reperfusion (I/R) injury. (
  • Left ventricular function was evaluated at 1 week after ischemia using high-resolution, 2D echocardiography (VisualSonics Vevo 770). (
  • HNG therapy enhanced left ventricular ejection fraction and preserved postischemic left ventricular dimensions (end-diastolic and end-systolic), resulting in improved cardiac function. (
  • Increased abundance of GRK2 [G protein-coupled receptor (GPCR) kinase 2] is associated with poor cardiac function in heart failure patients. (
  • Damage introduced by ischemia reperfusion injury (IR injury) is pivotal in diseases such as coronary heart disease (CHD) and stroke, causing substantial mortality and morbidity [ 1 , 2 ]. (
  • However, reperfusion is responsible for additional myocardial damage. (
  • 1 In 2003, Zhao et al reported that brief episodes of ischemia-reperfusion conducted cyclically after a prolonged period of ischemia (but before starting the reperfusion) reduced the damage produced by the reperfusion, thanks to ischemic postconditioning (PostC). (
  • However, reperfusion itself has the potential to exacerbate myocardial damage, a phenomenon known as reperfusion injury. (
  • This leads to improved recovery from acute cardiac damage. (
  • The number of cells with such deposits was markedly increased after 30 min of ischemia (19%), as well as after 20 min of ischemia followed by reperfusion (17%), prior to the development of irreversible myocardial damage. (
  • These results indicate that sarcolemmal permeability increases during the early stage of myocardial injury due to ischemia or ischemiareperfusion and contributes to the development of myocardial damage. (
  • However, this abrupt reperfusion frequently results in deleterious secondary damage termed ischemia-reperfusion (I/R) injury ( 2 ). (
  • However, reperfusion may cause additional heart damage. (
  • The results provide evidence for the potential role of CP in preventing microcirculatory disturbance and myocardial damage following I/R injury. (
  • In a variable proportion of patients presenting with ST-segment elevation myocardial infarction, ranging from 5% to 50%, primary percutaneous coronary intervention achieves epicardial coronary artery reperfusion but not myocardial reperfusion, a condition known as no-reflow. (
  • Prompt referral for mechanical reperfusion by urgent primary percutaneous coronary intervention (PPCI) represents the pivotal step in the current management of ST-segment elevation myocardial infarction (STEMI) ( 1 ). (
  • Estimate of the number of patients (pts) receiving optimal reperfusion according to Thrombolysis In Myocardial Infarction (TIMI) flow grade, myocardial blush grade (MBG), and ST-segment resolution (STR) of 100 patients without cardiogenic shock treated by primary percutaneous coronary intervention (PPCI). (
  • Levels of lysophosphatidylcholine, a toxic metabolite of phospholipase A2, were lowered by 30% in myocytes treated with urocortin for 24 h and by 50% with the irreversible iPLA2 inhibitor bromoenol lactone compared with controls. (
  • Severe myocardial ischemia may result in a characteristic pattern of metabolic and ultrastructural changes ( 2 ), which can lead to irreversible injury. (
  • Fstl1 transcript was also upregulated in response to myocardial stresses including transverse aortic constriction, ischemia/reperfusion injury, and myocardial infarction. (
  • 17 These data indicate that the autocrine/paracrine effects of factors secreted from Akt-activated cells could play significant roles in cardiac growth and maintenance. (
  • Myocytes were then plated in 6-well dishes (1 × 10 6 cells/well) in a 5% CO 2 incubator and maintained in DMEM solution containing 20% fetal bovine serum/0.1 mM Brdu for an additional 72 h. (
  • We use a range of approaches including cell biology, organ physiology, biochemistry and molecular biology to understand the intracellular processes that determine whether the cardiac cells will survive and repair, or undergo programmed cell death through apoptosis or necrosis. (
  • Because cardiomyocytes persist in the heart for decades, it has been assumed that cells sustain direct injury that results in eventual cytotoxicity. (
  • However, in collaboration with Dr. Asa Gustafsson ( BioScience Center ), we now have evidence that anthracyclines cause early senescence of cardiac stem cells that are needed for life-long growth and repair, resulting in a limited ability of the heart to respond to physiologic stress. (
  • The major objective of this study was to determine whether urocortin, a member of the corticotrophin-releasing factor (CRF) family, protects adult rat cardiomyocytes from ischemia that has been simulated by glucose deprivation and acidosis. (
  • In normal cardiac myocytes, La 3+ was localized exclusively in the extracellular space. (
  • Transient receptor potential vanilloid channel 2 (TRPV2) is required for normal cardiac contractility. (
  • Warm ischemia occurs after the blood supply has been cut off while the organ is still in the donor. (
  • DCD donors do not develop the physiological changes of DBD donors, but suffer from prolonged warm ischemia times during cardiac arrest. (
  • A prolonged period of ischemia leads to death of cardiac myocyte (myocardial infarction). (
  • 6 7 8 9 10 It has been reported that apoptosis is a significant contributor to myocardial cell death as a result of reperfusion injury. (
  • 25 In intact animals, cardiac myocyte apoptosis occurs during myocardial infarction, 26-29 especially followed by reperfusion, 30,31 heart failure 32-38 and various cardiomyopathic states, 39 myocarditis, 40 and transplant rejection. (
  • 41 The strength of the data differ for these syndromes but are most compelling for ischemia-reperfusion injury and heart failure. (
  • We know that levels of GRK2 are increased in chronic heart failure, but studies have also shown that increases of GRK2 levels are one of the first changes observed after acute heart damages such as heart attack and ischemia," Dr. Koch said. (
  • Sci Rep, 2017), and pulmonary hypertension (Circulation, 2011), our most important translational accomplishments have focused on cell death in heart disease - specifically in the most common and lethal cardiac syndromes: myocardial infarction (heart attack) and heart failure. (
  • In animal models, GRK2 contributes to the pathogenesis of heart failure after ischemia-reperfusion (IR) injury. (
  • In patients with heart failure (HF), splanchnic hypoperfusion causes ischemia and intestinal edema, allowing bacterial translocation and bacterial metabolites to enter the blood circulation via an impaired intestinal barrier. (
  • Phosphodiesterase type 3A (PDE3A), but not type 3B (PDE3B), contributes to the adverse cardiac remodeling induced by pressure overload. (