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.
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.
Damage inflicted on the body as the direct or indirect result of an external force, with or without disruption of structural continuity.
A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (CORONARY ARTERY DISEASE), to obstruction by a thrombus (CORONARY THROMBOSIS), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (MYOCARDIAL INFARCTION).
The 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.
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 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)
NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).
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.
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.
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.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
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.
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.
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).
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
Elements of limited time intervals, contributing to particular results or situations.
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 dialdehyde of malonic acid.
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 circulation of blood through the CORONARY VESSELS of the HEART.
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.
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.
Injuries incurred during participation in competitive or non-competitive sports.
Penetrating and non-penetrating injuries to the spinal cord resulting from traumatic external forces (e.g., WOUNDS, GUNSHOT; WHIPLASH INJURIES; etc.).
The hollow, muscular organ that maintains the circulation of the blood.
Synthetic or natural substances which are given to prevent a disease or disorder or are used in the process of treating a disease or injury due to a poisonous agent.
The mitochondria of the myocardium.
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.
Solutions which, upon administration, will temporarily arrest cardiac activity. They are used in the performance of heart surgery.
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.
Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).
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 movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.
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.
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).
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 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).
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.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
Solutions used to store organs and minimize tissue damage, particularly while awaiting implantation.
Contractile activity of the MYOCARDIUM.
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.
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.
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)
Prolonged dysfunction of the myocardium after a brief episode of severe ischemia, with gradual return of contractile activity.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
The process by which chemical compounds provide protection to cells against harmful agents.
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.
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
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.
Enzymes of the transferase class that catalyze the conversion of L-aspartate and 2-ketoglutarate to oxaloacetate and L-glutamate. EC
An enzyme that catalyzes the conversion of L-alanine and 2-oxoglutarate to pyruvate and L-glutamate. (From Enzyme Nomenclature, 1992) EC
The act of constricting.
Non-human animals, selected because of specific characteristics, for use in experimental research, teaching, or testing.
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.
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.
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.
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.
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.
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.
Sulfhydryl acylated derivative of GLYCINE.
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.
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.
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 circulation of the BLOOD through the MICROVASCULAR NETWORK.
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.
10-carbon saturated monocarboxylic acids.
Organic compounds containing both the hydroxyl and carboxyl radicals.
Use of infusions of FIBRINOLYTIC AGENTS to destroy or dissolve thrombi in blood vessels or bypass grafts.
General or unspecified injuries involving the leg.
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)
The circulation of BLOOD through the LIVER.
Cell adhesion molecule and CD antigen that mediates the adhesion of neutrophils and monocytes to activated platelets and endothelial cells.
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).
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.
A XANTHINE OXIDASE inhibitor that decreases URIC ACID production. It also acts as an antimetabolite on some simpler organisms.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
Proteins involved in the transport of specific substances across the membranes of the MITOCHONDRIA.
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.
A partial or complete return to the normal or proper physiologic activity of an organ or part following disease or trauma.
The veins and arteries of the HEART.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Pathological processes of the LIVER.
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 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).
The transference of a part of or an entire liver from one human or animal to another.
Damage or trauma inflicted to the eye by external means. The concept includes both surface injuries and intraocular injuries.
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.
Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor.
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.
The section of the alimentary canal from the STOMACH to the ANAL CANAL. It includes the LARGE INTESTINE and SMALL INTESTINE.
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.
The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.
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.
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.
General or unspecified injuries to the neck. It includes injuries to the skin, muscles, and other soft tissues of the neck.
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.
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.
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.
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.
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.
A trisaccharide occurring in Australian manna (from Eucalyptus spp, Myrtaceae) and in cottonseed meal.
A ubiquitous stress-responsive enzyme that catalyzes the oxidative cleavage of HEME to yield IRON; CARBON MONOXIDE; and BILIVERDIN.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
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)
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.
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)
White blood cells. These include granular leukocytes (BASOPHILS; EOSINOPHILS; and NEUTROPHILS) as well as non-granular leukocytes (LYMPHOCYTES and MONOCYTES).
Examinations used to diagnose and treat heart conditions.
General or unspecified injuries involving organs in the abdominal cavity.
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.
Fibrinolysin or agents that convert plasminogen to FIBRINOLYSIN.
An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.
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.
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.
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.
The circulation of blood through the BLOOD VESSELS of the BRAIN.
General or unspecified injuries involving the arm.
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 statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.
Injuries resulting when a person is struck by particles impelled with violent force from an explosion. Blast causes pulmonary concussion and hemorrhage, laceration of other thoracic and abdominal viscera, ruptured ear drums, and minor effects in the central nervous system. (From Dorland, 27th ed)
General or unspecified injuries to the hand.
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.
General or unspecified injuries to the chest area.
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.
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.
The univalent radical OH. Hydroxyl radical is a potent oxidizing agent.
A vasodilator used in angina of effort or ischemic heart disease.
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)
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.
The property of blood capillary ENDOTHELIUM that allows for the selective exchange of substances between the blood and surrounding tissues and through membranous barriers such as the BLOOD-AIR BARRIER; BLOOD-AQUEOUS BARRIER; BLOOD-BRAIN BARRIER; BLOOD-NERVE BARRIER; BLOOD-RETINAL BARRIER; and BLOOD-TESTIS BARRIER. Small lipid-soluble molecules such as carbon dioxide and oxygen move freely by diffusion. Water and water-soluble molecules cannot pass through the endothelial walls and are dependent on microscopic pores. These pores show narrow areas (TIGHT JUNCTIONS) which may limit large molecule movement.
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.
Injuries involving the vertebral column.
A CALCIUM-dependent, constitutively-expressed form of nitric oxide synthase found primarily in ENDOTHELIAL CELLS.
The number of times the HEART VENTRICLES contract per unit of time, usually per minute.
Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.
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.
Injuries to the knee or the knee joint.
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.
The relationship between the dose of an administered drug and the response of the organism to the drug.
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).
Gases or volatile liquids that vary in the rate at which they induce anesthesia; potency; the degree of circulation, respiratory, or neuromuscular depression they produce; and analgesic effects. Inhalation anesthetics have advantages over intravenous agents in that the depth of anesthesia can be changed rapidly by altering the inhaled concentration. Because of their rapid elimination, any postoperative respiratory depression is of relatively short duration. (From AMA Drug Evaluations Annual, 1994, p173)
Dilation of an occluded coronary artery (or arteries) by means of a balloon catheter to restore myocardial blood supply.
Recording of the moment-to-moment electromotive forces of the HEART as projected onto various sites on the body's surface, delineated as a scalar function of time. The recording is monitored by a tracing on slow moving chart paper or by observing it on a cardioscope, which is a CATHODE RAY TUBE DISPLAY.
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
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)
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.
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.
Relatively complete absence of oxygen in one or more tissues.
A proteolytic enzyme in the serine protease family found in many tissues which converts PLASMINOGEN to FIBRINOLYSIN. It has fibrin-binding activity and is immunologically different from UROKINASE-TYPE PLASMINOGEN ACTIVATOR. The primary sequence, composed of 527 amino acids, is identical in both the naturally occurring and synthetic proteases.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
A subtype of ADENOSINE RECEPTOR that is found expressed in a variety of locations including the BRAIN and endocrine tissues. The receptor is generally considered to be coupled to the GI, INHIBITORY G-PROTEIN which causes down regulation of CYCLIC AMP.
Classification system for assessing impact injury severity developed and published by the American Association for Automotive Medicine. It is the system of choice for coding single injuries and is the foundation for methods assessing multiple injuries or for assessing cumulative effects of more than one injury. These include Maximum AIS (MAIS), Injury Severity Score (ISS), and Probability of Death Score (PODS).
The circulation of blood through the BLOOD VESSELS supplying the abdominal VISCERA.
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.
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 group of compounds that contain the general formula R-OCH3.
The urea concentration of the blood stated in terms of nitrogen content. Serum (plasma) urea nitrogen is approximately 12% higher than blood urea nitrogen concentration because of the greater protein content of red blood cells. Increases in blood or serum urea nitrogen are referred to as azotemia and may have prerenal, renal, or postrenal causes. (From Saunders Dictionary & Encyclopedia of Laboratory Medicine and Technology, 1984)
A tripeptide with many roles in cells. It conjugates to drugs to make them more soluble for excretion, is a cofactor for some enzymes, is involved in protein disulfide bond rearrangement and reduces peroxides.
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.
Compounds that selectively bind to and activate ADENOSINE A2 RECEPTORS.
Specialized phagocytic cells of the MONONUCLEAR PHAGOCYTE SYSTEM found on the luminal surface of the hepatic sinusoids. They filter bacteria and small foreign proteins out of the blood, and dispose of worn out red blood cells.
An azo dye used in blood volume and cardiac output measurement by the dye dilution method. It is very soluble, strongly bound to plasma albumin, and disappears very slowly.
General or unspecified injuries to the soft tissue or bony portions of the face.
General or unspecified injuries to the heart.
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.
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.
A form of ischemia-reperfusion injury occurring in the early period following transplantation. Significant pathophysiological changes in MITOCHONDRIA are the main cause of the dysfunction. It is most often seen in the transplanted lung, liver, or kidney and can lead to GRAFT REJECTION.
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.
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.
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.
A subclass of adenosine A2 receptors found in LEUKOCYTES, the SPLEEN, the THYMUS and a variety of other tissues. It is generally considered to be a receptor for ADENOSINE that couples to the GS, STIMULATORY G-PROTEIN.
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.
An endogenous 105-kDa plasma glycoprotein produced primarily by the LIVER and MONOCYTES. It inhibits a broad spectrum of proteases, including the COMPLEMENT C1R and the COMPLEMENT C1S proteases of the CLASSICAL COMPLEMENT PATHWAY, and the MANNOSE-BINDING PROTEIN-ASSOCIATED SERINE PROTEASES. C1-INH-deficient individuals suffer from HEREDITARY ANGIOEDEMA TYPES I AND II.
One of the three polypeptide chains that make up the TROPONIN complex. It inhibits F-actin-myosin interactions.
A subfamily of the Muridae consisting of several genera including Gerbillus, Rhombomys, Tatera, Meriones, and Psammomys.
Drugs used to cause dilation of the blood vessels.
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)
Inorganic or organic salts and esters of nitric acid. These compounds contain the NO3- radical.
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.
Heterocyclic compounds in which an oxygen is attached to a cyclic nitrogen.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
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.
The main structural component of the LIVER. They are specialized EPITHELIAL CELLS that are organized into interconnected plates called lobules.
Streptococcal fibrinolysin . An enzyme produced by hemolytic streptococci. It hydrolyzes amide linkages and serves as an activator of plasminogen. It is used in thrombolytic therapy and is used also in mixtures with streptodornase (STREPTODORNASE AND STREPTOKINASE). EC 3.4.-.
A photographic fixative used also in the manufacture of resins. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), this substance may reasonably be anticipated to be a carcinogen (Merck Index, 9th ed). Many of its derivatives are ANTITHYROID AGENTS and/or FREE RADICAL SCAVENGERS.
A glycogen synthase kinase that was originally described as a key enzyme involved in glycogen metabolism. It regulates a diverse array of functions such as CELL DIVISION, microtubule function and APOPTOSIS.
A derivative of the NIACINAMIDE that is structurally combined with an organic nitrate. It is a potassium-channel opener that causes vasodilatation of arterioles and large coronary arteries. Its nitrate-like properties produce venous vasodilation through stimulation of guanylate cyclase.
General or unspecified injuries to the posterior part of the trunk. It includes injuries to the muscles of the back.
A class of cell surface receptors that prefer ADENOSINE to other endogenous PURINES. Purinergic P1 receptors are widespread in the body including the cardiovascular, respiratory, immune, and nervous systems. There are at least two pharmacologically distinguishable types (A1 and A2, or Ri and Ra).
A potentially lethal cardiac arrhythmia that is characterized by uncoordinated extremely rapid firing of electrical impulses (400-600/min) in HEART VENTRICLES. Such asynchronous ventricular quivering or fibrillation prevents any effective cardiac output and results in unconsciousness (SYNCOPE). It is one of the major electrocardiographic patterns seen with CARDIAC ARREST.
Abnormal fluid accumulation in TISSUES or body cavities. Most cases of edema are present under the SKIN in SUBCUTANEOUS TISSUE.
Traumatic injuries to the cranium where the integrity of the skull is not compromised and no bone fragments or other objects penetrate the skull and dura mater. This frequently results in mechanical injury being transmitted to intracranial structures which may produce traumatic brain injuries, hemorrhage, or cranial nerve injury. (From Rowland, Merritt's Textbook of Neurology, 9th ed, p417)
"Phosphorylation of GSK-3β mediates intralipid-induced cardioprotection against ischemia/reperfusion injury". Anesthesiology. ... reperfusion, and activation of the reperfusion injury salvage kinase pathway (RISK). The mitochondrial accumulation of ... Myocardial damage with the resumption of blood flow after an ischemic event is termed "reperfusion injury". The mitochondrial ... Perrelli MG, Pagliaro P, Penna C (June 2011). "Ischemia/reperfusion injury and cardioprotective mechanisms: Role of ...
Sustained protection by acadesine against ischemia- and reperfusion-induced injury. Studies in the transplanted rat heart. ... 5-Aminoimidazole-4-carboxamide-1- β - d -ribofuranoside Increases Myocardial Glucose Uptake during Reperfusion and Induces Late ... "MECHANISMS OF ADENOSINE MONOPHOSPHATE-ACTIVATED PROTEIN KINASE-INDUCED PRECONDITIONING IN ISCHEMIA/REPERFUSION." Department of ... AICAR has been used clinically to treat and protect against cardiac ischemic injury. The drug was first used in the 1980s as a ...
[email protected] nanozyme was developed to treat reperfusion-induced injury in ischemic stroke. Peroxidase-like activity of Fe3O4 was ... "Highly bioactive zeolitic imidazolate framework-8-capped nanotherapeutics for efficient reversal of reperfusion-induced injury ... The same year, 2014, it was reported that a carboxylated fullerene (C3) was neuroprotective post-injury in an in-vivo primate ... preventing retinal degeneration induced by intracellular peroxides (toxic reactive oxygen intermediates). This was seen as ...
SOD1-enacapsulated polyketal nanoparticles are able to scavenge reperfusion-injury induced ROS. Furthermore, this treatment ... Polyketal nanoparticles have also been used in the infarcted mouse heart to prevent ischemia-reperfusion injury caused by ... dismutase encapsulated in polyketal microparticles to rat myocardium and protection from myocardial ischemia-reperfusion injury ...
"Atorvastatin protects against ischemia-reperfusion injury in fructose-induced insulin resistant rats". Cardiovascular Drugs and ... "Synthesis and pharmacological evaluation of novel arginine analogs as potential inhibitors of acetylcholine-induced relaxation ...
Zheng YQ, Liu JX, Wang JN, Xu L (2006). "Effects of crocin on reperfusion-induced oxidative/nitrative injury to cerebral ... 2006). "Protective effects of carotenoids from saffron on neuronal injury in vitro and in vivo". Biochim Biophys Acta. 1770 (4 ...
During normal embryologic processes, or during cell injury (such as ischemia-reperfusion injury during heart attacks and ... Bcl10 has been shown to induce apoptosis and to activate NF-kappaB. This protein is reported to interact with other CARD domain ... Accordingly, these processes regulating apoptosis during clinical processes such as cancer and ischemia-reperfusion injury. ... BinCARD has reportedly suppressed NF-kappa B activation induced by BCL10 hereby decreasing the amounts of phosphorylated Bcl10 ...
"Exercise-induced overexpression of angiogenic factors and reduction of ischemia/reperfusion injury in stroke". Current ... This induces a release of proteolytic enzymes from the vasculature. These enzymes target a particular point on the blood vessel ... Application of specific compounds that may inhibit or induce the creation of new blood vessels in the body may help combat such ... Growth factors such as bFGF and VEGF can induce capillary growth into the tumor, which some researchers suspect supply required ...
Injury to the myocardium also occurs during re-perfusion. This might manifest as ventricular arrhythmia. The re-perfusion ... These symptoms are likely induced by a massive surge of catecholamines from the sympathetic nervous system, which occurs in ... Kloner R, Hale SL (15 September 2016). "Reperfusion Injury: Prevention and Management". In Morrow DA (ed.). Myocardial ... Buja LM (July 2005). "Myocardial ischemia and reperfusion injury". Cardiovascular Pathology. 14 (4): 170-5. doi:10.1016/j. ...
... protecting against ischaemia-reperfusion injury, and doxorubicin-induced cardiomyopathy. Carnosine demonstrated neuroprotective ...
... vascular ischemia-reperfusion injuries to various organs including the heart and hind limb; allograph Transplant rejection of ... acid-induced lung injury, cystic fibrosis, pleurisy, brain inflammation and the inflammatory component of Alzheimer's disease; ... "Emerging roles of pro-resolving lipid mediators in immunological and adaptive responses to exercise-induced muscle injury". ... "Lipoxin A4-induced heme oxygenase-1 protects cardiomyocytes against hypoxia/reoxygenation injury via p38 MAPK activation and ...
The deletion of p66SHC also protects from ischemia/reperfusion brain injuries through blunted production of free radicals.[14] ... When protein kinase C is induced by hyperglycemia, p66SCH is induced which then leads to oxidative stress. When the coagulated ... induced apoptosis - mediating steroid action through the redox signaling pathway. P52SHC and p66SHC have been found in steroid ... A rise in p66SHC promotes stress induced apoptosis.[8] p66SHC functionally is also involved in regulating oxidative and stress ...
... and renal injury induced by ischemia-reperfusion". Journal of the American Society of Nephrology. 15 (8): 2152-60. doi:10.1097/ ... and cardiac damage induced by oxidative stress and ischemia-reperfusion". The Journal of Pharmacology and Experimental ...
Zheng YQ, Liu JX, Wang JN, Xu L (2006). "Effects of crocin on reperfusion-induced oxidative/nitrative injury to cerebral ... traumatic brain injury, spinal cord injury, and acute management of neurotoxin consumption (i.e. methamphetamine overdoses). ... Herrera-Mundo N, Sitges M (2013). "Vinpocetine and α-tocopherol prevent the increase in DA and oxidative stress induced by 3- ... Caffeine induces neuronal glutathione synthesis by promoting cysteine uptake, leading to neuroprotection. More neuroprotective ...
Platelets protect against myocardial dysfunction and injury induced by ischemia and reperfusion in isolated rat hearts. ... Mehta's thesis topic was "studies on experimental myocardial reperfusion" which he completed under the direction of Prof. Tom ... Critical role of AT1 receptor expression after ischemia-reperfusion in isolated rat hearts: Beneficial effect of antisense ... Small concentrations of oxLDL induce capillary tube formation from endothelial cells viaLOX-1- dependent redox-sensitive ...
Succinate accumulation under hypoxic conditions has been implicated in the reperfusion injury through increased ROS production ... High concentrations of succinate will mimic the hypoxia state by suppressing PHDs, therefore stabilizing HIF1α and inducing the ... In animal models, pharmacological inhibition of ischemic succinate accumulation ameliorated ischemia-reperfusion injury. As of ... a new therapeutic target for myocardial reperfusion injury". Cardiovascular Research. 111 (2): 134-141. doi:10.1093/cvr/cvw100 ...
Zheng, Pengfei (2017-02-20). "Plin5 alleviates myocardial ischaemia/reperfusion injury by reducing oxidative stress through ... Medium and high concentrations of ROS can induce apoptosis and eventually cause necrosis through oxidative stress. PLIN ... deficiency in PLIN5 initiates excessive phosforilation of PI3K/Akt which contributes to ischemia-reperfusion injury aggravation ...
PKCδ has been implicated in depressing cardiac function and cell death after ischemia-reperfusion injury as well as promoting ... "Mitochondrial kinase signalling pathways in myocardial protection from ischaemia/reperfusion-induced necrosis". Cardiovasc. Res ... have been reported to have cardio-protective effects after ischemic-reperfusion injury. There were reductions in mitochondrial ... protects the heart against ischemia-reperfusion injury". Pflügers Arch. 457 (5): 979-988. doi:10.1007/s00424-008-0583-5. PMID ...
... protonophore uncoupler capable of protecting mammals from acute renal ischemic-reperfusion injury and cold-induced microtubule ... "Mitochondrial uncoupler BAM15 reverses diet-induced obesity and insulin resistance in mice". nature. Retrieved 16 June 2020. ...
... sulfate glycosaminoglycan mimetic improves pressure ulcer healing in a rat model of cutaneous ischemia-reperfusion injury. ... 2008 Mar-Apr;16(2):294-9. Morvan et al, An engineered biopolymer prevents mucositis induced by 5-fluorouracil in hamsters. Am J ... After injury, the extracellular matrix, and thereby also the heparan sulfate is broken down by different local enzymes, ... Blanquaert et al, Heparan like molecules induce the repair of skul defects. Bone 1995;17(6):499-506. Lazarus et al, Definitions ...
... may also help to reduce reperfusion injury, damage caused by oxidative stress when the blood ... Polderman, Kees H (2008). "Induced hypothermia and fever control for prevention and treatment of neurological injuries". The ... "Hypophosphatemia and hypomagnesemia induced by cooling in patients with severe head injury". J Neurosurg. 94 (5): 697-705. doi: ... This is done in an attempt to reduce the risk of tissue injury following lack of blood flow. Periods of poor blood flow may be ...
"Effect of low-level laser therapy on lung injury induced by hindlimb ischemia/reperfusion in rats". Lasers in Medical Science ... "Low-level light therapy induces mucosal healing in a murine model of dextran-sodium-sulfate induced colitis". Photomedicine and ... Lim, Jinhwan (2010-05-03). "Effects of low-level light therapy on streptozotocin-induced diabetic kidney". Journal of ... Kaya, Göksel Şimşek (2011-06-01). "The use of 808-nm light therapy to treat experimental chronic osteomyelitis induced in rats ...
... protects the isolated rat heart from the myocardial injuries produced by ischemia and reperfusion. Planta Med, 1993 ... A higher dose of 1980 mg per day has no effect, which is possibly due to the oxidative stress that is induced by flavonoids in ... Kwon, J.T., et al., Effects of Cyclobuxine D on Drug-induced Contractions of the Isolated Rat Uterine Muscle and Potassium- ... Cyclobuxine was in this way able to suppress the damage (myocardial injury) produced by ischemia. As indicated above, research ...
In studies of mice models, a high-fat diet can induce greater injury to the kidney with renal ischemia-reperfusion as compared ... "Renal ischemia/reperfusion injury; from pathophysiology to treatment". Journal of Renal Injury Prevention. 4 (2): 20-27. doi: ... Researchers have found that IL-17C is activated in kidney injury. In hypoxia-induced studies of mice, an upregulation of the ... EGF- lower levels of EGF mRNA and proteins in the kidneys are indicative of injury after kidney ischemia and reperfusion. KIM-1 ...
... causing a one hundredfold increase in catalytic activity in treatment of ischemia-reperfusion injuries. M40401 was also found ... mimetic properties protects lungs from radiation-induced injury". Free Radical Biology and Medicine 33 (6): 857-63. Retrieved ... "A metalloporphyrin superoxide dismutase mimetic protects against paraquat-induced endothelial cell injury, in vitro". J ... Researchers found MnTBAP reversed obesity and induced faster wound healing in diabetic mice. MnTBAP has the ability to prevent ...
Cavar I (2011). "Anti-thromboxane B2 antibodies protect against acetaminophen-induced liver injury in mice". Journal of ... such as ischemia-reperfusion injury., hepatic inflammatory processes, acute hepatotoxicity etc. TxB2, a stable degradation ... "Effects of selective cyclooxygenase inhibitors on ischemia/reperfusion-induced hepatic microcirculatory dysfunction in mice". ... High-dose naproxen can induce near-complete suppression of platelet thromboxane throughout the dosing interval and appears not ...
Thus, cyclophilins may function in cardioprotection during ischemia-reperfusion injury. Currently, cyclophilin expression is ... Studies have shown that PPID protects human keratinocytes from UVA-induced apoptosis, so medication and therapies that inhibit ... such as ischemic reperfusion injury, AIDS, and cancer. Like other cyclophilins, PPID forms a β-barrel structure with a ... Jandova J, Janda J, Sligh JE (Mar 2013). "Cyclophilin 40 alters UVA-induced apoptosis and mitochondrial ROS generation in ...
He also found that prevention of LPC accumulation can protect heart from ischemia/reperfusion injury. In 1997 Ehsan Hoque was ... induced cardiac injury. As a young boy, Hoque was constantly bullied for wearing heavy eyeglasses and taking longer to do ... concentrating on ischemic reperfusion injury of the heart, and neuroendocrinology with a focus on aging. Hoque has published ... Dilazep attenuates lysophosphatidylcholine-induced mechanical and metabolic derangements in the isolated, working rat heart". ...
Ischemia reperfusion injuryEdit. Succinate accumulation under hypoxic conditions has been implicated in the reperfusion injury ... HIF1 is known to induce transcription of more than 60 genes, including genes involved in vascularization and angiogenesis, ... In animal models, pharmacological inhibition of ischemic succinate accumulation ameliorated ischemia-reperfusion injury.[29] As ... a new therapeutic target for myocardial reperfusion injury". Cardiovascular Research. 111 (2): 134-141. doi:10.1093/cvr/cvw100 ...
Cavar I (2011). "Anti-thromboxane B2 antibodies protect against acetaminophen-induced liver injury in mice". Journal of ... Ito Y (2003). "Effects of selective cyclooxygenase inhibitors on ischemia/reperfusion-induced hepatic microcirculatory ... such as ischemia-reperfusion injury.,[2] hepatic inflammatory processes,[3] acute hepatotoxicity [4] etc. TxB2, a stable ... Yokoyama Y (2005). "Role of thromboxane in producing hepatic injury during a hepatic stress disorder". Arch. Surg. 140 (8): 801 ...
... Si-Ming Wei,1,2 Yu-Min Huang,3 and ... The pathophysiologic mechanism of testicular damage is an ischemia-reperfusion injury. Testicular ischemia-reperfusion leads to ... "Diosmetin protects against ischemia/reperfusion-induced acute kidney injury in mice," The Journal of Surgical Research, vol. ... on testicular torsion/detorsion-induced ischemia/reperfusion injury attributable to excess reactive oxygen species released by ...
... Eirini Pantazi,1 Emma Folch-Puy,1 ... Z. Gao and Y.-H. Li, "Antioxidant stress and anti-inflammation of PPARα on warm hepatic ischemia-reperfusion injury," PPAR ... Ischemia-reperfusion injury (IRI) is a limiting factor for the outcome of many clinical conditions and although the extensive ... Ischemia-reperfusion injury (IRI) remains a frequent complication in surgery, especially in case of steatotic livers that ...
... induced acute kidney injury (AKI) is regulated by transcriptional factors and microRNAs (miRs). However, modulation of miRs by ... The CCAAT enhancer binding protein beta (C/EBP-β) increased the expression of miR-16 after I/R injury. The ChIP and luciferase ... Our results indicated that miR-16 was transactivated by C/EBP-β resulting in aggravated I/R induced AKI and that urinary miR-16 ... Figure 2: The expression of urinary microRNA(miR)-16 was induced by ischemia-reperfusion (I/R) injury in the kidneys.. ...
Neuroprotection of Cyperus esculentus L. orientin against cerebral ischemia/reperfusion induced brain injury.. Jing SQ1, Wang ... We found that CLO protected CoCl2-induced HT22 cells against ischemia/reperfusion injury by lowering lipid peroxidation and ... Cyperus esculentus L. orientin (CLO); antioxidants; caspase-3; cerebral ischemia/reperfusion injury; cobalt chloride; lipid ... leaves against ischemia/reperfusion (I/R) injury using standard orientin as control. For in vitro studies, we treated HT22 ...
Histone Deacetylase Inhibition Blunts Ischemia/Reperfusion Injury by Inducing Cardiomyocyte AutophagyCLINICAL PERSPECTIVE. Min ... Histone Deacetylase Inhibition Blunts Ischemia/Reperfusion Injury by Inducing Cardiomyocyte AutophagyCLINICAL PERSPECTIVE ... Histone Deacetylase Inhibition Blunts Ischemia/Reperfusion Injury by Inducing Cardiomyocyte AutophagyCLINICAL PERSPECTIVE ... Histone Deacetylase Inhibition Blunts Ischemia/Reperfusion Injury by Inducing Cardiomyocyte AutophagyCLINICAL PERSPECTIVE ...
To find effective therapeutic interventions for tourniquet-induced acute IR injuries, our current study investigated effect of ... To find effective therapeutic interventions for tourniquet-induced acute IR injuries, our current study investigated effect of ... on tourniquet-induced acute IR injury in mouse hindlimb. In C57/BL6 mice, a tourniquet was placed on unilateral hindlimb (left ... on tourniquet-induced acute IR injury in mouse hindlimb. In C57/BL6 mice, a tourniquet was placed on unilateral hindlimb (left ...
During cerebral ischemia/reperfusion (I/R) injury, DRAM1 protein expression is increased, and autophagy is activated. However, ... Furthermore, DRAM1 knockdown aggravates OGD/R-induced cell injury and significantly blocks autophagy through decreasing ... inhibits the expression of DRAM1 and LC3II/I and exacerbates OGD/R-induced cell injury. ... The aim of this study is to investigate whether DRAM1 mediates autophagy activation in cerebral I/R injury and to explore its ...
Activation of sensory neurons reduces ischemia/reperfusion-induced acute renal injury in rats. Download Prime PubMed App to ... Ghrelin-induced gastroprotection against ischemia-reperfusion injury involves an activation of sensory afferent nerves and ... Activation of sensory neurons reduces ischemia/reperfusion-induced acute renal injury in rats.. Anesthesiology. 2009 Feb; 110(2 ... "Activation of Sensory Neurons Reduces Ischemia/reperfusion-induced Acute Renal Injury in Rats." Anesthesiology, vol. 110, no. 2 ...
Whether Propofol can reduce myocardial ischemia-reperfusion injury induced by hepatic ischemia-reperfusion ... ... Current Mechanistic Concepts in Ischemia and Reperfusion Injury.. Ischemia-reperfusion injury is associated with serious ... Ischemia-reperfusion injury has never been di.... The Effect of Pregabalin Given Preoperatively on the Tourniquet Induced ... Does Caffeine Reduce Dipyridamole-Induced Protection Against Ischemia-Reperfusion Injury?. The purpose of this project is to ...
Ischemia-reperfusion (IR) cycle in the myocardium is associated with activation of an injurious cascade, thus leading to new ... Ischemia-reperfusion (IR) cycle in the myocardium is associated with activation of an injurious cascade, thus leading to new ... Damage occurs during both ischemia and post-ischemic reperfusion in animal and human models. The mechanisms that contribute to ... Both types of anesthetic conditioning reduce, albeit not to the same degree, the extent of myocardial injury. This review ...
Luteolin Inhibits Ischemia/Reperfusion-Induced Myocardial Injury in Rats via Downregulation of microRNA-208b-3p.. [Chen Bian, ... LUT pretreatment conveys anti-apoptotic effects after myocardial I/R injury by decreasing miR-208b-3p and increasing Ets1 ... Recent researches have suggested that LUT can carry out cardioprotective effects during ischemia/reperfusion (I/R). However, ... there have no reports on whether LUT can exert protective effects against myocardial I/R injury through the actions of specific ...
Significant up-regulation of Glutamate transporter-1 was found after 3, 6, 24, 72 hours of reperfusion. The present study showed ... However, brain ischemic postconditioning (six cycles of 10 s/10 s reperfusion/re-occlusion) significantly reduced neuronal death ... we found that most neurons in the CA1 region died after 10 minutes of ischemia and is followed by 72 hours of reperfusion. ... Ischemic postconditioning refers to several transient reperfusion and ischemia cycles after an ischemic event and before a long ...
... *Authors: *Haiying Zhu ... reperfusion injury (CIRI) and the impact of curcumin pretreatment. A total of 60 rats were randomly divided into the normal ... The protective effects of curcumin on intestine and remote organs against mesenteric ischemia/reperfusion injury. Turk J ... reperfusion injury in rats. Experimental and Therapeutic Medicine 14.5 (2017): 4047-4052. ...
... Fu, Jinrong ... Complement activation augments myocardial cell injury and apoptosis during ischemia/reperfusion (I/R), whereas complement ... The aim of this study was to determine whether C1INH protects against myocardial cell injury via an anti-apoptotic activity or ... In a rat model of acute myocardial infarction (AMI) induced by I/R, administration of C1INH protected against cardiomyocytic ...
Novel Rat Model of Ischemic Cardiomyopathy Induced by Repetitive Myocardial Ischemia/Reperfusion Injury While Conscious ... reperfusion, so the influence of sympathetic denervation on myocardial ischemia - reperfusion injury was investigated in the ... Canine myocardial reperfusion injury : Its reduction by the combined administration of superoxide dismutase and catalase JOLLY ... Study of the mechanism of hydrogen peroxide and hydroxyl free radical-induced cellular injury and calcium overload in cardiac ...
Abstract 11402: Cardioprotective Effects Of mTOR Against Ex Vivo Ischemia-reperfusion Injury In Diet-induced Obese Mice. ... Abstract 11402: Cardioprotective Effects Of mTOR Against Ex Vivo Ischemia-reperfusion Injury In Diet-induced Obese Mice ... Abstract 11402: Cardioprotective Effects Of mTOR Against Ex Vivo Ischemia-reperfusion Injury In Diet-induced Obese Mice ... Abstract 11402: Cardioprotective Effects Of mTOR Against Ex Vivo Ischemia-reperfusion Injury In Diet-induced Obese Mice ...
... 1 ... G. lucidum treatment was found to have prevented the T/D-induced I/R injury by decreasing MDA levels of the testis. SOD, CAT ... Though several compounds have been used to heal ischemia-reperfusion (I/R) injury in animal models of testicular torsion, few ... To investigate the protective effect of Ganoderma lucidum on testicular torsion/detorsion (T/D)-induced ischemia-reperfusion (I ...
Emulsified Isoflurane Preconditioning Reduces Lung Injury Induced By Hepatic Ischemia/Reperfusion in Rats. Int J Med Sci 2011; ... Emulsified Isoflurane Preconditioning Reduces Lung Injury Induced By Hepatic Ischemia/Reperfusion in Rats Xin Lv1,2 *, Zhen- ... Reperfusion was allowed to proceed for 4 h before sacrifice of the animals. Lung injury was observed histologically. Neutrophil ... Objective: To investigate whether emulsified isoflurane preconditioning could reduce lung injury induced by hepatic I/R in rats ...
Cardiac ischemia-reperfusion (I/R) injury remains a challenge for clinicians, which initiates with energy metabolism disorder. ... The present study was designed to investigate the protective effect of notoginsenoside R1 (NR1) on I/R-induced cardiac injury ... ATP5D modulation contributes to the protection of notoginsenoside NR1 against ischemia-reperfusion-induced myocardial injury.. ... We found that NR1 pretreatment ameliorated myocardial infarction, histological injury, and cardiac function induced by I/R. ...
Vitexin attenuates myocardial ischemia/reperfusion injury in rats by regulating mitochondrial dysfunction induced by ... Empagliflozin attenuates ischemia and reperfusion injury through LKB1/AMPK signaling pathway. In conclusion, EMPA can trigger ... Tangshen Formula Alleviates Hepatic Steatosis by Inducing Autophagy Through the AMPK/SIRT1 Pathway ... In conclusion, TSF improved lipid accumulation and hepatic steatosis by inducing the AMPK/SIRT1 pathway-mediated autophagy. ...
... to investigate whether CA could provide neuroprotection against oxidative stress caused by cerebral ischemia-reperfusion injury ... it is shown here that CA has the effect of relieving cerebral ischemia reperfusion-induced oxidative stress injury via the Nrf2 ... provides neuroprotection against cerebral ischemia reperfusion-induced oxidative stress injury via the Nrf2 signalling pathway ... provides neuroprotection against cerebral ischemia reperfusion-induced oxidative stress injury via the Nrf2 signalling pathway ...
Recent evidence suggests that gallic acid (GA) reverses oxidative stress in rat model of streptozotocin-induced dementia, but ... dysfunction are frequently implicated in the pathology of secondary neuronal damage following cerebral ischemia/reperfusion. ... Keywords: Cerebral ischemia/reperfusion injury; Gallic acid; Hypoxia/reoxygenation injury; Mitochondrial dysfunction; ... To further assess the effects of GA on cerebral ischemia/reperfusion injury, 2, 3, 5-triphenyl-tetrazolium chloride (TTC) ...
Berberine Ameliorates MCAO Induced Cerebral Ischemia/Reperfusion Injury via Activation of the BDNF-TrkB-PI3K/Akt Signaling ... lipoic acid protects against cerebral ischemia/reperfusion-induced injury in rats.. *HO-1 attenuates hippocampal neurons injury ... Berberine Ameliorates MCAO Induced Cerebral Ischemia/Reperfusion Injury via Activation of the BDNF-TrkB-PI3K/Akt Signaling ... "Berberine Ameliorates MCAO Induced Cerebral Ischemia/Reperfusion Injury Via Activation of the BDNF-TrkB-PI3K/Akt Signaling ...
Conclusion ME may protect ischemia/reperfusion induced brain injury by increase in antioxidant activity, decrease in lipid ... ME may protect ischemia/reperfusion induced brain injury by increase in antioxidant activity, decrease in lipid proxidation and ... Neuroprotective Effect of Mentha longifolia L. Extract on Ischemia/reperfusion-induced Brain Injury in Male Wistar Rats ...
... Guang-Xing Bian1), Gui- ... The aim of this study is to investigate if MA also protected against myocardial ischemia-reperfusion injury in vivo. The ... These results suggest that MA has the protective effect on myocardial ischemia-reperfusion injury. This protection ability ... has shown protect effect on isolated rat hearts and isolated cardiomyocytes against reperfusion injury in our previous studies ...
Here, we have evaluated the effect of estradiol on the local gut injury induced by I/R in male rats. I/R was induced by the ... Estradiol Modulates Local Gut Injury Induced by Intestinal Ischemia-Reperfusion in Male Rats. ... In conclusion, estradiol blunts intestinal injury induced by I/R by modulating chemokines release and leukocyte trafficking. ... Morphometric analysis of the gut showed I/R induced a reduction of villous height that was prevented by estradiol. White blood ...
Renoprotective Effects of l-Carnosine on Ischemia/Reperfusion-Induced Renal Injury in Rats. Hayato Kurata, Toshihide Fujii, ... Renoprotective Effects of l-Carnosine on Ischemia/Reperfusion-Induced Renal Injury in Rats. Hayato Kurata, Toshihide Fujii, ... Renoprotective Effects of l-Carnosine on Ischemia/Reperfusion-Induced Renal Injury in Rats. Hayato Kurata, Toshihide Fujii, ... Renoprotective Effects of l-Carnosine on Ischemia/Reperfusion-Induced Renal Injury in Rats ...
... ... induced testis injury. Animals were divided into four groups of IR, honey + ischaemia- reperfusion (HIR), vitamin C + ischaemia ... reperfusion (VIR) and carbohydrates + ischaemia- reperfusion (CIR). The testes were examined for spermatogenesis index. ... This study was conducted to survey the protective effect of pre-treatment with Persian honey during post-ischaemia reperfusion ...
Abstract 385: Amelioration of Heart Transplantation-Induced Ischemia-Reperfusion Injury by Melatonin and Ghrelin in Rats. ... Abstract 385: Amelioration of Heart Transplantation-Induced Ischemia-Reperfusion Injury by Melatonin and Ghrelin in Rats ... Abstract 385: Amelioration of Heart Transplantation-Induced Ischemia-Reperfusion Injury by Melatonin and Ghrelin in Rats ... Abstract 385: Amelioration of Heart Transplantation-Induced Ischemia-Reperfusion Injury by Melatonin and Ghrelin in Rats ...
Prostaglandin E1 protects cardiomyocytes against hypoxia-reperfusion induced injury via the miR-21-5p/FASLG axis Mingxiang Tang ... 47] showed that PGE1 exerts an anti-inflammatory effect that ameliorates renal ischemia/reperfusion injury-induced gastric ... Prostaglandin E1 protects cardiomyocytes against hypoxia-reperfusion induced injury via the miR-21-5p/FASLG axis. Biosci Rep 20 ... it was shown to prevent ischemia/reperfusion injuries by inducing the production of pro- and anti-inflammatory cytokines [14]. ...
  • Combined therapy with extracorporeal shock wave and adipose-derived mesenchymal stem cells remarkably improved acute ischemia-reperfusion injury of quadriceps muscle," Oxidative Medicine and Cellular Longevity , vol. 2018, Article ID 6012636, 14 pages, 2018. (
  • This review focuses on cellular and pathophysiological concepts on the myocardial damage induced by IR and how anesthetic pharmacological agents commonly used could attenuate the functional and structural effects induced by oxidative stress in cardiac tissue. (
  • The purpose of our study was to investigate whether CA could provide neuroprotection against oxidative stress caused by cerebral ischemia-reperfusion injury (CIRI) and elucidate the underlying mechanism. (
  • Middle cerebral artery occlusion (MCAO)-induced damage was established in Sprague Dawley (SD) rats and PC12 cells were exposed to hydrogen peroxide (H 2 O 2 ) to imitate oxidative stress damage. (
  • Importantly, we constructed and validated Nrf2 knockdown PC12 cells to confirm the key role of Nrf2 in the neuroprotective effect of CA against oxidative stress injuries. (
  • In conclusion, it is shown here that CA has the effect of relieving cerebral ischemia reperfusion-induced oxidative stress injury via the Nrf2 signalling pathway. (
  • Oxidative stress and mitochondrial dysfunction are frequently implicated in the pathology of secondary neuronal damage following cerebral ischemia/reperfusion. (
  • Recent evidence suggests that gallic acid (GA) reverses oxidative stress in rat model of streptozotocin-induced dementia, but the roles and mechanisms of GA on cerebral ischemia/reperfusion injury remain unknown. (
  • Both etanercept and exogenous adiponectin supplementation (on day 3 posttrauma or 10 mins before reperfusion on day 7 posttrauma) markedly inhibited oxidative/nitrative stress and ischemia/reperfusion injury in posttraumatic ischemic/reperfused hearts of wild-type mice, whereas only adiponectin supplementation (but not tumor necrosis factor α inhibition) substantially attenuated posttraumatic ischemia/reperfusion injury in adiponectin knockout mice. (
  • Tumor necrosis factor α-induced downregulation of adiponectin and the resultant enhanced oxidative/nitrative stress are involved in exacerbated posttraumatic ischemic myocardial injury. (
  • Ischaemia-reperfusion injury resulting from interruption and restoration of blood flow might be related to free radical mediated oxidative stress and inflammation, and subsequently to post-surgery related complications. (
  • The administration of valproic acid decreased all the parameters of lung injury, oxidative stress, apoptosis, and inflammation and some of its protection appeared to occur by increasing heme oxygenase-1 activity. (
  • The purpose of this study is to clarify the changes in hepatic microcirculation during liver ischemia and after reperfusion in the rat and the potential beneficial effects of Naloxone as pretreatment, in respect to microcirculation and oxidative stress. (
  • Liver microcirculation was assessed by laser-Doppler flowmetry at baseline, at the end of the ischemia period [30min or 60min, respectively] and at the end of the reperfusion period, while oxidative stress was assessed by means of MDA at the same time periods. (
  • Previous clinical and animal studies have identified that oxidative stress and inflammation are main pathological components in renal IR injury. (
  • The general objective of my research was to investigate the mechanism by which renal ischemia-reperfusion led to oxidative stress and inflammatory responses in the liver. (
  • Ischemia - reperfusion (IR) injury results from inflammation and oxidative stress , among other factors. (
  • The aim of the present study was to investigate whether the intake of BN prevents or reduces IR kidney injury and inflammation , improving renal function and decreasing oxidative stress . (
  • Low intake of BN prior to IR-induced kidney injury improves renal function by inhibition of macrophage infiltration and oxidative stress . (
  • Objective: Ischemia/reperfusion (I/R) injury is an important cause of myocardial damage by means of oxidative, inflammatory, and apoptotic mechanisms. (
  • Oxidative stress induced with renal I/R injury directly affects glomerular and tubular epithelium through reactive oxygen species. (
  • M. T. Droy-Lefaix, Y. Drouet, G. Geraud and P. Braquet, The amplificative role of PAF-acether in the oxidative stress following reperfusion of ischemic stomach, in: Oxygen radicals in biology and medicine, M. G. Simic and K. A. Taylor, eds. (
  • Toxic reactive oxygen species (ROS) generated by induced oxidative stress in the episodes of cerebral ischemia-reperfusion (CIR) plays major role in neurodegeneration. (
  • As the prime source of ROS generation, neuronal mitochondria, the cellular energy metabolic centre experience severe damage because of CIR-induced oxidative stress. (
  • Thus L-ascorbic acid loaded polylactide nanocapsules were prepared and fed orally to assess the role of nanocapsulated ascorbic acid (NAA) against CIR induced oxidative injury in mitochondrial region of rat brains. (
  • Results showed that in comparison to free ascorbic acid (AA), NAA exerted better protection to the brain mitochondria by preventing oxidative damage in ROS mediated CIR injury. (
  • Sibani Sarkar, Abhishek Mukherjee, Snehasikta Swarnakar and Nirmalendu Das, "Nanocapsulated Ascorbic Acid in Combating Cerebral Ischemia Reperfusion- Induced Oxidative Injury in Rat Brain", Current Alzheimer Research (2016) 13: 1363. (
  • Quercetin and rutin may ameliorate insecticide induced oxidative stress in human erythrocytes. (
  • Selected antioxidants have a protective effect against beta-cyfluthrin-induced oxidative stress in human erythrocytes in vitro. (
  • A mixture of curcumin, hesperidin and rutin ameliorates hepatic oxidative stress caused by STZ-induced hyperglycemia. (
  • Celecoxib administration prevented the IR-induced functional, histopathological and oxidative changes in both genders by similar degrees. (
  • Influence of remote ischemic conditioning and tramadol hydrochloride on oxidative stress in kidney ischemia/reperfusion injury in rats. (
  • Hearts from I/R group showed significant increase in oxidative stress levels and marked myocardial injury as compared to control. (
  • Significant improvement in oxidative stress, apoptosis parameters and cardiac injury was observed in I/R hearts when subjected to IPC. (
  • Two hours after reperfusion, rats were euthanized for estimation of oxidative stress markers (malondialdehyde and reduced glutathione). (
  • Therefore, the dose of 20 mg/kg i.p. was used to evaluate the neuroprotective effect by using diffusion-weighted imaging (30 min after reperfusion), assessing the neurological deficit (24 h after middle cerebral artery occlusion) and estimating oxidative stress markers (72 h after middle cerebral artery occlusion). (
  • Crocin, a pharmacologically active component of Crocus sativus L. (saffron), has been reported to be useful in the treatment of oxidative stress injury. (
  • Effects of antioxidant gene therapy on retinal neurons and oxidative stress in a model of retinal ischemia/reperfusion. (
  • Protective effect of aqueous saffron extract (Crocus sativus L.) and crocin, its active constituent, on renal ischemia-reperfusion-induced oxidative damage in rats. (
  • Protective effects of glucosamine on oxidative-stress and ischemia/reperfusion-induced retinal injury. (
  • Protective Effects of Crocus Sativus L. Extract and Crocin against Chronic-Stress Induced Oxidative Damage of Brain, Liver and Kidneys in Rats. (
  • Effects of crocin on reperfusion-induced oxidative/nitrative injury to cerebral microvessels after global cerebral ischemia. (
  • Oxidative stress plays a major role in the biochemical and pathological changes associated with myocardial ischemic-reperfusion injury (IRI). (
  • In the present study, the effect of chronic oral administration of raw garlic homogenate on oxidative stress induced by ischemic-reperfusion injury in isolated rat heart was investigated. (
  • Oxidative stress induced cellular damage as indicated by ultrastructural changes, like disruption of myofilament, Z-band architecture along with mitochondrial changes were significantly less. (
  • The study strongly suggests that chronic garlic administration prevents oxidative stress and associated ultrastructural changes, induced by myocardial ischemic-reperfusion injury. (
  • In view of this observation, the present study was designed to investigate whether this property of garlic could offer protection against oxidative stress arising out of ischemic-reperfusion injury in isolated rat heart. (
  • Effects of vagus nerve stimulation on cognitive functioning in rats with cerebral ischemia reperfusion," Journal of Translational Medicine , vol. 14, no. 1, p. 101, 2016. (
  • Neuroprotection of Cyperus esculentus L. orientin against cerebral ischemia/reperfusion induced brain injury. (
  • Results showed that CLO could decrease neurological deficit score, attenuate brain water content, and reduce cerebral infarct volume, leading to neuroprotection during cerebral ischemia-reperfusion injury. (
  • During cerebral ischemia/reperfusion (I/R) injury, DRAM1 protein expression is increased, and autophagy is activated. (
  • The aim of the present study was to observe the dynamic changes of the growth arrest and DNA damage‑inducible 153 (GADD153) gene and caspase‑12 in the brain tissue of rats with cerebral ischemia‑reperfusion injury (CIRI) and the impact of curcumin pretreatment. (
  • ERS is the key link of cerebral ischemia-reperfusion injury (CIRI) ( 8 ). (
  • Here we investigated the potential roles and mechanisms of GA in hypoxia/reoxygenation induced by sodium hydrosulfite (Na2S2O4) in vitro and cerebral ischemia/reperfusion induced by middle cerebral artery occlusion (MCAO) in vivo. (
  • To further assess the effects of GA on cerebral ischemia/reperfusion injury, 2, 3, 5-triphenyl-tetrazolium chloride (TTC) staining, dUTP nick-end labeling (TUNEL) assay, and Cytochrome C (Cyt C) release were performed in MCAO rats. (
  • The results support that GA is useful against cerebral ischemia/reperfusion injury as a potential protective agent. (
  • The rat middle cerebral artery occlusion (MCAO) model was established to investigate the neuroprotective effect of pelargonidin on cerebral ischemia/reperfusion injury and to investigate its potential mechanism(s) of action. (
  • Our datas demonstrated that pelargonidin ameliorated neurological function deficits in MCAO rats and its potential mechanism of action was associated with overexpression of the Nrf2/HO-1 signaling pathway, which may provide a new approach to the treatment of cerebral ischemia or cerebral ischemia/reperfusion injury. (
  • In this study, we investigated the protective effects of CAR on cerebral ischemia/reperfusion injury in a middle cerebral artery occlusion mouse model. (
  • Recent evidences suggest that cerebral ischemia-reperfusion insult plays significant role in pathogenic diseases like Alzheimer's disease (AD) and other neurodegenerative diseases. (
  • Cardiac denervation protected myocyte against ischemia - reperfusion injury through decreasing direct NE toxicity, but not through decreasing NE-derived free radicals. (
  • Our recent report using transgenic mice with cardiac-specific overexpression of mTOR (mTOR-Tg) showed that cardiac mTOR protects the heart against ischemia/reperfusion (I/R) injury. (
  • To address this question, we studied the effect of overexpression of cardiac mTOR on cardiac function following I/R in mice with high-fat diet (HFD)-induced obesity using mTOR-Tg mice. (
  • These findings suggest that cardiac mTOR is sufficient to substantially limit the metabolic syndrome-induced cardiac dysfunction following I/R in a mouse model of obesity with glucose intolerance and insulin resistance. (
  • Cardiac ischemia-reperfusion (I/R) injury remains a challenge for clinicians, which initiates with energy metabolism disorder. (
  • The present study was designed to investigate the protective effect of notoginsenoside R1 (NR1) on I/R-induced cardiac injury and underlying mechanism. (
  • We found that NR1 pretreatment ameliorated myocardial infarction, histological injury, and cardiac function induced by I/R. Furthermore, similar to the effect of Y-27632, NR1 improved H9c2 cell viability, maintained actin skeleton and mitochondria morphology, and attenuated apoptosis induced by oxygen and glucose deprivation/reoxygenation. (
  • These results prove NR1 as an agent able to prevent I/R-induced energy metabolism disorder via inhibiting ROCK and enhancing mitochondrial ATP synthase δ-subunits, which at least partially contributes to its protection against cardiac I/R injury. (
  • Global myocardial ischemia reperfusion (I/R), which is often obligatory during cardiac surgery, induce an inflammatory response in the transplanted heart. (
  • However, the mechanism by which PGE1 contributes to the amelioration of cardiac injury remains unclear. (
  • Trauma significantly sensitized myocardium to ischemia/reperfusion injury as evidenced by increased apoptosis, enlarged infarct size, and decreased cardiac function. (
  • Muscular exercise is a countermeasure to protect against IR-induced cardiac injury in both young and old animals. (
  • Cardiac Ischemia/Reperfusion Injury: The Beneficial Effects of Exercise. (
  • To evaluate differences in cardiac resistance against myocardial ischaemia and reperfusion injury, cardiac surrogate parameters including maximal ST-elevation, arrhythmias and infarct size were assessed. (
  • In this study on ischaemia-induced and reperfusion-induced injury, we found that the most widely used cardioprotective drugs in CAD unfavourably impacted the cardiac outcomes in rats after ischaemic preconditioning. (
  • In the present investigation, the effect of Curcuma longa (Cl) and Ocimum sanctum (Os) on myocardial apoptosis and cardiac function was studied in an ischemia and reperfusion (I-R) model of myocardial injury. (
  • Ischemia-reperfusion injury (IRI) is a leading cause of acute kidney injury (AKI) that arises from a variety of conditions, including decreased cardiac output, renal vascular occlusion, or kidney transplantation ( 1 ). (
  • When compared to nonpreconditioned controls, preceding preconditioning improved postischemic cardiac performance and significantly decreased test ischemia/reperfusion-induced formation of free nitrotyrosine measured in the perfusate as a marker for cardiac endogenous ONOO(-) formation. (
  • We conclude that classic preconditioning inhibits ischemia/reperfusion-induced cardiac formation of ONOO(-) and that subsequent periods of ischemia/reperfusion result in a gradual attenuation of ischemia/reperfusion-induced ONOO(-) generation. (
  • Background/Aims: This study was designed to investigate the dose-dependent protective effect of ivabradine, a specific inhibitor of the cardiac sinoatrial node, on renal ischemia-reperfusion (I/R) injury in rats. (
  • Limited microRNAs (miRNAs, miRs) have been reported to be necessary for exercise-induced cardiac growth and essential for protection against pathological cardiac remodeling. (
  • Inhibition of miR-17-3p in vivo attenuated exercise-induced cardiac growth including cardiomyocyte hypertrophy and expression of markers of myocyte proliferation. (
  • Importantly, mice injected with miR-17-3p agomir were protected from adverse remodeling after cardiac ischemia/reperfusion injury. (
  • Collectively, these data suggest that miR-17-3p contributes to exercise-induced cardiac growth and protects against adverse ventricular remodeling. (
  • miR-17-3p may represent a novel therapeutic target to promote functional recovery after cardiac ischemia/reperfusion. (
  • 3. Chen Y, Liu Z, Xie X. Hydrogen sulphide attenuates renal and cardiac injury after total hepatic ischemia and reperfusion. (
  • Protective effect of crocin against reperfusion- induced cardiac arrhythmias in anaesthetized rats. (
  • Resveratrol enhanced cardiac Sirt1 activity but failed to mimic CR-induced cardioprotection in eNOS −/− mice. (
  • This study investigated the effect of probucol, a potent antioxidant, on testicular torsion/detorsion-induced ischemia/reperfusion injury attributable to excess reactive oxygen species released by neutrophils. (
  • Abundant amounts of reactive oxygen species are produced during ischemia-reperfusion [ 2 ]. (
  • We have reported that curcumin [ 5 ] and rutin [ 6 ] can protect against testicular torsion/detorsion-induced ischemia/reperfusion injury in rats by reducing reactive oxygen species. (
  • We found that CLO protected CoCl 2 -induced HT22 cells against ischemia/reperfusion injury by lowering lipid peroxidation and reactive oxygen species formation as well as decreasing protein oxidation. (
  • Some evidence implicates reactive oxygen species (ROS) as a probable cause of myocardial injury in prooxidant clinical settings. (
  • They also showed that granulocytic myeloid-derived suppressor cells played a role in the beneficial effects induced by G-CSF via arginase-1 and reactive oxygen species. (
  • Furthermore, these splenic cells effectively suppressed in vitro T cell activation mainly through arginase-1 and reactive oxygen species, and their adoptive transfer attenuated renal injury. (
  • Upon reperfusion, molecular oxygen undergoes sequential reduction to form reactive oxygen species, including superoxide anion and hydroxyl radical, in addition to hydrogen peroxide. (
  • Background In donor kidneys subjected to ischemia-reperfusion injury during kidney transplant, phagocytes coexpressing the F4/80 and CD11c molecules mediate proinflammatory responses and trigger adaptive immunity in transplantation through antigen presentation. (
  • E-selectin protein expression, myeloperoxidase activity, and malondialdehyde level were significantly increased, and testicular spermatogenesis was significantly decreased in the ipsilateral testes in the ischemia-reperfusion group, compared with the control group. (
  • Low-amplitude, left vagus nerve stimulation significantly attenuates ventricular dysfunction and infarct size through prevention of mitochondrial dysfunction during acute ischemia-reperfusion injury," Heart Rhythm , vol. 10, no. 11, pp. 1700-1707, 2013. (
  • Treatment with dexamethasone at the beginning of reperfusion (1 mg/kg, i.p.) significantly inhibited expression of TNFα and IL-1β, reduced rupture of the muscle sarcolemma and infarct size (24.8 ± 2.0%), and improved direct muscle stimulation-induced gastrocnemius muscle contraction in 24-h IR mice. (
  • Furthermore, DRAM1 knockdown aggravates OGD/R-induced cell injury and significantly blocks autophagy through decreasing autophagosome-lysosome fusion. (
  • Increases in renal tissue levels of 6-keto-prostaglandin F1alpha at 1 h after reperfusion were significantly inhibited by pretreatment with capsazepine, CGRP(8-37), and indomethacin. (
  • Pretreatment with capsazepine, CGRP(8-37), indomethacin, and denervation of primary sensory nerves significantly increased blood urea nitrogen and serum creatinine levels, renal vascular permeability, renal tissue levels of myeloperoxidase activity, cytokine-induced neutrophil chemoattractant, and tumor necrosis factor-alpha, and decreased renal tissue blood flow. (
  • Reperfusion of the transplanted graft significantly increased plasma levels of 8-iso-PGF 2α . (
  • Acute post-injury administration of azithromycin significantly prevented RGC death. (
  • Compared with the ischemic reperfusion group, BALF total protein content increases significantly, while lung D/W decreases significantly in the intervention group. (
  • Radix ophiopogonison extract can significantly reduce the degree of acute lung injury. (
  • Naloxone pretreatment seemed to protect liver parenchyma, since MDA levels were significantly decreased in relation to placebo treated rats, in both 30min ischemia/ 60min reperfusion and 60min ischemia/60min reperfusion groups. (
  • Both tissue levels of CGRP and the expression of immunohistochemical CGRP in the liver were significantly increased in rats subjected to I/R 1 hour after reperfusion. (
  • AT (250 U/kg, i.v.) significantly enhanced the I/R-induced increase in both hepatic levels of CGRP and the expression of immunohisto-chemical CGRP. (
  • Furthermore, AT-induced increase in hepatic level of 6-keto-PGF1a, a stable metabolite of PGI 2 , were significantly inhibited by CPZ, CGRP (8-37), a CGRP receptor antagonist, and L-nitro-arginine-methyl-ester (L-NAME), a non-selective inhibitor of NOS. (
  • In the simvastatin treated group, intestinal tissue injury, TNF-α level, and tissue malondealdehyde levels were significantly lower than in the I/R group (p (
  • Similarly, in vitro data showed that minocycline significantly induced the expression of MCPIP1 in primary neuron-glial cells, cortical neurons, and reduced oxygen glucose deprivation (OGD)-induced cell death. (
  • The amount of TNF-α as an index of acute inflammatory except the 3rd day significantly decreased on the other day of reperfusion (7th, 147th and 287th days). (
  • We found that CAR (50 mg/kg) significantly reduced infarct volume and improved neurological deficits after 75 min of ischemia and 24 h of reperfusion. (
  • HMGB1 was measured in plasma samples obtained pre-, intra- and post-transplant from OLT recipients (n=51) and was significantly elevated in initial liver flush (LF) obtained after reperfusion in all patients. (
  • Bisaramil significantly inhibited the increase of the superoxide-radical generating capacity of PMNs during the reperfusion. (
  • COX-2 −/− livers after I/R injury showed significantly decreased levels of IL-2, as well as IL-12, a cytokine known to have a central role in Th1 effector cell differentiation. (
  • I/R injury, an Ag-independent event, causes up to 10% of early transplant failures and can lead to a significantly higher incidence of acute and chronic rejections ( 1 ). (
  • Similarly, crocin (50 mg/kg) treatment also significantly increased the level of activity of GSH, enhanced the activity of T-SOD, and decreased the activity level of ROS and MDA after IR injury. (
  • No studies investigating the function of C/EBP-β in the kidney have been reported except for the ER stress induced renal C/EBP-β and the suppression of NF-κB-dependent gene expression in response to LPS in mice 17 . (
  • In C57/BL6 mice, a tourniquet was placed on unilateral hindlimb (left hindlimb) at the hip joint for 3 h, and then released for 24 h to induce IR. (
  • Glucose intolerance and insulin resistance induced by HFD determined by glucose and insulin tolerance tests were comparable between HFD-WT and HFD-mTOR-Tg mice. (
  • Exercise of obese mice induces cardioprotection and oxygen sparing in hearts exposed to high-fat load. (
  • The authors demonstrate in mice that such injury is sufficient to dampen donor renal macrophages' ability to present antigens, skewing them toward a proreparative phenotype. (
  • Methods: C57BL/6 mice suffering 30mins hepatic ischemia process were sacrificed after 1h reperfusion to build murine warm hepatic IRI model. (
  • Conclusion: GSP could protect liver against IRI: particularly in high-fat diet induced obese mice. (
  • Song X, Xu H, Feng Y, Li X, Lin M, Cao L. Protective Effect of Grape Seed Proanthocyanidins against Liver Ischemic Reperfusion Injury: Particularly in Diet-Induced Obese Mice. (
  • WT and LysM-eGFP mice treated with reparixin or saline were subjected to 60 min of ischemia followed by different times of reperfusion. (
  • Focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) for 2 h in male C57BL/6 mice and MCPIP1 knockout mice followed by 24- or 48-h reperfusion. (
  • MCPIP1-deficient mice failed to evoke minocycline-treatment-induced tolerance compared with that of the control MCPIP1-deficient group without minocycline treatment. (
  • however, intracerebroventricular post-treatment reduced infarct volume even when the mice were treated with CAR at 6 h after reperfusion. (
  • Complement component 5a receptor 2 (C5AR2) deficient mice are protected from inflammation and fibrosis in response to ischemia reperfusion injury. (
  • Here, we investigated this possibility in mice by studying the role of conventional DCs (cDCs) in liver ischemia/reperfusion (I/R) injury, a model of sterile inflammation. (
  • Mangiferin induces islet regeneration in aged mice. (
  • 8. Jalili C, Tabatabaei H, Kakaberiei S, Roshankhah S, Salahshoor MR. Protective role of crocin against nicotine-induced damages on male mice liver. (
  • Crocin attenuates cisplatin-induced liver injury in the mice. (
  • To find effective therapeutic interventions for tourniquet-induced acute IR injuries, our current study investigated effect of dexamethasone, an anti-inflammatory drug, on tourniquet-induced acute IR injury in mouse hindlimb. (
  • The data suggest that one-time treatment with dexamethasone at the beginning of reperfusion only reduced structural and functional impairments of the skeletal muscle but not the NMJ through inhibiting inflammatory cytokines. (
  • Based on this fact, inhibition of production and release of inflammatory cytokines is likely considered as one of the strategies for limb acute IR injury. (
  • Such activation reduces acute renal injury by attenuating inflammatory responses through enhanced endothelial PGI2 production. (
  • The aim of this study was to determine whether C1INH protects against myocardial cell injury via an anti-apoptotic activity or anti-inflammatory effect. (
  • Intestinal ischemia and reperfusion (I/R) triggers a systemic inflammatory response characterized by leukocyte mobilization from the bone marrow, release of cytokines to the circulation, and increased microvascular permeability, leading to high mortality. (
  • We investigated the molecular mechanisms responsible for exacerbation of ischemic myocardial injury after nonlethal mechanical trauma with a special focus on the role of tumor necrosis factor α and its potential downstream effector adiponectin, a novel adipokine with anti-inflammatory and cardioprotective properties. (
  • In addition to local damage to the bowel, II/R leads to remote organ dysfunction ( 5 , 6 ), particularly in the lung, resulting in acute lung injury (ALI) ( 3 , 7 ), characterized by an excess elevation of pro-inflammatory cytokines and activated neutrophils ( 8 - 10 ). (
  • 1 Intestinal I/R is associated with the exacerbation of intestinal injury and a systemic inflammatory response leading to progressive distal organ impairment, finally resulting in cardiocirculatory, respiratory, hepatic, and renal failure. (
  • Azithromycin affords neuroprotection by modifying the inflammatory state of the retina following ischemia/reperfusion injury suggesting its potential repurposing for glaucoma treatment. (
  • During IR injury, an intense inflammatory process occurs in the liver. (
  • Depletion of mast cells prior to IRI resulted in improved renal function due to diminished local inflammatory cytokine/chemokine levels and neutrophil recruitment to the kidneys after the acute injury phase (48 h post-IRI). (
  • Minocycline, a broad-spectrum tetracycline antibiotic, has shown anti-inflammatory and neuroprotective effects in ischemic brain injury. (
  • The present study seeks to determine whether monocyte chemotactic protein-induced protein 1 (MCPIP1), a recently identified modulator of inflammatory reactions, is involved in the cerebral neuroprotection conferred by minocycline treatment in the animal model of focal cerebral ischemia and to elucidate the mechanisms of minocycline-induced ischemic brain tolerance. (
  • Because of its anti-inflammatory and antioxidant properties, the Brazil nut (BN) might attenuate IR renal injury . (
  • Simultaneously, local ischaemia in the reperfused tissue is extended to the whole body systemically through these activated inflammatory cells and, possibly, results in secondary detectable tissue damage in endothelial cells of the systemic circulation inducing prolonged DNA damage even in the early reperfusion period. (
  • The aim of this study was to investigate the role of PARG on the modulation of the inflammatory response caused by splanchnic ischemia and reperfusion. (
  • These results suggest that PARG activity modulates the inflammatory response in ischemia/reperfusion and participates in end (target) organ damage under these conditions. (
  • Our results implicate inflammatory monocytes as mediators of liver I/R injury and reveal that cDCs respond to DAMPS during sterile inflammation, providing the host with protection from progressive tissue damage. (
  • A persistent inflammatory response might be associated with long-term changes following acute ischaemia/reperfusion. (
  • Renal ischemia and reperfusion injury (IRI) is considered an inflammatory syndrome. (
  • Baicalein attenuates radiation-induced inflammatory process in mouse kidney. (
  • In addition, the H 2 O 2 -induced injury in Nrf2-knockdown PC12 cells was more serious than it was in control cells, and CA-mediated neuroprotection was exclusively inhibited by the knock down of Nrf2 in PC12 cells. (
  • Much evidence demonstrates that inflammation is an important factor to cause acute IR injury. (
  • Renal macrophages are key cells in controlling processes related to inflammation or repair after ischemia-reperfusion injury. (
  • After injury, however, resident renal macrophages coexpressing these surface markers acquire a proreparative phenotype, which is pivotal in controlling inflammation and fibrosis. (
  • CXC chemokines mediate hepatic inflammation following reperfusion. (
  • IR induced liver injury and inflammation, as evidenced by high levels of alanine aminotransferase and myeloperoxidase activity, chemokine and cytokine production, and histological outcome. (
  • Ischaemic/reperfusion injury resulted in persistent inflammation and tubulointerstital fibrosis with decreased creatinine clearance and increased urinary albumin excretion at 4 and 8 weeks. (
  • These results suggest that macrophages play an important role in mediating persistent inflammation and fibrosis after ischaemia/reperfusion leading to a development of chronic kidney disease. (
  • Monocyte retention, activation phenotype and the effects of their depletion by intravenous clodronate-liposome treatment on lung inflammation and injury were determined. (
  • Early studies have demonstrated that probucol can attenuate ischemia-reperfusion injury in the kidney, heart, and brain [ 8 - 10 ]. (
  • Methods We used mouse models of ischemia-reperfusion injury to investigate whether G-CSF can attenuate renal injury by increasing infiltration of myeloid-derived suppressor cells into kidney tissue. (
  • Based on the characteristics of dexmedetomidine, we hypothesized that dexmedetomidine could attenuate intestinal mucosal injury and mortality in rats after intestinal I/R. (
  • This study was designed to investigate whether n-3 PUFAs attenuate ischemia/reperfusion (I/R) induced intestinal barrier injury by activating I-FABP-PPARγ pathway. (
  • Development of new strategies to attenuate hepatic I/R injury is important for achieving a better clinical outcome. (
  • Baicalein could attenuate intestinal ischemia-reperfusion injury induced acute lung injury. (
  • To investigate the protective effect of Ganoderma lucidum on testicular torsion/detorsion (T/D)-induced ischemia-reperfusion (I/R) injury. (
  • These results suggest that MA has the protective effect on myocardial ischemia-reperfusion injury. (
  • This study was conducted to survey the protective effect of pre-treatment with Persian honey during post-ischaemia reperfusion on ischaemia-reperfusion (IR)-induced testis injury. (
  • These findings suggested that both melatonin and ghrelin have a promising graft protective effect against transplant induced global I/R injury. (
  • 7 Either in vivo or in vitro , dexmedetomidine has demonstrated a protective effect against the I/R injury of heart, kidney, brain, and testis in animal models. (
  • Quantitative determination of Radix ophiopogonison and its protective effect on intestinal ischemia reperfusion-induced lung injury in rats. (
  • In conclusion, these data suggest that the naphthalene-prazosin derivative exerts a cardio protective effect via the calcium channels activation and consequently induces changes in the left ventricular pressure levels. (
  • The study showed that TEL has a protective effect against TIR injury. (
  • Protective Effect of Folic Acid against Apoptosis Induced by Ischemia/Reperfusion Injury in Rat Liver', Iranian Journal of Pharmaceutical Sciences , 3(4), pp. 229-238. (
  • Herein, we have evaluated the therapeutic potential of P8RI, via a putative protective effect on neutrophil activation, in an experimental model of acute mesenteric ischemia/reperfusion. (
  • 6. Padma VV, Sowmya P, Felix TA, Baskaran R, Poornima P. Protective effect of gallic acid against lindane induced toxicity in experimental rats. (
  • Banerjee, Sanjay K. / Inhibition of SGLT1 abrogates preconditioning-induced cardioprotection against ischemia-reperfusion injury . (
  • Caloric restriction (CR) confers cardioprotection against ischemia-reperfusion injury (IRI). (
  • I/R caused significant increases in the lung edema, pulmonary arterial pressure, lung injury scores, tumor necrosis factor-α, and cytokine-induced neutrophil chemoattractant-1 concentrations in bronchoalveolar lavage fluid. (
  • The number of neutrophils in the liver increased between 6 and 24 h of reperfusion, whereas the distance traveled, velocity, neutrophil size and shape, and cluster formation reached a maximum 6 h after reperfusion and then decreased gradually. (
  • Imaging of the liver by confocal IVM was successfully implemented to describe neutrophil behavior in vivo during liver injury by IR. (
  • Mesenteric ischemia/reperfusion-induced neutrophil activation leads to a massive cleavage and shedding of the most extracellular domains of CD31 into plasma, enhancing the deleterious effect of neutrophil activation. (
  • Preventive administration of P8RI, a CD31-agonist peptide, could decrease I/R-induced intestinal injury by potentially limiting neutrophil activation. (
  • The lack of COX-2 expression resulted in decreased levels of CXCL2, a neutrophil-activating chemokine, reduced infiltration of MMP-9-positive neutrophils, and impaired late macrophage activation in livers after I/R injury. (
  • Dexamethasone protects against tourniquet-induced acute ischemia-reperfusion injury in mouse hindlimb," Frontiers in Physiology , vol. 9, p. 244, 2018. (
  • Gan, J. DRAM1 Protects Neuroblastoma Cells from Oxygen-Glucose Deprivation/Reperfusion-Induced Injury via Autophagy. (
  • Yu M, Jiang Y, Feng Q, Ouyang Y, Gan J. DRAM1 Protects Neuroblastoma Cells from Oxygen-Glucose Deprivation/Reperfusion-Induced Injury via Autophagy. (
  • 2014. "DRAM1 Protects Neuroblastoma Cells from Oxygen-Glucose Deprivation/Reperfusion-Induced Injury via Autophagy. (
  • Activation of the adenosine receptor protects against ischemia-reperfusion injury (pharmacologic preconditioning). (
  • The present study was designed to investigate how PGE1 protects against hypoxia/reoxygenation (H/R)-induced injuries by regulating microRNA-21-5p (miR-21-5p) and fas ligand (FASLG). (
  • CONCLUSIONS: Intravenous administration of rhEpo protects the heart against cold global I/R. Apoptosis does not seem to play a major role in the process of tissue injury in this model. (
  • In conclusion, the results of this study indicate that Naloxone pretreatment protects the liver from ischemia/ reperfusion hepatocellular injury. (
  • Diosmin protects rat retina from ischemia/reperfusion injury. (
  • Bisaramil inhibited the elevation of the plasma concentration of MDA and GSSG during the reperfusion and abolished the decrease in the plasma concentration of GSH during the occlusion and reperfusion. (
  • Conclusions: Infrarenal abdominal aortic occlusion and reperfusion causes lung injury. (
  • METHODS: Anesthetized rats were subjected to 45 min of renal ischemia/reperfusion. (
  • Methods: H9c2 cells underwent oxygen glucose deprivation (OGD) followed by reperfusion to simulate cardiomyocytes ischemia/reperfusion injury. (
  • Methods Isolated perfused C57BL/6 murine lungs were subjected to warm ischaemia (2 hours) and reperfusion (2 hours) under normoxic conditions. (
  • Methods Hearts isolated from SD male rats were subjected to either ischemia-reperfusion injury (I/R) (15 min global ischemia followed by 20 min reperfusion) or ischemic preconditioning (IPC) (3 cycles of 2 min global ischemia separated by 3 min reperfusion) followed by I/R in presence and absence of phlorizin, an SGLT1 inhibitor. (
  • METHODS: Arteries were isolated from hearts exposed to a well-established rat ischemia/reperfusion model. (
  • S-nitroso human serum albumin treatment reduces ischemia/reperfusion injury in skeletal muscle via nitric oxide release," Circulation , vol. 105, no. 25, pp. 3032-3038, 2002. (
  • We have previously demonstrated that antithrombin (AT) reduces ischemia/reperfusion (I/R)-induced liver injury by inhibiting leukocyte activation through the promotion of hepatic production of prostacyclin (PGI2) [ 1 ]. (
  • Complement activation augments myocardial cell injury and apoptosis during ischemia/reperfusion (I/R), whereas complement system inhibition with C1 inhibitor (C1INH), a serine protease inhibitor, exerts markedly cardioprotective effects. (
  • In cultured H9c2 rat cardiomyocytic cells, C1INH blocked hypoxia/reoxygenation-induced apoptosis in the absence of sera associated with inhibition of cytochrome c translocation and suppression of caspase-3 activation. (
  • Therefore, these studies support the hypothesis that C1INH, in addition to inhibition of activation of the complement and contact systems, improves outcome in I/R-mediated myocardial cell injury via an anti-apoptotic activity independent of serine protease inhibitory activity. (
  • The authors examined whether HDAC inhibition provided protection against ischemia-reperfusion (I/R) lung injury in rats by up-regulating HO-1 activity. (
  • TRPV4 inhibition also diminished renal IR-induced increase in AKI biomarkers. (
  • TRPV4 inhibition also blunted Ang II-induced increase in renal vascular resistance (RVR) and hypoperfusion in the pigs. (
  • Conclusion Present study indicated that inhibition of SGLT1 by phlorizin abrogated the beneficial effect of ischemic-preconditioning and for the first time, provides evidence that SGLT1 plays a crucial role in ischemic preconditioning-induced cardioprotection. (
  • Baicalein represses TGF-β1-induced fibroblast differentiation through the inhibition of miR-21. (
  • Thus, the aim of this study is to investigate the possible effect and the mechanism of berberine against cerebral ischemic injury using the middle cerebral artery occlusion (MCAO) model. (
  • Melatonin (10, 20 and 40 mg/kg i.p.) was administered four times in an animal at the time of middle cerebral artery occlusion, 1 h after middle cerebral artery occlusion, at the time of reperfusion and 1 h after reperfusion. (
  • The primary pathophysiology of testicular torsion and detorsion is testicular ischemia-reperfusion injury. (
  • However, the effect of probucol on testicular ischemia-reperfusion injury has not been evaluated previously. (
  • Male Wistar rats were subjected to 60-min ischemia and subsequent reperfusion. (
  • Emulsified isoflurane preconditioning markedly attenuated hepatic I/R-induced lung injury in rats, which may be hopefully applied to the clinical treatment of organ injury caused by hepatic surgery, transplantation or hemorrhagic shock. (
  • Prostaglandin I2 (PGI2) produced by endothelial cells improves ischemia/reperfusion-induced acute renal injury by inhibiting leukocyte activation in rats. (
  • Activation of sensory neurons increases endothelial PGI2 production by releasing calcitonin gene-related peptide (CGRP) in rats with hepatic ischemia or reperfusion. (
  • We examined here whether activation of sensory neurons increases PGI2 endothelial production, thereby reducing ischemia/reperfusion-induced acute renal injury. (
  • Hepatic ischemia/reperfusion-induced injury is accompanied by free radical production, leading to endothelial cell destruction, adhesion of neutrophils and plugging of the hepatic sinusoids and thus to blood microcirculation flow reduction. (
  • Recent studies have demonstrated that CGRP increases the endothelial production of nitric oxide (NO). Since NO has been shown to activate endothelial cyclooxygenase-1 (COX-1) activity, we further examined whether AT-induced increase in hepatic level of PGI 2 can be mediated by nitric oxide synthase (NOS) activation. (
  • In this process, CGRP-induced activation of endothelial NOS and COX-1 could be critically involved. (
  • comment on the paper 'Dynamics of serum-induced endothelial cell apoptosis in patients with myocardial Infarction' by Forteza et al. (
  • However, it remains unclear whether endothelial nitric oxide (NO) synthase (eNOS) plays a role in CR-induced cardioprotection and Sirt1 activation. (
  • however, the tourniquet and subsequent release results in serious acute ischemia-reperfusion (IR) injury in the skeletal muscle and neuromuscular junction (NMJ). (
  • Vagus nerve stimulation mediates protection from kidney ischemia-reperfusion injury through α 7nAChR + splenocytes," The Journal of Clinical Investigation , vol. 126, no. 5, pp. 1939-1952, 2016. (
  • Hepatic ischemia-reperfusion injury is a common pathophysiological process in liver surgery. (
  • Shikonin attenuated hepatic ischemia/reperfusion injury by inhibiting apoptosis and autophagy. (
  • Liver ischemia-reperfusion (IR) injury is a complication of several systemic pathologies, including trauma and shock. (
  • Using a COX-2-deficient mouse model, we present data that suggest that COX-2 has an active role in liver ischemia/reperfusion (I/R) injury. (
  • This research aimed to test the impact of liver ischemia/reperfusion (IR) insult on the activity of antioxidant enzymes, functional enzymes, histological, and hemodynamic parameters of heart, as well as protective function of crocin on these variables in rats. (
  • OBJECTIVE: Cardioprotective properties of recombinant human Erythropoietin (rhEpo) have been shown in in vivo regional or ex vivo global models of ischemia-reperfusion (I/R) injury. (
  • Percentage difference in radioactivity (counts/pixel) between experimental and control thenar muscle at 60 and 240 minutes after reperfusion. (
  • We investigated the effect of angiotensin II receptor blocker Telmisartan (TEL) (10 mg/kg i.m. 30 min before the reperfusion) on experimental TIR injury in rats. (
  • Repeated remote ischemic preconditioning and isoflurane anesthesia in an experimental model of renal ischemia-reperfusion injury. (
  • We have evaluated the preventive therapeutic potential of an engineered synthetic octapeptide (P8RI), which restores the inhibitory intracellular signaling of cleaved CD31, in an experimental model of acute mesenteric ischemia/reperfusion. (
  • Intravascular lung-marginated monocytes have been shown to play key roles in experimental acute lung injury, but their contribution to lung ischaemia-reperfusion injury post transplantation is unknown. (
  • In this study the aim was to characterize Ca(2+) sensitivity in coronary arteries following experimental ischemia/reperfusion injury. (
  • Hearts were subjected to a preconditioning protocol (three intermittent periods of global ischemia/reperfusion of 5 min duration each) followed by a test ischemia/reperfusion (30 min global ischemia and 15 min reperfusion). (
  • Isolated perfused hearts were subjected to 25-min global ischemia followed by 60-min reperfusion. (
  • We adopt the oxygen-glucose deprivation and reperfusion (OGD/R) Neuro-2a cell model to mimic cerebral I/R conditions in vitro , and RNA interference is used to knock down DRAM1 expression in this model. (
  • Results: Propofol enhanced the survival of H9c2 cells, decreased ROS levels and inhibited apoptosis during oxygen glucose deprivation/reperfusion (OGD/R) injury. (
  • Low-level vagus nerve stimulation attenuates myocardial ischemic reperfusion injury by antioxidative stress and antiapoptosis reactions in canines," Journal of Cardiovascular Electrophysiology , vol. 27, no. 2, pp. 224-231, 2016. (
  • Baicalein attenuates lung injury induced by myocardial ischemia and reperfusion. (
  • I/R was induced by the clamping of the superior mesenteric artery for 45 min, followed by 2 h of reperfusion. (
  • The rats underwent II/R injury with occlusion of the superior mesenteric artery and coeliac artery to induce ischemia for 40 min, and were subsequently reperfused for 0‑48 h. (
  • Intestinal ischaemia was induced by superior mesenteric artery ligation with microvascular clamps for 60 minutes, and after ischaemia, blood perfusion was released into the tissue and a reperfusion phase was started, which lasted for 3 hours. (
  • In a randomized, controlled, and experimenter-blinded preclinical study, mesenteric ischemia/reperfusion (I/R) was induced in Wistar rats by superior mesenteric artery occlusion for 30 min followed by 4 h of reperfusion. (
  • Cerebral ischemic injury remains associated with high mortality rates and lacks effective therapeutic intervention. (
  • Therapeutic approaches blocking tumor necrosis factor α production or restoring adiponectin might have prophylactic value against secondary myocardial ischemic injury after a primary nonlethal mechanical trauma. (
  • These findings may contribute to the development of an IL‑6‑RNAi‑based therapeutic strategy for the treatment of II/R‑induced ALI. (
  • These findings elucidate protective roles of G-CSF-induced myeloid-derived suppressor cells against ischemia-reperfusion injury and indicate that human studies investigating the therapeutic potential of myeloid-derived suppressor cells and G-CSF in renal ischemia-reperfusion injury are warranted. (
  • Study on therapeutic effect and its related mechanism of anemoside B4 on ischemia reperfusion injury induced by renal artery and vein ligation in rats]. (
  • Innate immune signaling induced by IRI provides many potential therapeutic targets for improving OLT outcome, and patient-specific screening of DAMPs/PRRs during OLT could be a novel diagnostic strategy for identifying IRI risk. (
  • 1. Bolisetty S, Zarjou A, Agarwal A. Heme oxygenase 1 as a therapeutic target in acute kidney 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. (
  • The data also suggest that potential valuable therapeutic approaches in liver I/R injury may result from further studies aimed at identifying specific COX-2-derived prostanoid pathways. (
  • A better understanding of the molecular pathophysiology of I/R injury may eventually lead to advanced therapeutic strategies that could improve the success rate of organ transplantation. (
  • Retention and activation of intravascular monocytes in perfused murine and human donor lungs suggests an important and previously unrecognised role as passenger leukocytes contributing to lung injury and primary graft dysfunction, emphasising their potential as therapeutic targets in lung transplantation. (
  • Although antioxidant administration during reperfusion injury has been shown to reduce the severity of the ischemic reperfusion injury, yet some properties of antioxidants such as cytotoxicity [ 3 ], pro-oxidant activity [ 4 ] or high molecular weight in case of SOD, limited their therapeutic application. (
  • Our in vitro and in vivo studies demonstrate that MCPIP1 is an important mediator of minocycline-induced protection from brain ischemia. (
  • For in vitro studies, we treated HT22 cells with CoCl 2 as an in vitro ischemic injury model. (
  • D. A. Parks, G. B. Bulkley, D. N. Granger, S. R. Hamilton and J. M. Mc Cord, Ischemic injury in the cat small intestine role of Superoxide radicals, Gastroenterology 82:9 (1986). (
  • 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). (
  • Morphologic observations of the ischemic myocardial tissue undergoing reperfusion suggest that reperfusion injury is a true pathologic phenomenon and a distinct entity from the preceding ischemic injury. (
  • Results G-CSF treatment before ischemia-reperfusion injury subsequently attenuated acute renal dysfunction, tissue injury, and tubular apoptosis. (
  • Stroke is a group of diseases associated with sudden rupture of cerebral vessels or brain tissue injury caused by blockage of blood flow to the brain and is characterized by high morbidity, mortality and disability rates. (
  • Therefore, the role of endothelin receptor antagonism in IR-induced-tissue injury carries great interest. (
  • Oxygen free radicals, formed during I/R, have been proposed as one of the main causes of tissue injury and play important role in I/R injury. (
  • Leucocytes have been shown to play an important role in the development of tissue injury after I/R. Accordingly, numerous studies have shown that even short-time I/R-induced DNA damage can be investigated in human peripheral leucocytes using the alkaline single-cell gel-electrophoresis assay (comet assay). (
  • During ischemia-reperfusion, oxygen-derived free radicals mediate tissue injury. (
  • Ischemia-reperfusion (IR) tissue injury is the resultant pathology from a combination of factors, including tissue hypoxia, followed by tissue damage associated with re-oxygenation. (
  • Effects of propofol pretreatment on myocardial cell apoptosis and SERCA2 expression in rats with hepatic ischemia/reperfusion. (
  • F. Clostre, A. Etienne, J. M. Mencia-Huerta and P. Braquet, Prevention of the platelet-activating factor induced gastrointestinal damages by BN 52021 and BN 52063, in: Ginkgolides -chemistry, biology, pharmacology and clinical perspectives, P. Braquet, ed. (
  • Peroxidase (MPO) and plasma lipid peroxidation product Malondialdehyde (MDA) play important roles in the pathogenesis of Multiple Organ Dysfunction Syndrome (MODS) caused by intestinal ischemia reperfusion-induced remote organ injury [ 6 , 7 ]. (
  • AKI is often associated with dysfunction of remote organs also known as distant organ injury. (
  • Rationale Primary graft dysfunction in lung transplant recipients derives from the initial, largely leukocyte-dependent, ischaemia-reperfusion injury. (
  • Objective To define the role of donor intravascular monocytes in lung transplant-related acute lung injury and primary graft dysfunction. (
  • Resident lung mononuclear phagocytes have been implicated in ischaemia-reperfusion injury and the development of primary graft dysfunction following lung transplantation, but the contribution of lung intravascular monocytes to lung transplant-related injury is not known. (
  • In conclusion, estradiol blunts intestinal injury induced by I/R by modulating chemokines release and leukocyte trafficking. (
  • The mortality caused by intestinal ischemia-reperfusion (I/R)-induced intestinal injury remains high, and few techniques or drugs are effective enough to use clinically. (
  • However, whether or not dexmedetomidine administration can provide protection against intestinal injury induced by intestinal I/R injury remains unclear. (
  • Therefore, the current experiment was designed to investigate the effects of different doses of dexmedetomidine (given before or after the ischemic phase) on intestinal injury after I/R injury and explore the potential mechanisms involved in the effects of dexmedetomidine. (
  • Low-level tragus stimulation for the treatment of ischemia and reperfusion injury in patients with ST-segment elevation myocardial infarction: a proof-of-concept study," JACC: Cardiovascular Interventions , vol. 10, no. 15, pp. 1511-1520, 2017. (
  • In a rat model of acute myocardial infarction (AMI) induced by I/R, administration of C1INH protected against cardiomyocytic apoptosis via normalization of ratio of the Bcl-2/Bax expression in the myocardial infarct area. (
  • It accounts for a great proportion of cell loss associated with myocardial infarction (MI) and / or ischemia-reperfusion (IR). (
  • Ischemia/reperfusion (I/R) injury represents a source of substantial morbidity and mortality in various statuses that is, coronary bypass, myocardial infarction, and so on. (
  • IR injury contributes to disease and mortality in a variety of pathologies, including myocardial infarction, ischemic stroke, acute kidney injury, trauma, circulatory arrest, sickle cell disease and sleep apnea. (