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.
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.
The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.
A 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)
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).
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 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.
NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).
The application of repeated, brief periods of vascular occlusion at the onset of REPERFUSION to reduce REPERFUSION INJURY that follows a prolonged ischemic event. The techniques are similar to ISCHEMIC PRECONDITIONING but the time of application is after the ischemic event instead of before.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
Injuries incurred during participation in competitive or non-competitive sports.
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
Penetrating and non-penetrating injuries to the spinal cord resulting from traumatic external forces (e.g., WOUNDS, GUNSHOT; WHIPLASH INJURIES; etc.).
Elements of limited time intervals, contributing to particular results or situations.
The dialdehyde of malonic acid.
Abrupt reduction in kidney function. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; ACUTE KIDNEY TUBULAR NECROSIS; and other less severe conditions.
A tissue or organ remaining at physiological temperature during decreased BLOOD perfusion or in the absence of blood supply. During ORGAN TRANSPLANTATION it begins when the organ reaches physiological temperature before the completion of SURGICAL ANASTOMOSIS and ends with reestablishment of the BLOOD CIRCULATION through the tissue.
A transferase that catalyzes formation of PHOSPHOCREATINE from ATP + CREATINE. The reaction stores ATP energy as phosphocreatine. Three cytoplasmic ISOENZYMES have been identified in human tissues: the MM type from SKELETAL MUSCLE, the MB type from myocardial tissue and the BB type from nervous tissue as well as a mitochondrial isoenzyme. Macro-creatine kinase refers to creatine kinase complexed with other serum proteins.
The pathological process occurring in cells that are dying from irreparable injuries. It is caused by the progressive, uncontrolled action of degradative ENZYMES, leading to MITOCHONDRIAL SWELLING, nuclear flocculation, and cell lysis. It is distinct it from APOPTOSIS, which is a normal, regulated cellular process.
Damage to any compartment of the lung caused by physical, chemical, or biological agents which characteristically elicit inflammatory reaction. These inflammatory reactions can either be acute and dominated by NEUTROPHILS, or chronic and dominated by LYMPHOCYTES and MACROPHAGES.
Synthetic or natural substances which are given to prevent a disease or disorder or are used in the process of treating a disease or injury due to a poisonous agent.
Localized reduction of blood flow to brain tissue due to arterial obstruction or systemic hypoperfusion. This frequently occurs in conjunction with brain hypoxia (HYPOXIA, BRAIN). Prolonged ischemia is associated with BRAIN INFARCTION.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
Treatment process involving the injection of fluid into an organ or tissue.
An anatomic severity scale based on the Abbreviated Injury Scale (AIS) and developed specifically to score multiple traumatic injuries. It has been used as a predictor of mortality.
The circulation of blood through the CORONARY VESSELS of the HEART.
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.
The hollow, muscular organ that maintains the circulation of the blood.
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).
Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).
The mitochondria of the myocardium.
Solutions which, upon administration, will temporarily arrest cardiac activity. They are used in the performance of heart surgery.
A tetrameric enzyme that, along with the coenzyme NAD+, catalyzes the interconversion of LACTATE and PYRUVATE. In vertebrates, genes for three different subunits (LDH-A, LDH-B and LDH-C) exist.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
General or unspecified injuries involving the leg.
The chilling of a tissue or organ during decreased BLOOD perfusion or in the absence of blood supply. Cold ischemia time during ORGAN TRANSPLANTATION begins when the organ is cooled with a cold perfusion solution after ORGAN PROCUREMENT surgery, and ends after the tissue reaches physiological temperature during implantation procedures.
The process by which organs are kept viable outside of the organism from which they were removed (i.e., kept from decay by means of a chemical agent, cooling, or a fluid substitute that mimics the natural state within the organism).
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
The process by which chemical compounds provide protection to cells against harmful agents.
Solutions used to store organs and minimize tissue damage, particularly while awaiting implantation.
A 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).
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).
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.
The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.
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
An enzyme that catalyzes the conversion of L-alanine and 2-oxoglutarate to pyruvate and L-glutamate. (From Enzyme Nomenclature, 1992) EC
Enzymes of the transferase class that catalyze the conversion of L-aspartate and 2-ketoglutarate to oxaloacetate and L-glutamate. EC
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.
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.
Damage or trauma inflicted to the eye by external means. The concept includes both surface injuries and intraocular injuries.
Non-human animals, selected because of specific characteristics, for use in experimental research, teaching, or testing.
Contractile activity of the MYOCARDIUM.
Highly reactive molecules with an unsatisfied electron valence pair. Free radicals are produced in both normal and pathological processes. They are proven or suspected agents of tissue damage in a wide variety of circumstances including radiation, damage from environment chemicals, and aging. Natural and pharmacological prevention of free radical damage is being actively investigated.
NECROSIS occurring in the MIDDLE CEREBRAL ARTERY distribution system which brings blood to the entire lateral aspects of each CEREBRAL HEMISPHERE. Clinical signs include impaired cognition; APHASIA; AGRAPHIA; weak and numbness in the face and arms, contralaterally or bilaterally depending on the infarction.
Naturally occurring or synthetic substances that inhibit or retard the oxidation of a substance to which it is added. They counteract the harmful and damaging effects of oxidation in animal tissues.
General or unspecified injuries to the neck. It includes injuries to the skin, muscles, and other soft tissues of the neck.
A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.
Substances that influence the course of a chemical reaction by ready combination with free radicals. Among other effects, this combining activity protects pancreatic islets against damage by cytokines and prevents myocardial and pulmonary perfusion injuries.
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.
Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids.
The act of constricting.
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.
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.
Sulfhydryl acylated derivative of GLYCINE.
The circulation of the BLOOD through the MICROVASCULAR NETWORK.
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.
General or unspecified injuries involving organs in the abdominal cavity.
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.
General or unspecified injuries involving the arm.
A XANTHINE OXIDASE inhibitor that decreases URIC ACID production. It also acts as an antimetabolite on some simpler organisms.
Pathological processes of the LIVER.
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.
General or unspecified injuries to the chest area.
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 partial or complete return to the normal or proper physiologic activity of an organ or part following disease or trauma.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
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.
10-carbon saturated monocarboxylic acids.
Organic compounds containing both the hydroxyl and carboxyl radicals.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Proteins involved in the transport of specific substances across the membranes of the MITOCHONDRIA.
Injuries involving the vertebral column.
The transference of a part of or an entire liver from one human or animal to another.
A nucleoside that is composed of ADENINE and D-RIBOSE. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter.
Injuries to the knee or the knee joint.
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.
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.
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.
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).
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.
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)
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.
A ubiquitous stress-responsive enzyme that catalyzes the oxidative cleavage of HEME to yield IRON; CARBON MONOXIDE; and BILIVERDIN.
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 termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.
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.
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 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.
A trisaccharide occurring in Australian manna (from Eucalyptus spp, Myrtaceae) and in cottonseed meal.
The veins and arteries of the HEART.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
An 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.
General or unspecified injuries to the soft tissue or bony portions of the face.
General or unspecified injuries to the heart.
Use of infusions of FIBRINOLYTIC AGENTS to destroy or dissolve thrombi in blood vessels or bypass grafts.
Examinations used to diagnose and treat heart conditions.
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.
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.
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.
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.
White blood cells. These include granular leukocytes (BASOPHILS; EOSINOPHILS; and NEUTROPHILS) as well as non-granular leukocytes (LYMPHOCYTES and MONOCYTES).
An iron-molybdenum flavoprotein containing FLAVIN-ADENINE DINUCLEOTIDE that oxidizes hypoxanthine, some other purines and pterins, and aldehydes. Deficiency of the enzyme, an autosomal recessive trait, causes xanthinuria.
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)
An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.
Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.
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.
General or unspecified injuries to the posterior part of the trunk. It includes injuries to the muscles of the back.
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.
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)
Injuries of tissue other than bone. The concept is usually general and does not customarily refer to internal organs or viscera. It is meaningful with reference to regions or organs where soft tissue (muscle, fat, skin) should be differentiated from bones or bone tissue, as "soft tissue injuries of the hand".
A relatively common sequela of blunt head injury, characterized by a global disruption of axons throughout the brain. Associated clinical features may include NEUROBEHAVIORAL MANIFESTATIONS; PERSISTENT VEGETATIVE STATE; DEMENTIA; and other disorders.
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.
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.
Traumatic injuries involving the cranium and intracranial structures (i.e., BRAIN; CRANIAL NERVES; MENINGES; and other structures). Injuries may be classified by whether or not the skull is penetrated (i.e., penetrating vs. nonpenetrating) or whether there is an associated hemorrhage.
A spectrum of clinical liver diseases ranging from mild biochemical abnormalities to ACUTE LIVER FAILURE, caused by drugs, drug metabolites, and chemicals from the environment.
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)
Injuries sustained from incidents in the course of work-related activities.
The univalent radical OH. Hydroxyl radical is a potent oxidizing agent.
A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.
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.
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.
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).
A CALCIUM-dependent, constitutively-expressed form of nitric oxide synthase found primarily in ENDOTHELIAL CELLS.
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 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 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
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
Damages to the CAROTID ARTERIES caused either by blunt force or penetrating trauma, such as CRANIOCEREBRAL TRAUMA; THORACIC INJURIES; and NECK INJURIES. Damaged carotid arteries can lead to CAROTID ARTERY THROMBOSIS; CAROTID-CAVERNOUS SINUS FISTULA; pseudoaneurysm formation; and INTERNAL CAROTID ARTERY DISSECTION. (From Am J Forensic Med Pathol 1997, 18:251; J Trauma 1994, 37:473)
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.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A vasodilator used in angina of effort or ischemic heart disease.
Injuries to the PERIPHERAL NERVES.
Harm or hurt to the ankle or ankle joint usually inflicted by an external source.
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)
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 adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter.
Relatively complete absence of oxygen in one or more tissues.
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)
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.
Increased intracellular or extracellular fluid in brain tissue. Cytotoxic brain edema (swelling due to increased intracellular fluid) is indicative of a disturbance in cell metabolism, and is commonly associated with hypoxic or ischemic injuries (see HYPOXIA, BRAIN). An increase in extracellular fluid may be caused by increased brain capillary permeability (vasogenic edema), an osmotic gradient, local blockages in interstitial fluid pathways, or by obstruction of CSF flow (e.g., obstructive HYDROCEPHALUS). (From Childs Nerv Syst 1992 Sep; 8(6):301-6)
The 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).
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)
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.
Injuries to blood vessels caused by laceration, contusion, puncture, or crush and other types of injuries. Symptoms vary by site and mode of injuries and may include bleeding, bruising, swelling, pain, and numbness. It does not include injuries secondary to pathologic function or diseases such as ATHEROSCLEROSIS.
Injuries caused by impact with a blunt object where there is no penetration of the skin.
The circulation of blood through the BLOOD VESSELS of the BRAIN.
The main structural component of the LIVER. They are specialized EPITHELIAL CELLS that are organized into interconnected plates called lobules.
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.
The number of times the HEART VENTRICLES contract per unit of time, usually per minute.
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.
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.
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.
A group of compounds that contain the general formula R-OCH3.
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.
Accidents on streets, roads, and highways involving drivers, passengers, pedestrians, or vehicles. Traffic accidents refer to AUTOMOBILES (passenger cars, buses, and trucks), BICYCLING, and MOTORCYCLES but not OFF-ROAD MOTOR VEHICLES; RAILROADS nor snowmobiles.
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.
One of the three polypeptide chains that make up the TROPONIN complex. It inhibits F-actin-myosin interactions.
Systems for assessing, classifying, and coding injuries. These systems are used in medical records, surveillance systems, and state and national registries to aid in the collection and reporting of trauma.
The circulation of blood through the BLOOD VESSELS supplying the abdominal VISCERA.
Injuries to tissues caused by contact with heat, steam, chemicals (BURNS, CHEMICAL), electricity (BURNS, ELECTRIC), or the like.
Fibrinolysin or agents that convert plasminogen to FIBRINOLYSIN.
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.
Inorganic or organic salts and esters of nitric acid. These compounds contain the NO3- radical.
Pathological processes of the KIDNEY or its component tissues.
General or unspecified injuries involving the foot.
General or unspecified injuries involving the fingers.
Wounds caused by objects penetrating the skin.
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.
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.
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 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.
Unforeseen occurrences, especially injuries in the course of work-related activities.
Deeply perforating or puncturing type intraocular injuries.
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.

Endothelin up-regulation and localization following renal ischemia and reperfusion. (1/4643)

BACKGROUND: Endothelin (ET), a potent vasoconstrictor, is known to play a role in ischemic acute renal failure. Although preproET-1 (ppET-1) mRNA is known to be up-regulated following ischemia/reperfusion injury, it has not been determined which component of the injury (ischemia or reperfusion) leads to initial gene up-regulation. Likewise, although ET-1 peptide expression has been localized in the normal kidney, its expression pattern in the ischemic kidney has not been determined. Therefore, the purpose of this study was twofold: (a) to determine whether ischemia alone or ischemia plus reperfusion is required for the up-regulation of ppET-1 mRNA to occur, and (b) to localize ET-1 peptide expression following ischemia in the rat kidney to clarify better the role of ET in the pathophysiology of ischemia-induced acute renal failure. METHODS: Male Lewis rats underwent clamping of the right renal vascular pedicle for either 30 minutes of ischemia (group 1), 60 minutes of ischemia (group 2), 30 minutes of ischemia followed by 30 minutes of reperfusion (group 3), or 60 minutes of ischemia followed by three hours of reperfusion (group 4). The contralateral kidney acted as a control. ppET-1 mRNA up-regulation and ET-1 peptide expression were examined using the reverse transcription-polymerase chain reaction and immunohistochemistry, respectively. RESULTS: Reverse transcription-polymerase chain reaction yielded a control (nonischemic) value of 0.6 +/- 0.2 densitometric units (DU) of ppET-1 mRNA in the kidney. Group 1 levels (30 min of ischemia alone) were 1.8 +/- 0.4 DU, a threefold increase (P < 0.05). Group 2 levels (60 min of ischemia alone) increased almost six times above baseline, 3.5 +/- 0.2 DU (P < 0.01), whereas both group 3 and group 4 (ischemia plus reperfusion) did not experience any further significant increases in mRNA levels (1.9 +/- 0.4 DU and 2.8 +/- 0.6 DU, respectively) beyond levels in group 1 or 2 animals subjected to similar ischemic periods. ET-1 peptide expression in the ischemic kidneys was significantly increased over controls and was clearly localized to the endothelium of the peritubular capillary network of the kidney. CONCLUSIONS: Initial ET-1 gene up-regulation in the kidney occurs secondary to ischemia, but reperfusion most likely contributes to sustaining this up-regulation. The marked increase of ET-1 in the peritubular capillary network suggests that ET-induced vasoconstriction may have a pathophysiological role in ischemic acute tubular necrosis.  (+info)

Hypothermic neuroprotection of peripheral nerve of rats from ischaemia-reperfusion injury. (2/4643)

Although there is much information on experimental ischaemic neuropathy, there are only scant data on neuroprotection. We evaluated the effectiveness of hypothermia in protecting peripheral nerve from ischaemia-reperfusion injury using the model of experimental nerve ischaemia. Forty-eight male Sprague-Dawley rats were divided into six groups. We used a ligation-reperfusion model of nerve ischaemia where each of the supplying arteries to the sciatic-tibial nerves of the right hind limb was ligated and the ligatures were released after a predetermined period of ischaemia. The right hind limbs of one group (24 rats) were made ischaemic for 5 h and those of the other group (24 rats) for 3 h. Each group was further divided into three and the limbs were maintained at 37 degrees C (36 degrees C for 5 h of ischaemia) in one, 32 degrees C in the second and 28 degrees C in the third of these groups for the final 2 h of the ischaemic period and an additional 2 h of the reperfusion period. A behavioural score was recorded and nerve electrophysiology of motor and sensory nerves was undertaken 1 week after surgical procedures. At that time, entire sciatic-tibial nerves were harvested and fixed in situ. Four portions of each nerve were examined: proximal sciatic nerve, distal sciatic nerve, mid-tibial nerve and distal tibial nerve. To determine the degree of fibre degeneration, each section was studied by light microscopy, and we estimated an oedema index and a fibre degeneration index. The groups treated at 36-37 degrees C underwent marked fibre degeneration, associated with a reduction in action potential and impairment in behavioural score. The groups treated at 28 degrees C (for both 3 and 5 h) showed significantly less (P < 0.01; ANOVA, Bonferoni post hoc test) reperfusion injury for all indices (behavioural score, electrophysiology and neuropathology), and the groups treated at 32 degrees C had scores intermediate between the groups treated at 36-37 degrees C and 28 degrees C. Our results showed that cooling the limbs dramatically protects the peripheral nerve from ischaemia-reperfusion injury.  (+info)

Does soluble intercellular adhesion molecule-1 (ICAM-1) affect neutrophil activation and adhesion following ischaemia-reperfusion? (3/4643)

OBJECTIVES: To examine the effect of reperfusion plasma and sICAM-1 on neutrophil integrin expression and neutrophil adhesion to determine if sICAM-1 has a potential role in the regulation of neutrophil adhesion. MATERIALS: Twenty-seven patients, 17 men and 10 women undergoing femorodistal surgery. Blood was taken preoperatively and from the femoral vein following the release of the cross-clamp. Neutrophils were obtained from five volunteers and incubated with phosphate buffered saline (PBS), preoperative plasma or reperfusion plasma with and without sICAM-1. Neutrophil expression of CD11b and adhesion were measured. MAIN RESULTS: Neutrophil CD11b expression did not change following incubation in the three media. Neutrophil adhesion increased significantly following exposure to reperfusion plasma compared to PBS or preoperative plasma (45.5 adhesion vs. 12.75%, p < 0.01 Mann-Whitney U-test). Soluble ICAM-1 decreased CD11b expression and adhesion in neutrophils exposed to reperfusion plasma only (CD11b expression fell from 15.9 to 3.4 mcf, p < 0.01 Mann-Whitney U-test and adhesion fell to 11.6% cells adhered, p < 0.01). CONCLUSION: An increase in CD11b expression is not required for an increase in neutrophil adhesion. The change in neutrophil adhesion produced by reperfusion plasma can be blocked by sICAM-1. Soluble ICAM-1 may have a physiological role in the regulation of neutrophil adhesion.  (+info)

Modification of postsynaptic densities after transient cerebral ischemia: a quantitative and three-dimensional ultrastructural study. (4/4643)

Abnormal synaptic transmission has been hypothesized to be a cause of neuronal death resulting from transient ischemia, although the mechanisms are not fully understood. Here, we present evidence that synapses are markedly modified in the hippocampus after transient cerebral ischemia. Using both conventional and high-voltage electron microscopy, we performed two- and three-dimensional analyses of synapses selectively stained with ethanolic phosphotungstic acid in the hippocampus of rats subjected to 15 min of ischemia followed by various periods of reperfusion. Postsynaptic densities (PSDs) from both area CA1 and the dentate gyrus were thicker and fluffier in postischemic hippocampus than in controls. Three-dimensional reconstructions of selectively stained PSDs created using electron tomography indicated that postsynaptic densities became more irregular and loosely configured in postischemic brains compared with those in controls. A quantitative study based on thin sections of the time course of PSD modification indicated that the increase in thickness was both greater and more long-lived in area CA1 than in dentate gyrus. Whereas the magnitude of morphological change in dentate gyrus peaked at 4 hr of reperfusion (140% of control values) and declined thereafter, changes in area CA1 persisted and increased at 24 hr of reperfusion (191% of control values). We hypothesize that the degenerative ultrastructural alteration of PSDs may produce a toxic signal such as a greater calcium influx, which is integrated from the thousands of excitatory synapses onto dendrites, and is propagated to the neuronal somata where it causes or contributes to neuronal damage during the postischemic phase.  (+info)

Intestinal reperfusion injury is mediated by IgM and complement. (5/4643)

Intestinal ischemia-reperfusion injury is dependent on complement. This study examines the role of the alternative and classic pathways of complement and IgM in a murine model of intestinal ischemia-reperfusion. Wild-type animals, mice deficient in complement factor 4 (C4), C3, or Ig, or wild-type mice treated with soluble complement receptor 1 were subjected to 40 min of jejunal ischemia and 3 h of reperfusion. Compared with wild types, knockout and treated mice had significantly reduced intestinal injury, indicated by lowered permeability to radiolabeled albumin. When animals deficient in Ig were reconstituted with IgM, the degree of injury was restored to wild-type levels. Immunohistological staining of intestine for C3 and IgM showed colocalization in the mucosa of wild-type controls and minimal staining for both in the intestine of Ig-deficient and C4-deficient mice. We conclude that intestinal ischemia-reperfusion injury is dependent on the classic complement pathway and IgM.  (+info)

Riluzole improves functional recovery after ischemia in the rat retina. (6/4643)

PURPOSE: Retinal ischemia leads to neuronal death. The effects of riluzole, a drug that protects against the deleterious effect of cerebral ischemia by acting on several types of ion channels and blocking glutamatergic neurotransmission, were investigated in a rat model of retinal ischemic injury. METHODS: Retinal ischemia was induced by increasing intraocular pressure above systolic blood pressure for 30 minutes. Electroretinograms were recorded before ischemia and at different periods of reperfusion. Riluzole was injected or topically applied to the eye before or after ischemia and twice daily during the reperfusion period. Retinas were harvested for histopathology (toluidine blue and silver-impregnation stainings, Tdt-dUTP terminal nick-end labeling [TUNEL] method) and immunohistochemistry for cytoskeletal glial fibrillary acid protein and c-jun NH2-terminal kinase (p-JNK). RESULTS: Ischemia for 30 minutes caused a reduction of a- and b-waves of the electroretinogram. Systemic and topical treatments with riluzole significantly enhanced the recovery of the reduced a- and b-waves after defined reperfusion times. Riluzole also prevented or attenuated ischemia-induced retinal cell death (necrosis and apoptosis) and reduced the activation of p-JNK, c-jun phosphorylation, and the increase of cytoskeletal proteins induced by ischemic injury. CONCLUSIONS: Riluzole acted in vivo as a potent neuroprotective agent against pressure-induced ischemia. Therefore, riluzole may be a major drug for use in protection against retinal injury.  (+info)

The effect of mannitol versus dimethyl thiourea at attenuating ischemia/reperfusion-induced injury to skeletal muscle. (7/4643)

OBJECTIVE: Mannitol is used as a treatment for skeletal muscle ischemia/reperfusion (I/R) injury in humans, despite the fact that its effectiveness in vivo is still disputed. The purpose of this study was to determine the efficacy of mannitol in attenuating I/R injury at the microcirculatory level. METHODS: The study was designed as an experimental study with male Wistar rats. The main outcome measures were intravital microscopy, which was used to measure capillary perfusion, capillary and venular red blood cell velocity (VRBC), and leukocyte-endothelial interactions in the extensor digitorum longus muscle of the rat hind limb before and after ischemia. In addition, tissue injury was assessed during reperfusion with the fluorescent vital dyes bisbenzimide and ethidium bromide. Dimethyl thiourea (DMTU), a highly effective therapeutic agent of experimental I/R injury, was used as a positive control. RESULTS: No-flow ischemia (2 hour) resulted in a 40% drop in capillary perfusion, a decline in capillary and venular VRBC, and increased leukocyte venular adherence and tissue infiltration. Tissue injury increased to a constant level during reperfusion. Mannitol attenuated capillary malperfusion during the first 60 minutes of reperfusion and prevented a decline in capillary VRBC. However, mannitol did not reduce tissue injury or leukocyte adherence and infiltration during reperfusion. By comparison, DMTU not only prevented the perfusion deficits and the increases in leukocyte venular adherence and tissue infiltration but significantly reduced the magnitude of tissue injury. CONCLUSION: Our findings suggest that mannitol may be of limited value for the prevention of early reperfusion-induced injury after no-flow ischemia in skeletal muscle. By comparison, DMTU was highly efficacious by not only reducing microvascular perfusion deficits but by also reducing leukocyte-endothelial cell interactions and the incidence of cellular injury.  (+info)

Bcl-2 inhibits ischemia-reperfusion-induced apoptosis in the intestinal epithelium of transgenic mice. (8/4643)

Little is known about the effects of ischemia-reperfusion on the inductive, commitment, or execution phases of apoptosis. We have created a genetically defined model to study the response of small intestinal epithelial cells to ischemia-reperfusion injury as a function of their proliferative status and differentiation. Occlusion of the superior mesenteric artery for 20 min in adult FVB/N or C57BL/6 mice results in the appearance of TUNEL-positive apoptotic cells in the jejunal epithelium within 4 h, with a maximum response occurring at 24 h. Stimulation of apoptosis is greater in postmitotic, differentiated epithelial cells located in the upper portions of villi compared with undifferentiated, proliferating cells in the crypts of Lieberkuhn (7-fold vs. 2-fold relative to sham-operated controls). Comparisons of p53(+/+) and p53(-/-) mice established that the apoptosis is p53 independent. To further characterize this response, we generated FVB/N transgenic mice that express human Bcl-2 in epithelial cells distributed from the base of crypts to the tips of their associated villi. The fivefold elevation in steady-state Bcl-2 concentration is not accompanied by detectable changes in the levels or cellular distributions of the related anti-apoptotic regulator Bcl-xL or of the proapoptotic regulators Bax and Bak and does not produce detectable effects on basal proliferation, differentiation, or death programs. The apoptotic response to ischemia-reperfusion is reduced twofold in the crypts and villi of transgenic mice compared with their normal littermates. These results suggest that both undifferentiated and differentiated cells undergo a commitment phase that is sensitive to Bcl-2. Forced expression of Bcl-2 also suppressed the p53-dependent death that occurs in proliferating crypt epithelial cells following gamma-irradiation. Thus suppressibility by Bcl-2 operationally defines a common feature of the apoptosis induced in the crypt epithelium by these two stimuli.  (+info)

The nuclear protein high-mobility group box 1 (HMGB1) is a key trigger for the inflammatory reaction during liver ischemia reperfusion injury (IRI). Hydrogen treatment was recently associated with down-regulation of the expression of HMGB1 and pro-inflammatory cytokines during sepsis and myocardial IRI, but it is not known whether hydrogen has an effect on HMGB1 in liver IRI. A rat model of 60 minutes 70% partial liver ischemia reperfusion injury was used. Hydrogen enriched saline (2.5, 5 or 10 ml/kg) was injected intraperitoneally 10 minutes before hepatic reperfusion. Liver injury was assessed by serum alanine aminotransferase (ALT) enzyme levels and histological changes. We also measured malondialdehyde (MDA), hydroxynonenal (HNE) and 8-hydroxy-guanosine (8-OH-G) levels as markers of the peroxidation injury induced by reactive oxygen species (ROS). In addition, pro-inflammatory cytokines including TNF-α and IL-6, and high mobility group box B1 protein (HMGB1) were measured as markers of post
TY - JOUR. T1 - Pirfenidone alleviates lung ischemia-reperfusion injury in a rat model. AU - Saito, Masao. AU - Chen-Yoshikawa, Toyofumi F.. AU - Suetsugu, Kimitaka. AU - Okabe, Ryo. AU - Takahagi, Akihiro. AU - Masuda, Satohiro. AU - Date, Hiroshi. PY - 2019/7. Y1 - 2019/7. N2 - Objective: Lung ischemia-reperfusion injury is among the complications seen after lung transplantation, resulting in morbidity and mortality. Pirfenidone, an antifibrotic agent for the treatment of idiopathic pulmonary fibrosis, is reported to have cytoprotective properties in various disease models. The purpose of this study was to investigate the effect of pirfenidone on lung ischemia-reperfusion injury. Methods: Male Lewis rats (260-290 g) were divided into 3 groups: sham group (n = 5), warm ischemia (WI) group (n = 10), and WI plus pirfenidone (WI+PFD) group (n = 10). The sham group underwent 210 minutes of perfusion without ischemia. The WI and WI+PFD groups underwent 90 minutes of warm ischemia and 120 minutes of ...
TY - JOUR. T1 - Methane attenuates hepatic ischemia/reperfusion injury in rats through antiapoptotic, anti-inflammatory, and antioxidative actions. AU - Ye, Zhouheng. AU - Chen, Quyang. AU - Zhang, Rongjia. AU - Nakao, Atsunori. AU - Fan, Danfeng. AU - Zhang, Ting. AU - Gu, Zhengyong. AU - Tao, Hengyi. AU - Sun, Xuejun. PY - 2015/9/1. Y1 - 2015/9/1. N2 - Hepatic ischemia/reperfusion (I/R) injury, which occurs in various diseases, introduces severe tissue damage and liver dysfunction. However, no promising therapies for such a significant condition currently exist. Methane has been suggested to exert a protective effect against intestinal I/R injury. In this study, we introduced methane to treat hepatic I/R injury to show its promising protective effect. Also, intraperitoneal injection with methane-rich saline, which could have potential clinical applications, was applied as a new method. Partial liver warm ischemia was applied in Sprague-Dawley rats for 60 min followed by succedent reperfusion. ...
TY - JOUR. T1 - Pseudomonas aeruginosa potentiates the lethal effect of intestinal ischemia-reperfusion injury. T2 - The role of in vivo virulence activation. AU - Fink, David. AU - Romanowski, Kathleen. AU - Valuckaite, Vesta. AU - Babrowski, Trissa. AU - Kim, Moses. AU - Matthews, Jeffrey B.. AU - Liu, Donald. AU - Zaborina, Olga. AU - Alverdy, John C.. PY - 2011/12/1. Y1 - 2011/12/1. N2 - Background: Experimental models of intestinal ischemia-reperfusion (IIR) injury are invariably performed in mice harboring their normal commensal flora, even though multiple IIR events occur in humans during prolonged intensive care confinement when they are colonized by a highly pathogenic hospital flora. The aims of this study were to determine whether the presence of the human pathogen Pseudomonas aeruginosa in the distal intestine potentiates the lethality of mice exposed to IIR and to determine what role any in vivo virulence activation plays in the observed mortality. Methods: Seven- to 9-week-old ...
TY - JOUR. T1 - Impact of epoxyeicosatrienoic acids in lung ischemia-reperfusion injury.. AU - Townsley, Mary I.. AU - Morisseau, Christophe. AU - Hammock, Bruce. AU - King, Judy A.. PY - 2010/2. Y1 - 2010/2. N2 - OBJECTIVE: Epoxyeicosatrienoic acids (EETs) are protective in both myocardial and brain ischemia, variously attributed to activation of K(ATP) channels or blockade of adhesion molecule upregulation. In this study, we tested whether EETs would be protective in lung ischemia-reperfusion injury. METHODS: The filtration coefficient (K(f)), a measure of endothelial permeability, and expression of the adhesion molecules vascular cell adhesion molecule (VCAM) and intercellular adhesion molecule (ICAM) were measured after 45 minutes ischemia and 30 minutes reperfusion in isolated rat lungs. RESULTS: K(f) increased significantly after ischemia-reperfusion alone vs time controls, an effect dependent upon extracellular Ca(2+) although not on the EET-regulated channel TRPV4. Inhibition of ...
TY - JOUR. T1 - (−)-Phenserine inhibits neuronal apoptosis following ischemia/reperfusion injury. AU - Chang, Cheng Fu. AU - Lai, Jing Huei. AU - Wu, John Chung Che. AU - Greig, Nigel H.. AU - Becker, Robert E.. AU - Luo, Yu. AU - Chen, Yen Hua. AU - Kang, Shuo Jhen. AU - Chiang, Yung Hsiao. AU - Chen, Kai Yun. PY - 2017/12/15. Y1 - 2017/12/15. N2 - Stroke commonly leads to adult disability and death worldwide. Its major symptoms are spastic hemiplegia and discordant motion, consequent to neuronal cell death induced by brain vessel occlusion. Acetylcholinesterase (AChE) is upregulated and allied with inflammation and apoptosis after stroke. Recent studies suggest that AChE inhibition ameliorates ischemia-reperfusion injury and has neuroprotective properties. (−)-Phenserine, a reversible AChE inhibitor, has a broad range of actions independent of its AChE properties, including neuroprotective ones. However, its protective effects and detailed mechanism of action in the rat middle cerebral ...
Protective Role of p70S6K in Intestinal Ischemia-Reperfusion Injury in Mice. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
TY - JOUR. T1 - Effect of adenoviral catalase gene transfer on renal ischemia/reperfusion injury in rats. AU - Yang, Chih Ching. AU - Hsu, Ship Ping. AU - Chen, Kuo Hsin. AU - Chien, Chiang Ting. N1 - Publisher Copyright: © 2015 by The Chinese Physiological Society and Airiti Press Inc.. PY - 2015. Y1 - 2015. N2 - Ischemia/reperfusion (I/R) may through overt H 2 O 2 -induced pathophysiologic mechanisms lead to renal dysfunction. We explore whether catalase (CAT) protein overexpression by adenoviral CAT gene (Adv-CAT) transfection may improve ischemia/reperfusion-induced renal dysfunction. We augmented renal CAT expression by intrarenal arterial Adv-CAT administration with renal venous clamping in avertin-anesthetized female Wistar rats. After Adv-CAT transfection, we examined the CAT expression, location and effects on blood urea nitrogen (BUN) and urinary tubular injury biomarkers by biochemical assays, microcirculation by a laser perfusion imager, renal H 2 O 2 amount by a chemiluminescent ...
Purpose: Liver ischemia reperfusion injury (IRI) remains a clinical problem associated with both surgical and non-surgical settings. Innate immune-dominated inflammation drives the pathogenesis of liver injuries. Although the activation of liver inflammation by IR have been studied extensively, few has been focused on the inflammation resolution in the disease process.. *Methods: In a murine liver partial warm ischemia model, we characterized the inflammation resolution during IR at histological, cellular and molecular levels. The role of Kupffer cells (KCs) was determined by clodronate-liposome (CL)-mediated depletion, and their functional mechanisms were explored by the inhibition of KC efferocytosis via TIM-4 blocking Abs, during the recovery stage of liver IRI (three doses at 24h, day 3 and day5 post reperfusion).. *Results: The restoration of liver homeostasis from a 90 min ischemia lasts for 7 days, as defined by: (i) repair of hepatocellular damage, (ii) clearance of infiltrating ...
Background: Cerebral ischemia-reperfusion injury (CIRI) can cause brain tissue inflammation, neuronal degeneration, and apoptosis. There is increasing evidence that microRNAs (miRNA) exert neuroprotective effects by regulating the inflammatory process during cerebral ischemia-reperfusion injury. Additionally, it is increasingly acknowledged that neuroinflammation is regulated by Toll-like receptor 4 (TLR4). However, it is unclear whether miRNA can exert its neuroprotective effects by regulating TLR4-mediated inflammation. Methods: The effects of BMSCs over-expressing miR-202-3p on CIRI, angiogenesis in midbrain tissue, and the release of inflammatory factors (IFs) in the serum were measured using in vivo rat models. We also used SH-SY5Y cells to establish an ischemia-reperfusion in vitro cell model. The interaction between miR-202-3p and TLR4 was analyzed by overexpressing miR-202-3p and knocking down TLR4. Knockdown of TLR4 was performed using siRNA. Results:
TY - JOUR. T1 - Role of the bronchial circulation in ischemia-reperfusion lung injury. AU - Pearse, D. B.. AU - Wagner, E. M.. PY - 1994/1/1. Y1 - 1994/1/1. N2 - Bronchial arterial (BA) perfusion could modify pulmonary arterial (PA) ischemia-reperfusion (IR) injury by promoting clearance of peribronchial edema or limiting edema formation through maintenance of pulmonary vessel integrity via bronchopulmonary anastomotic or pulmonary vasa vasorum flow. The purpose of this study was to determine the effect of BA perfusion on IR injury in isolated sheep lungs. In 12 lungs (BA++) the BA was perfused throughout 30 min of PA ischemia and 180 min of reperfusion. In 12 lungs (BA- +) BA perfusion was begun with PA reperfusion, and in 15 lungs (BA--) the BA was never perfused. After 180 min, extravascular lung water was less (P , 0.05) in BA++ and BA-+ lungs [4.70 ± 0.16 and 4.57 ± 0.18 g/g blood-free dry lung (bfdl)] than in BA-- lungs (5.23 ± 0.19 g/g bfdl). The reflection coefficient for albumin was ...
There is a very little information about the protective effect of lycopene (LYC) against hepatic ischemia-reperfusion injury. The present study was designed to examine the possible protective effect of the strong antioxidant and anti-inflammatory agent, LYC, on hepatic ischemia/reperfusion injury. For this purpose, rats were subjected to 45 min of hepatic ischemia followed by 60 min of reperfusion period. LYC at the doses of 2.5 and 5 mg/kg body weight (bw) were injected intraperitoneally, 60 min prior to ischemia. Upon sacrification, hepatic tissue samples were used for the measurement of catalase (CAT) activity and malondialdehyde (MDA) levels. Also, aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) were assayed in serum samples. As a result of the use of LYC at the doses of 2.5 and 5 mg/kg bw; while improvements of the ALT, AST, LDH and MDA values were partial and dose-dependent, the improvement of CAT activity was total and dose-independent (p , ...
TY - JOUR. T1 - Cannabinoid-2 receptor mediates protection against hepatic ischemia/reperfusion injury. AU - Bátkai, Sándor. AU - Osei-Hyiaman, Douglas. AU - Pan, Hao. AU - El-Assal, Osama. AU - Rajesh, Mohanraj. AU - Mukhopadhyay, Partha. AU - Hong, Feng. AU - Harvey-White, Judith. AU - Jafri, Anjum. AU - Haskó, G.. AU - Huffman, John W.. AU - Gao, Bin. AU - Kunos, George. AU - Pacher, Pál. PY - 2007/6. Y1 - 2007/6. N2 - Hepatic ischemia-reperfusion (I/R) injury continues to be a fatal complication that can follow liver surgery or transplantation. We have investigated the involvement of the endocannabinoid system in hepatic I/R injury using an in vivo mouse model. Here we report that I/R triggers several-fold increases in the hepatic levels of the endocannabinoids anandamide and 2-arachidonoylglycerol, which originate from hepatocytes, Kupffer, and endothelial cells. The I/R-induced increased tissue endocannabinoid levels positively correlate with the degree of hepatic damage and serum ...
Pulmonary ischemia-reperfusion injury (IRI) is a clinical syndrome of acute lung injury that occurs after lung transplantation or remote organ ischemia. IRI causes early mortality and has no effective therapies. While NK cells are innate lymphocytes capable of recognizing injured cells, their roles in acute lung injury are incompletely understood. Here, we demonstrated that NK cells were increased in frequency and cytotoxicity in 2 different IRI mouse models. We showed that NK cells trafficked to the lung tissue from peripheral reservoirs and were more mature within lung tissue. Acute lung ischemia-reperfusion injury was blunted in a NK cell-deficient mouse strain but restored with adoptive transfer of NK cells. Mechanistically, NK cell NKG2D receptor ligands were induced on lung endothelial and epithelial cells following IRI, and antibody-mediated NK cell depletion or NKG2D stress receptor blockade abrogated acute lung injury. In human lung tissue, NK cells were increased at sites of ...
PubMed journal article: Activation of sensory neurons reduces ischemia/reperfusion-induced acute renal injury in rats. Download Prime PubMed App to iPhone, iPad, or Android
TY - JOUR. T1 - Adenosine and inosine exert cytoprotective effects in an in vitro model of liver ischemia-reperfusion injury. AU - Modis, Katalin. AU - Gero, Domokos. AU - Stangl, Rita. AU - Rosero, Olivér. AU - Szijártó, Attila. AU - Lotz, Gábor. AU - Mohácsik, Petra. AU - Szoleczky, Petra. AU - Coletta, Ciro. AU - Szabo, Csaba. PY - 2013/2. Y1 - 2013/2. N2 - Liver ischemia represents a common clinical problem. In the present study, using an in vitro model of hepatic ischemia-reperfusion injury, we evaluated the potential cyto-protective effect of the purine metabolites, such as adenosine and inosine, and studied the mode of their pharmacological actions. The human hepatocellular carcinoma-derived cell line HepG2 was subjected to combined oxygen-glucose deprivation (COGD; 0-14-24 h), followed by re-oxygenation (0-4-24 h). Adenosine or inosine (300-1,000 μM) were applied in pretreatment. Cell viability and cytotoxicity were measured by the 3-(4,5-dimethyl-2-thiazolyl)-2, ...
Background: Ischemia and reperfusion (I/R) injury is a serious and common complication after liver surgery and transplantation. We previously showed that three days of preoperative fasting protects against hepatic I/R injury. The protective effect was induced by the absence of protein, since a protein-free diet induced similar protection. To investigate whether total protein or single essential amino acids are responsible, we investigated the effects of a three-day preoperative amino acid free diet on hepatic I/R injury in mice.. Materials and methods: Male C57BL/6 mice were randomized into four groups (n=6/group). Three days before the induction of hepatic I/R injury they received either a control diet, a leucin-free, methionine-free or tryptophan-free diet. Bodyweight was recorded during the dietary intervention and after surgery. Hepatic I/R injury was induced by clamping 70% of the liver for 75 minutes. Serum ALAT and LDH levels and the percentage of necrosis in liver tissue were used to ...
Discussion. In this study, we used the ischemia/reperfusion model developed for kidney function and injury studies at the Department of Anesthesiology, Botucatu Medical School. This model consists of right nephrectomy in all animals, followed by randomization of the animals into four groups of 10 animals per group: Ischemia, Ischemia + drug, Non-ischemia, and Non-ischemia + drug. Thus, parecoxib was tested in two groups, in the presence and absence of I/R (IP and NIP groups), and NGAL levels were measured in all groups at four times to evaluate renal function.. Nephrectomy followed by ischemia/reperfusion may trigger mechanisms of renal preconditioning, reducing histological lesions and preserving or facilitating recovery of renal function in the ischemic kidney. For instance, animals that had not been nephrectomized prior to ischemia/reperfusion had oliguric renal failure, whereas animals that had been nephrectomized prior to I/R developed polyuric renal failure with better prognosis and ...
The Hamid Rabb Lab is involved in translational research aimed at understanding the molecular pathogenesis of kidney ischemia/reperfusion injury. Were interested in the development of novel treatments for kidney IRI.. Research Areas: kidney diseases, kidney ischemia/reperfusion injuries, nephrology ...
BACKGROUND: In contrast with various pre-clinical studies, recent clinical trials suggest that high dose erythropoietin (EPO) treatment following kidney transplantation does not improve short-term outcome and that it even increases the risk of thrombotic events. ARA290 is a non-erythropoietic EPO derivative and does not increase the risk of cardiovascular events, but potentially has cytoprotective capacities in prevention of renal ischemia/reperfusion injury. METHODS: Eight female Dutch Landrace pigs were exposed to unilateral renal ischemia for 45 minutes with simultaneous cannulation of the ureter of the ischemic kidney. ARA290 or saline was administered by an intravenous injection at 0, 2, 4 and 6 hours post-reperfusion. The animals were sacrificed seven days post-reperfusion. RESULTS: ARA290 increased glomerular filtration rate during the observation period of seven days. Furthermore, ARA290 tended to reduce MCP-1 and IL-6 expression 15 minutes post-reperfusion. Seven days post-reperfusion ARA290
To explore the effects of propofol post-conditioning (PPC) on hepatic ischaemia/reperfusion injury (HIRI) and the potential mechanisms that might be involved in the interaction of Brahma-related gene1(BRG1) and Nuclear-related factor 2(Nrf2). Patients were randomized into PPC(n = 16) and non-PPC(NPC)( n = 21) groups. Propofol(2 mg/kg) was infused within 10 min. of the onset of liver reperfusion during liver transplantation in the PPC group. Liver function tests, as well as Brg1, Nrf2, Heme oxygenase-1(HO-1) and NADPH:quinone oxidoreductase1(NQO1) expression levels were evaluated. CMV-Brg1 mice were designed to investigate the role of Brg1 overexpression during HIRI. Brg1 and Nrf2 siRNA were used to examine the relationship between Brg1 and Nrf2/HO-1 pathways in propofol-mediated effects in a human hepatocyte(L02) hypoxia/reoxygenation(H/R) model. In patients, PPC attenuated both donor liver pathological and function injury, and reducing oxidative stress markers, compared to the NPC group, 24 hrs ...
Myocardial infarction (MI) induces cardiac remodeling. This may increase the susceptibility of the infarcted heart to subsequent ischemic events. While chronic angiotensin II blockade is cardioprotective post-MI, the acute effects of angiotensin II i
1. Aihara T, Shiraishi M, Hiroyasu S, Hatsuse K, Mochizuki H, Seki S. et al. Ulinastatin, a protease inhibitor, attenuates hepatic ischemia/reperfusion injury by downregulating TNF-alpha in the liver. Transplant Proc. 1998;30:3732-4 doi:S0041-1345(98)01214-7 [pii] 2. Yang YL, Li JP, Xu XP, Dou KF, Yue SQ, Li KZ. Protective effects of tumor necrosis factor alpha antibody and ulinastatin on liver ischemic reperfusion in rats. World J Gastroenterol. 2004;10:3161-4 3. Klune JR, Dhupar R, Cardinal J, Billiar TR, Tsung A. HMGB1: endogenous danger signaling. Mol Med. 2008;14:476-84 doi:10.2119/2008-00034.Klune 4. Kang R, Livesey KM, Zeh HJ 3rd, Lotze MT, Tang D. HMGB1 as an autophagy sensor in oxidative stress. Autophagy. 2011;7:904-6 doi:15704 [pii] 5. Fan J, Li Y, Levy RM, Fan JJ, Hackam DJ, Vodovotz Y. et al. Hemorrhagic shock induces NAD(P)H oxidase activation in neutrophils: role of HMGB1-TLR4 signaling. J Immunol. 2007;178:6573-80 6. Tang D, Shi Y, Kang R, Li T, Xiao W, Wang H. et al. Hydrogen ...
TY - JOUR. T1 - Interleukin-10 delivery via mesenchymal stem cells. T2 - A novel gene therapy approach to prevent lung ischemia-reperfusion injury. AU - Manning, Eddie. AU - Pham, Si. AU - Li, Sen. AU - Vazquez-Padron, Roberto I. AU - Mathew, James. AU - Ruiz, Phillip. AU - Salgar, Shashikumar K.. PY - 2010/6/1. Y1 - 2010/6/1. N2 - Ischemia-reperfusion (IR) injury is an important cause of primary graft failure in lung transplantation. In this study, viral interleukin-10 (vIL-10)-engineered mesenchymal stem cells (MSCs) were tested for their ability to prevent lung IR injury. Bone marrow-derived MSCs were transduced with rvIL-10-retrovirus. After 120min of warm left lung ischemia, rats received ∼15×106 vIL-10-engineered MSCs (MSC-vIL-10), empty vector-engineered MSCs (MSC-vec), or saline intravenously. Mean blood oxygenation (PaO2/FiO2 ratio, mmHg) was measured at 4hr, 24hr, 72hr, and 7 days. As early as 4hr post-IR injury with MSC-vIL-10 treatment, blood oxygenation was significantly (p,0.05) ...
Objective To evaluate the impact of miR-148a on hepatic ischemia/reperfusion (I/R) injury via inhibiting Ca(2+)/calmodulin-dependent protein kinase IIα (CaMKIIα), and analyze the potential mechanism. Methods Liver I/R model was built in mice. Expression of CaMKIIα was detected in the hepatic tissues by Western blotting. The mRNA levels of miR-148a, CaMKIIα, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were analyzed by quantitative real-time PCR (qRT-PCR). HE staining was performed to observe morphological changes of the livers in each group. TUNEL was used to evaluate the degree of hepatocellular apoptosis in each group. Results After hepatic I/R injury, the expression of miR-148a increased, and it was negatively correlated with CaMKIIα. After therapy with exogenous miR-148a mimics, the protein expression of CaMKIIα, the mRNA levels of TNF-α and IL-1β, the degree of inflammatory cell infiltration and liver cell necrosis, and the level of hepatocellular apoptosis were all
TY - JOUR. T1 - Reduced ischemia and reperfusion injury following exercise training. AU - Libonati, Joseph R.. AU - Gaughan, John P.. AU - Hefner, Colleen A.. AU - Gow, Andrew. AU - Paolone, Albert M.. AU - Houser, Steven R.. PY - 1997. Y1 - 1997. N2 - We examined the effects of two exercise training modalities, i.e., low intensity endurance and sprint running, on in vitro, isovolumic myocardial performance following ischemia and reperfusion. Rats ran on a treadmill 5 d · wk-1 for 6 wk at the following levels: endurance; 20 m · min-1, 0% grade, 60 min · d-1 and sprint; five 1-min runs at 75 m · min-1, 15% grade interspersed with 1-min active recovery runs at 20 m · min-1, 15% grade. Both endurance and sprint training significantly improved exercise tolerance relative to control (P ,0.05) on two graded exercise tests. Buffer perfused hearts of control (N = 18), endurance (N = 20), and sprint (N = 13) trained animals underwent no-flow ischemia (20 min) and reperfusion (30 min) in a ...
The goal of this study was to determine the protective effect of ticagrelor against ischemia-reperfusion injury in the kidney of rats via histological examination, biochemical parameters, and immunohistochemical analysis. Thirty male rats were randomized into five groups. The animals received ticagrelor 5 mg/kg, 10 mg/kg and 20 mg/kg or normal saline 0.1 mL/kg (control) orally before the procedure. The shame group only had laparatomy.An ischemia-reperfusion injury was done by clamping the renal hilus. There was less malondealdehyde assay (MDA) in ticagrelor groups than the control group, and this decrease was statistically significant (P= 0.001 in all ticagrelor received groups). The glutathione peroxidase (GPx) and glutathione reductase (GR) were elevated in ticagrelor groups at all doses. Similar findings were observed in all treatment groups. The 5 mg ticagrelor treated group had no changes in glomerules and tubules relative to the control group via histology. Dilated tubular structures were ...
We used COX-2-deficient mice to investigate the role of COX-2 in the mechanisms of liver I/R injury. Our data demonstrate that COX-2−/− mice, compared with their WT counterparts, were significantly less susceptible to liver I/R reperfusion injury. COX-2−/− mice showed reduced sGPT and sGOT levels after I/R injury, which indicate that liver damage was reduced in these mice as compared with WT controls. Inflammatory processes are mediated by multiple molecular mechanisms, and COX-2 is a major inflammatory mediator (44). Our observation that the lack of COX-2 confers a protective role in liver I/R injury is supported by our own celecoxib studies, in which selective COX-2 inhibition ameliorated mouse liver I/R injury. This observation is also supported by other publications, in which COX-2 inhibition was beneficial in rat liver I/R injury (22, 23).. Bcl-2 and Bcl-xL play an important role in inhibition of apoptotic cell death and are essential for maintenance of major organ systems (49). ...
TY - JOUR. T1 - Dexamethasone protects from renal ischemia/reperfusion injury. T2 - A possible association with SGK-1. AU - Rusai, Krisztina. AU - Prokai, A.. AU - Juanxing, C.. AU - Meszaros, K.. AU - Szalay, B.. AU - Pásti, K.. AU - Müller, V.. AU - Heemann, U.. AU - Lutz, J.. AU - Tulassay, T.. AU - Szabo, A.. PY - 2013/6/1. Y1 - 2013/6/1. N2 - Previous experimental data suggest that steroids might have protective effects during hypoxic/ischemic injury of various organs. In this study, the association between dexamethason (Dexa) treatment and the anti-apoptotic SGK-1 was tested in ischemic renal injury. In vitro, HK-2 cells were exposed to 24 h hypoxia, and the effect of Dexa incubation on SGK-1 expression / activation and on cell death was studied. In an in vivo rat model of unilateral renal IR, animals were treated with Dexa, and serum renal function parameters, tissue injury and SGK-1 expression and localization were examined after different reperfusion times (2 h, 4 h and 24 h). Dexa at ...
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Ischemia/reperfusion (I/R) injury remains a major complication of liver resection, transplantation, and hemorrhagic shock. Although the mechanisms that contribute to hepatic I/R are complex and diverse involving the interaction of cell injury in hepatocytes, immune cells, and endothelium, mitochondrial dysfunction is a cardinal event culminating in hepatic reperfusion injury. Mitochondrial autophagy, so-called mitophagy, is a key cellular process that regulates mitochondrial homeostasis and eliminates damaged mitochondria in a timely manner. Growing evidence accumulates that I/R injury is attributed to defective mitophagy. This review aims to summarize the current understanding of autophagy and its role in hepatic I/R injury and highlight the various therapeutic approaches that have been studied to ameliorate injury.
TY - JOUR. T1 - Absence of glutathione peroxidase-1 exacerbates cerebral ischemia-reperfusion injury by reducing post-ischemic microvascular perfusion. AU - Wong, Connie Hoi Yee. AU - Bozinovski, Steven. AU - Hertzog, Paul John. AU - Hickey, Michael John. AU - Crack, Peter J. PY - 2008. Y1 - 2008. N2 - Mice deficient in the anti-oxidant enzyme glutathione peroxidase-1 (Gpx1) have a greater susceptibility to cerebral injury following a localized ischemic event. Much of the response to ischemia-reperfusion is caused by aberrant responses within the microvasculature, including inflammation, diminished endothelial barrier function (increased vascular permeability), endothelial activation, and reduced microvascular perfusion. However, the role of Gpx1 in regulating these responses has not been investigated. Wild-type and Gpx1-/- mice underwent focal cerebral ischemia via mid-cerebral artery occlusion followed by measurement of cerebral perfusion via laser Doppler and intravital microscopy. ...
TY - JOUR. T1 - Ex vivo application of carbon monoxide in UW solution prevents transplant-induced renal ischemia/reperfusion injury in pigs. AU - Yoshida, J.. AU - Ozaki, K. S.. AU - Nalesnik, M. A.. AU - Ueki, S.. AU - Castillo-Rama, M.. AU - Faleo, G.. AU - Ezzelarab, M.. AU - Nakao, A.. AU - Ekser, B.. AU - Echeverri, G. J.. AU - Ross, M. A.. AU - Stolz, D. B.. AU - Murase, N.. PY - 2010/4. Y1 - 2010/4. N2 - I/R injury is a major deleterious factor of successful kidney transplantation (KTx). Carbon monoxide (CO) is an endogenous gaseous regulatory molecule, and exogenously delivered CO in low concentrations provides potent cytoprotection. This study evaluated efficacies of CO exposure to excised kidney grafts to inhibit I/R injury in the pig KTx model. Porcine kidneys were stored for 48 h in control UW or UW supplemented with CO (CO-UW) and autotransplanted in a 14-day follow-up study. In the control UW group, animal survival was 80% (4/5) with peak serum creatinine levels of 12.0 ± 5.1 ...
Orexin A (OXA) is a neuroprotective peptide that exerts protective effects on multiple physiological and pathological processes. Activation of autophagy is linked to the occurrence of cerebral ischemia-reperfusion injury (CIRI); however, its function remains incompletely understood. In this study, OXA was sought to exert its neuroprotective role by regulating autophagy in oxygen and glucose deprivation and reoxygenation (OGD/R) model and middle cerebral artery occlusion (MCAO) model of rats, and to elucidate the underlying molecular mechanisms. Acridine orange (AO) staining was used to evaluate autophagic vacuoles. Cell viability was measured by CCK8. The levels of p-ERK1/2, t-ERK1/2, p-mTOR, LC3B, Beclin 1, and p62 were evaluated by western blotting. Apoptosis rate was detected by Hoechst 33342 staining and Terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling (TUNEL). OXA treatment alleviated neuronal apoptosis and significantly inhibited autophagy activity. Mechanistically, OXA ...
TY - JOUR. T1 - Intestinal P-glycoprotein expression is multimodally regulated by intestinal ischemia-reperfusion. AU - Terada, Yusuke. AU - Ogura, Jiro. AU - Tsujimoto, Takashi. AU - Kuwayama, Kaori. AU - Koizumi, Takahiro. AU - Sasaki, Shunichi. AU - Maruyama, Hajime. AU - Kobayashi, Masaki. AU - Yamaguchi, Hiroaki. AU - Iseki, Ken. PY - 2014/6/2. Y1 - 2014/6/2. N2 - Purpose. Reactive oxygen species (ROS) have multiple physiological effects that are amount-dependent. ROS are one of the causes of intestinal ischemia-reperfusion (I/R) injury. In this study, we investigated whether the amount of ROS and the degree of intestinal I/R injury affect the expression level of P-glycoprotein (P-gp). Methods. We used hydrogen peroxide (H2O2) as ROS in in vitro experiments. Intestinal I/R model rats, which were subjected 15-min ischemia (I/R-15), were used in in vivo experiments. Results. P-gp expression in Caco-2 cells was increased in response to 1 μM of H2O2 but decreased upon exposure to 10 mM of ...
Abstract. Background: Increasing evidences suggest that innate immunity is involved in cerebral ischemia-reperfusion (I/R) injury, but the liable innate immune receptors have not been completely elucidated. Here, we explored the role of the nucleotide-binding oligomerization domain (NOD)2, a member of the cytosolic NOD-like receptor family, in acute focal cerebral I/R injury.. Methods: An in vivo middle cerebral artery occlusion (MCAO) model that in wild type (WT) and NOD2 deficient (NOD2-/-) mice and in vitro model of oxygen glucose deprivation and reoxygenation (OGD/R) in cultured primary microglia and astrocytes were used to investigate the expression of NOD2 and explore the roles of NOD2 in ischemic stroke.. Results: Our results showed that NOD2 expression was significantly increased in microglia and astrocytes in response to the I/R insult. Pretreatment with muramyl dipeptide, an extrinsic ligand of NOD2, significantly increased the infarct volume and neurological dysfunction in mice ...
Remote ischemic preconditioning (RIPC) initiates endogenous protective pathways in the brain from a distance and represents a new, promising paradigm in neuroprotection against cerebral ischemia-reperfusion (I/R) injury. However, the underlying mechanism of RIPC-mediated cerebral ischemia tolerance is complicated and not well understood. We reported previously that preactivation of Notch1 mediated the neuroprotective effects of cerebral ischemic preconditioning in rats subjected to cerebral I/R injury. The present study seeks to further explore the role of crosstalk between the Notch1 and NF-κB signaling pathways in the process of RIPC-induced neuroprotection. Middle cerebral artery occlusion and reperfusion (MCAO/R) in adult male rats and oxygen-glucose deprivation and reoxygenation (OGD/R) in primary hippocampal neurons were used as models of I/R injury in vivo and in vitro, respectively. RIPC was induced by a 3-day procedure with 4 cycles of 5 min of left hind limb ischemia followed by 5 min of
TY - JOUR. T1 - β-hydroxybutyrate attenuates renal ischemia-reperfusion injury through its anti-pyroptotic effects. AU - Tajima, Takaya. AU - Yoshifuji, Ayumi. AU - Matsui, Ayumi. AU - Itoh, Tomoaki. AU - Uchiyama, Kiyotaka. AU - Kanda, Takeshi. AU - Tokuyama, Hirobumi. AU - Wakino, Shu. AU - Itoh, Hiroshi. N1 - Funding Information: This work was partially supported by grants from the Ministry of Education, Culture, Science, Sports and Technology of Japan (26253053, 16H05315). The authors are grateful to Professor Ikuo Kimura, Dr. Junki Miyamoto, and Dr. Junichiro Irie for helpful discussions and to Novartis Pharmaceuticals for helpful support to provide the place to perform research. Publisher Copyright: © 2019 International Society of Nephrology. PY - 2019/5. Y1 - 2019/5. N2 - Ketone bodies including β-hydroxybutyrate (β-OHB) have been shown to protect against ischemic tissue injury when present at low concentrations. We evaluated the impact of β-OHB on renal ischemia/reperfusion injury ...
The objective of the present study was to determine whether preischemic administration of syringic acid (SA) would attenuate renal ischemia-reperfusion injury (IRI). Rats were divided into three groups: Sham group; IR group; and IR + SA group. The effects of SA were examined using biochemical parameters including serum ischemia-modified albumin (IMA), total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), tissue superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and malondialdehyde (MDA). The apoptosis status and histopathological changes were evaluated. After calculating the score for each histopathological change, the total score was obtained by summing all the scores. In the SA group, MDA, IMA, TOS, and OSI decreased significantly compared to the IR group. After SA administration, the increase in GPx activity was found to be significant. Apoptosis decreased significantly in the SA group compared with the IR group. The total score ...
Principal Investigator:WAKIDA Yasushi, Project Period (FY):1995 - 1997, Research Category:Grant-in-Aid for Scientific Research (C), Section:一般, Research Field:Circulatory organs internal medicine
Protective Effect of Pharmacological Preconditioning of Total Flavones of Abelmoschl Manihot on Cerebral Ischemic Reperfusion Injury in Rats. The present study was to investigate the effect of pharmacological preconditioning of total flavones of Abelmoschl Manihot (TFA) on cerebral ischemic reperfusion injury in rats. Rat cerebral isch.... ...
TY - JOUR. T1 - Cloning and expression of rat caspase-6 and its localization in renal ischemia/reperfusion injury. AU - Singh, Amar B.. AU - Kaushal, Varsha. AU - Megyesi, Judit K.. AU - Shah, Sudhir V.. AU - Kaushal, Gur P.. PY - 2002/1/1. Y1 - 2002/1/1. N2 - Background. Caspase-6 is an important member of the executioner caspases in the caspase family of cell death proteases. The executioner caspases are the major active caspases detected in apoptotic cells and are generally considered to mediate the execution of apoptosis by cleaving and inactivating intracellular proteins. However, the complete characterization of mRNA and protein of caspase-6 in rat and its expression in normal kidney and in disease state has not been previously elucidated. Methods. A rat kidney cortex λgt10 cDNA library was screened to isolate the full-length caspase-6 cDNA. The recombinant caspase-6 protein was characterized by expression in bacteria and by transient transfection in mammalian cells. The expression in ...
Ischemia/reperfusion injury (IRI) remains a major problem in organ transplantation, which represents the main cause of graft dysfunction posttransplantation. Hepatic IRI is characterized by an excessive inflammatory response within the liver. Mesenchymal stem cells (MSCs) have been shown to be immunomodulatory cells and have the therapeutic action on IRI in several organs. However, the mechanism of regulatory effect of MSCs on IRI remains unclear. In the present study, we examined the impact of MSCs on hepatic inflammatory response such as neutrophil influx and liver damage in a rat model of 70% hepatic IRI. Treatment with MSCs protected rat against hepatic IRI, with significantly decreased serum levels of liver enzymes, attenuated hepatic neutrophil infiltration, reduced expression of apoptosis-associated proteins, and ameliorated liver pathological injury. MSCs also significantly enhanced the intracellular activation of p38 MAPK phosphorylation, which led to decreased expression of CXCR2 on the
Abstract: : Purpose: To evaluate the expression of heme oxygenase-1 (HO-1), which is a heme-catabolizing enzyme induced by oxidative stress and acts against oxidant-induced tissue injury, on ischemia-reperfusion injury in the rat retina. Methods: Retinal ischemia was induced in male 8weeks SD rats by increasing the intraocular pressure to 110 mmHg for 45 minutes. At 6, 12, 24, and 48 hours after reperfusion, rat eyes were enucleated. Expression of HO-1 and HO-2, a constitutive isoform, in mRNA level in the retina was determined by using RT-PCR and that of protein levels were also studied by using Western blotting analysis. For immunohistochemical double-labeling, sections were incubated with antibodies against HO-1 and S-100. To evaluate possible neuroprotective effects of hemin, an inducer of HO-1, we injected 150 mg/kg of hemin intraperitoneally before the ischemia. The degree of retinal damage was assessed by electroretinogram (ERG) recording on 1, 2 and 4 weeks thereafter, by measuring the ...
Introduction/Aim Ischemia Reperfusion injury is a poorly understood entity with wide-ranging clinical implications touching on most fields of clinical medicine. Using skin flap and hind limb models of injury in the mouse we attempt to reduce ischemia reperfusion injury by targeting different parts of the ischemia reperfusion injury pathway. Methods Dorsal lateral thoracic artery island skin flaps (3.5x1.5 cm) were elevated in C57BL/6 mice and rendered ischemic for 10 hours by placing a 7 mm microclamp on the vascular pedicle followed by 7 days of reperfusion. Hind-limb ischemia (was achieved with orthodontic rubber bands applied above the greater trochanter of male C57BL/6 mice using a McGivney Haemorrhoid Ligator. Limbs underwent ischemia for two hours followed by 24 hours reperfusion prior to euthanasia. Animals were treated with intravenous Poloxamer 188 and P8 IgM-binding protein to assess their effect on ischemiareperfusion injury. Results Administration of P188 prior to ischemia gave an ...
AngII (angiotensin II), ACE (angiotensin I-converting enzyme) and the AT(1) receptor (AngII type I receptor) are associated with the inflammatory process and microvascular dysfunction of AKI (acute kidney injury) induced by renal I/R (ischaemia/reperfusion). However, Ang-(1-7) [angiotensin-(1-7)], ACE2 (angiotensin I-converting enzyme 2) and the Mas receptor also play a role in renal disease models. Therefore, in the present study, we have examined the renal profile of Ang-(1-7), ACE2 and the Mas receptor in renal I/R and compared them with that of AngII, ACE and the AT(1) receptor. Male Wistar rats were submitted to left nephrectomy and ischaemia (45 min) followed by reperfusion (2 or 4 h) in the right kidney. At 4 h of reperfusion, renal AngII was increased (P , 0.01) and renal Ang-(1-7) was decreased substantially (P , 0.05), although plasma levels of both angiotensins were unchanged. in addition, renal I/R decreased the renal mRNA expression of renin (P , 0.05), AT(1) receptors (P , 0.001) ...
AIM To investigate the protective effects of metallothionein induced by Zn 2+ on ischemia/reperfusion myocardium in isolated rat heart. METHODS 32 Sprague-Dawley rats were randomly divided into 4 groups (n=8, respectively): control group, ischemia/reperfusion (I/R) group, Zn 2+ pretreated group (ZPC), PD98059 (inhibitor of extracellular signal regulated protein kinase)+Zn 2+ pretreated group (PZPC). The levels of creatime kinase (CK), lacatate dehydrogenase (LDH) and adenosine triphosphate (ATP), which indicated myocardium injury, and the cardiac function(LVSP and±dp/dt max), were observed in this study. The expression levels of MT were valued by the 109Cd/hemoglobin affinity assays. RESULTS The expression level of MT was higher in ZPC group than in control group and I/R group. Compared with I/R group, the level of LDH and CK was reduced, ATP content was increased, and cardiac function (LVSP and±dp/dt max) was improved (P0.01) in ZPC group. The correspond data between
The present study aimed to investigate the protective effects of rhein on cerebral ischemic/reperfusion (I/R) injury in rats. The present study focused on the effect of rhein on oxidative stress and apoptotic factors, which are considered to serve an important role in the onset of I/R injury. Sprague‑Dawley rats were subjected to middle cerebral artery occlusion. Neurological functional scores (NFSs) were evaluated according to the Zea Longas score criteria and the area of brain infarct was determined by triphenyltetrazolium chloride staining. The morphology of the nerve cells in the cortex was observed following hematoxylin and eosin staining. In addition, levels of oxidative stress were assessed by measuring the levels of superoxide dismutase (SOD), glutathione‑peroxidase (GSH‑Px), catalase (CAT) and malondialdehyde (MDA). Levels of B‑cell lymphoma-2 (Bcl‑2), apoptosis regulator Bax (BAX), caspase-9, caspase‑3 and cleaved caspase‑3 expression were analyzed using western blot ...
TY - JOUR. T1 - Activation of BNIP3-mediated mitophagy protects against renal ischemia-reperfusion injury. AU - Tang, Chengyuan. AU - Han, Hailong. AU - Liu, Zhiwen. AU - Liu, Yuxue. AU - Yin, Lijun. AU - Cai, Juan. AU - He, Liyu. AU - Liu, Yu. AU - Chen, Guochun. AU - Zhang, Zhuohua. AU - Yin, Xiao-Ming. AU - Dong, Zheng. PY - 2019/9/12. Y1 - 2019/9/12. N2 - Acute kidney injury (AKI) is a syndrome of abrupt loss of renal functions. The underlying pathological mechanisms of AKI remain largely unknown. BCL2-interacting protein 3 (BNIP3) has dual functions of regulating cell death and mitophagy, but its pathophysiological role in AKI remains unclear. Here, we demonstrated an increase of BNIP3 expression in cultured renal proximal tubular epithelial cells following oxygen-glucose deprivation-reperfusion (OGD-R) and in renal tubules after renal ischemia-reperfusion (IR)-induced injury in mice. Functionally, silencing Bnip3 by specific short hairpin RNAs in cultured renal tubular cells reduced ...
The principal objectives of this were to determine whether hepatocyte membrane potentials (PD) are altered during liver transplantation and whether such changes may be of pathophysiologic importance in ischemia/reperfusion injury and graft survival. Livers of adult male Sprague-Dawley rats (N = 3-4/group) were impaled with intracellular microelectrodes prior to and at various time periods for six hours following complete hepatic resection. Just prior to resection each liver was perfused with preservation solutions associated with high (normal saline, NS), moderate (Eurocollins, EC) and low (University of Wisconsin solution, UW) risks of reperfusion injury. To determine whether changes are of pathophysiologic importance, the NS solution was modified (addition of 0.1% ethanol) to achieve similar PD changes as those observed with UW. Liver transplants were then performed using a nonarterialized, cuff technique in adult Lewis rats where the donor livers had been perfused and preserved for six hours ...
Targeting ischemia/reperfusion injury[edit]. Main article: Reperfusion injury. With reperfusion comes ischemia/reperfusion (IR ... Grace, P. A. (May 1994). "Ischaemia-reperfusion injury". The British Journal of Surgery. 81 (5): 637-647. doi:10.1002/bjs. ... "Revisiting Cerebral Postischemic Reperfusion Injury: New Insights in Understanding Reperfusion Failure, Hemorrhage, and Edema ... Yellon, Derek M.; Hausenloy, Derek J. (2007-09-13). "Myocardial Reperfusion Injury". New England Journal of Medicine. 357 (11 ...
Ischemia reperfusion injuryEdit. Succinate accumulation under hypoxic conditions has been implicated in the reperfusion injury ... 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 ... "Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS". Nature. 515 (7527): 431-5. Bibcode: ...
After MI, the myocardium suffers from reperfusion injury which leads to death of cardiomyocytes and detrimental remodelling of ... Transfection of cardiac myocytes with human HGF reduces ischemic reperfusion injury after MI. The benefits of HGF therapy ... Yellon, D. M.; Hausenloy, D. J. (2007). "Myocardial Reperfusion Injury". New England Journal of Medicine. 357 (11): 1121-1135. ... It is produced and proteolytically cleaved to its active state in response to cellular injury or during apoptosis. HGF binds to ...
Injury to the myocardium also occurs during re-perfusion. This might manifest as ventricular arrhythmia. The re-perfusion ... 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. ... injury is a consequence of the calcium and sodium uptake from the cardiac cells and the release of oxygen radicals during re- ...
RIC not only confers protection against ischemia-reperfusion injury, but also increases cerebral blood flow, which may ... "Automated Remote Ischemic Conditioning Device Easier to Use than Manual Cuff to Reduce Reperfusion Injury". www.abstractsonline ... This "conditioning" activates the body's natural protective physiology against reperfusion injury and the tissue damage caused ... Hausenloy, Derek J.; Yellon, Derek M. (2016). "Ischaemic conditioning and reperfusion injury". Nature Reviews Cardiology. 13 (4 ...
They speculated that the effect was related to its antioxidant action on the initial ischemia/reperfusion injury of the renal ... Thus, free radical-mediated reperfusion injury was seen to contribute to the process of innate and subsequent adaptive immune ... Kalogeris T, Baines CP, Krenz M, Korthuis RJ (2012). "Cell biology of ischemia/reperfusion injury". International Review of ... "Acute kidney injury", Wikipedia, 2020-06-13, retrieved 2020-06-16 Anders HJ, Schaefer L (July 2014). "Beyond tissue injury- ...
Pretreatment it reduced reperfusion injury in volunteers. It has been shown to increase myocardial perfusion and left ...
Ischemia-reperfusion injury of the appendicular musculoskeletal system. References[edit]. .mw-parser-output .reflist{font-size: ... Myoglobin is a sensitive marker for muscle injury, making it a potential marker for heart attack in patients with chest pain.[ ... In humans, myoglobin is only found in the bloodstream after muscle injury.[11][12][13] ... Myoglobin is not specific for myocardial necrosis, however, especially in the presence of skeletal muscle injury and renal ...
... renal ischemia-reperfusion injury, and polycystic kidney disease. The protective role of EETs in these animal model diseases ... ischemic versus reperfusion injury". American Journal of Physiology. Heart and Circulatory Physiology. 291 (2): H537-42. doi: ... ventricle contraction immediately after blockade of coronary artery blood flow in animal models of ischemia-reperfusion injury ... EETs also reduce the size of heart enlargement that occurs long after these experiment-induced injuries. Humans with ...
Reperfusion injury, i.e. postpulmonary thromboendartectomy or lung transplantation. *Swimming induced pulmonary edema also ... Acute lung injury may also cause pulmonary edema through injury to the vasculature and parenchyma of the lung. Acute lung ... This damage may be direct injury or injury mediated by high pressures within the pulmonary circulation. When directly or ... Transfusion associated Acute Lung Injury (TRALI) is a specific type of blood-product transfusion injury that occurs when the ...
H 2S donors reduce myocardial injury and reperfusion complications. Increased H 2S levels within the body will react with ... Non-safety related ) "Reduction of Ischemia-Reperfusion Mediated Cardiac Injury in Subjects Undergoing Coronary Artery Bypass ... PKG also limits smooth muscle cell proliferation, reducing intima thickening following AMI injury, ultimately decreasing ...
Nrf2 augments skeletal muscle regeneration after ischaemia-reperfusion injury. J Pathol. 2014 Dec;234(4):538-47. doi: 10.1002/ ... Hölzle worked on micro circulatory characteristics of these transplants and with the phenomenon of the reperfusion injury. ... A novel laser-Doppler flowmetry assisted murine model of acute hindlimb ischemia-reperfusion for free flap research. PLoS One. ...
August 2019). "Targeting PFKFB3 alleviates cerebral ischemia-reperfusion injury in mice". Scientific Reports. 9 (1): 11670. doi ... PFKFB3 inhibitor alleviates motor discoordination and brain infarct injury The Warburg effect, proposed by Otto Warbug in 1956 ...
Nitric oxide can contribute to reperfusion injury when an excessive amount produced during reperfusion (following a period of ... H 2S donors reduce myocardial injury and reperfusion complications. Increased H 2S levels within the body will react with ... Non-safety related ) "Reduction of Ischemia-Reperfusion Mediated Cardiac Injury in Subjects Undergoing Coronary Artery Bypass ... potential to be used to prevent the development of a series of pathological conditions including ischemia reperfusion injury, ...
May 2010). "Exosome secreted by MSC reduces myocardial ischemia/reperfusion injury". Stem Cell Research. 4 (3): 214-22. doi: ...
Ischemia results from the dysfunction and, combined with reperfusion injury, causes the tissue damage that leads to the wounds ... As in other chronic ulcers, reperfusion injury damages tissue. Though treatment of the different chronic wound types varies ... reperfusion injury, and bacterial colonization. Ischemia is an important factor in the formation and persistence of wounds, ... repeated bouts of ischemia-reperfusion injury, and bacterial colonization with resulting inflammatory host response. Since more ...
... has also been shown to prevent oxidative and reperfusion injury in heart and liver tissues. Bucillamine has both ... Prevents Transplantation-Associated Reperfusion Injury". Proceedings of the National Academy of Sciences. 99 (13): 8915-8920. ... It is hypothesized that similar processes related to reactive oxygen species (ROS) are involved in acute lung injury during ... giving it vastly superior function in restoring glutathione and therefore greater potential to prevent acute lung injury during ...
... helps to prevent cardiac dysfunction after ischemia-reperfusion injuries. Mitochondrial ROS production and oxidative mtDNA ...
Thus, cyclophilins may function in cardioprotection during ischemia-reperfusion injury. PPIB contributes to the replication and ... such as ischemic reperfusion injury, AIDS, and cancer. It is also associated with viral infections. In eukaryotes, cyclophilins ...
Suspension trauma Reperfusion injury, a similar but separate condition Thomassen; et al. (2009). "Does the horizontal position ...
... protects both liver and blood vessel tissues against hepatic ischemia and reperfusion (blood circulatory system) injury ... December 2007). "Pivotal Advance: Cannabinoid-2 receptor agonist HU-308 protects against hepatic Ischemia-reperfusion injury by ... being critical steps not only in reperfusion injury, but also atherosclerosis and other inflammatory disorders, is very ... has been shown to protect against tissue damage in various experimental models of ischemic-reperfusion injury, atherosclerosis/ ...
"Histone deacetylase inhibition reduces myocardial ischemia-reperfusion injury in mice". FASEB Journal. 22 (10): 3549-60. doi: ...
... or during cell injury (such as ischemia-reperfusion injury during heart attacks and strokes) or during developments and ... The VDAC2 protein has been implicated in cardioprotection against ischemia-reperfusion injury, such as during ischemic ... "Past and present course of cardioprotection against ischemia-reperfusion injury". Journal of Applied Physiology. 103 (6): 2129- ... IBD, the equivalent HIV in birds, can compromise their immune systems and even cause fatal injury to the lymphoid organ, ...
Most notably, SOD1 is pivotal in reactive oxygen species (ROS) release during oxidative stress by ischemia-reperfusion injury, ... In addition, SOD1 has been implicated in cardioprotection against ischemia-reperfusion injury, such as during ischemic ... "Past and present course of cardioprotection against ischemia-reperfusion injury". Journal of Applied Physiology. 103 (6): 2129- ... During ischemia reperfusion, ROS release substantially contribute to the cell damage and death via a direct effect on the cell ...
... or during cell injury (such as ischemia-reperfusion injury during heart attacks and strokes) or during developments and ... In addition, VDAC3 has been implicated in cardioprotection against ischemia-reperfusion injury, such as during ischemic ... "Past and present course of cardioprotection against ischemia-reperfusion injury". Journal of Applied Physiology. 103 (6): 2129- ...
Tilney, N. L.; Guttmann, R. D. (1997-10-15). "Effects of initial ischemia/reperfusion injury on the transplanted kidney". ...
"The role of the complement system in ischemia-reperfusion injury". Shock. 21 (5): 401-9. doi:10.1097/00024382-200405000-00002. ... atypical hemolytic uremic syndrome and ischemia-reperfusion injuries, and rejection of transplanted organs. The complement ... "Deficiency in complement C1q improves histological and functional locomotor outcome after spinal cord injury". The Journal of ... "Quantitative analysis of cellular inflammation after traumatic spinal cord injury: evidence for a multiphasic inflammatory ...
Reperfusion injury may be studied with everted hamster pouches also. To simulate reperfusion, one method is to tie a cuff ... Bertuglia, S; Marchiafava, PL; Colantuoni, A (June 1996). "Melatonin prevents ischemia reperfusion injury in hamster cheek ...
Ischaemic postconditioning protects against reperfusion injury via the SAFE pathway. Lydia Lacerda, Sarin Somers, Lionel H. ... This pathway allows ischaemic postconditioning that helps protect against reperfusion injury. This path involves the activation ... pathway against reperfusion injury: Does it go beyond the RISK pathway?". Journal of Molecular and Cellular Cardiology. 47 (1 ...
Evidence that myocardial "stunning" is a manifestation of reperfusion injury". Circ. Res. 65 (3): 607-22. doi:10.1161/01.res. ... This reversible reduction of function of heart contraction after reperfusion is not accounted for by tissue damage or reduced ... The generation of oxygen-derived [free radicals] during the initial period of reperfusion after ischemia is believed to ... Two leading hypotheses implicate reperfusion-induced oxygen free-radical damage and altered calcium flux resulting in ...
Oxidants interfere with the normal brain chemistry and cause further damage (this is known as "reperfusion injury"). ... which have a role in reperfusion injury after asphyxia.[26] Research by Ola Didrik Saugstad and others led to new international ... Brain injury may still occur in a TIA lasting only a few minutes. Having a TIA is a risk factor for eventually having a stroke. ... Jun Chen, Zao C. Xu, Xiao-Ming Xu, Animal Models of Acute Neurological Injuries, Humana Press; 1 edition, ISBN 978-1-60327-184- ...
... reperfusion injury - hemorrhagic transformation - cold exposure - rupture of an aneurysm or arteriovenous malformation (AVM) - ...
... from internal causes such as reperfusion injury. By locationEdit. *Wound, an injury in which skin is torn, cut or ... Illness and injuries during spaceflight. Injury severity scoreEdit. The injury severity score (ISS) is a medical score to ... Repetitive strain injury or other strain injury. *Other injuries from external physical causes, such as radiation poisoning, ... Traumatic injury, a body wound or shock produced by sudden physical collision or movement[9]*Avulsion injury ...
Influence on Vitamin C Bioavailability and Capacity to Protect Against Ischemia-Reperfusion Injury". Nutrition and Metabolic ...
... hepatic ischemia/reperfusion injury, colitis, osteoarthritis, lung injury, lung transplantation rejection, and neuropathic pain ... "MSHA - Occupational Illness and Injury Prevention Program - Health Topics - Carbon Monoxide". Retrieved 2017- ... potential to be used to prevent the development of a series of pathological conditions including ischemia reperfusion injury, ...
... which have a role in reperfusion injury after asphyxia.[15] Research by Ola Didrik Saugstad and others led to new international ... The corpses had no visible injuries, and were supplied to medical schools for money.[6] ... GBD 2015 Disease and Injury Incidence and Prevalence, Collaborators. (8 October 2016). "Global, regional, and national ... incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the ...
Protection: Cushions the plasma membrane and protects it from chemical injury. *Immunity to infection: Enables the immune ... "Shedding of the coronary endothelial glycocalyx: effects of hypoxia/reoxygenation vs ischaemia/reperfusion." British Journal of ...
en:Anterior cruciate ligament injury (8). *en:Antibiotic misuse (6) → 항생제 오용 ... en:Reperfusion therapy (3). *en:Reproductive health (31) → 재생산 건강 *en:Reproductive medicine (9) ...
Ischemia-reperfusion injury of the appendicular musculoskeletal system. *List of orthopedic implants ... Orthopedic surgeons use both surgical and nonsurgical means to treat musculoskeletal trauma, spine diseases, sports injuries, ...
Mechanical: vascular injury, pneumothorax (by placing pulmonary artery catheter), tracheal injury/stenosis (result of ... fat emboli and reperfusion pulmonary edema after lung transplantation or pulmonary embolectomy. However, the majority of these ... Comparison of two fluid-management strategies in acute lung injury". N Engl J Med. 354 (24): 2564-2575. doi:10.1056/ ... Pulmonary-artery versus central venous catheter to guide treatment of acute lung injury". N Engl J Med. 354 (21): 2213-2224. ...
... on myocardial ischemic reperfusion injury' in Molecular and Cellular Biochemistry vol. 289 (2006) pp. 55-63. PMID 16628469 ...
... atypical hemolytic uremic syndrome and ischemia-reperfusion injuries,[26][27] and rejection of transplanted organs.[28] ... "The Role of the Complement System in Ischemia-Reperfusion Injury". Shock. 21 (5): 401-9. doi:10.1097/00024382-200405000-00002. ... of the central nervous system such as Alzheimer's disease and other neurodegenerative conditions such as spinal cord injuries.[ ... "Deficiency in Complement C1q Improves Histological and Functional Locomotor Outcome after Spinal Cord Injury". Journal of ...
Endothelial injury: Injury to the endothelial causing platelet activation and aggregation *Common causes include: trauma, ... Main articles: Thrombolysis, Thrombosis prophylaxis, and Reperfusion therapy. This section needs more medical references for ... A thrombus is a healthy response to injury intended to prevent bleeding, but can be harmful in thrombosis, when clots obstruct ... A thrombus occurs when the hemostatic process, which normally occurs in response to injury, becomes activated in an uninjured ...
Ischemia-reperfusion injury of the appendicular musculoskeletal system. ReferencesEdit. *^ a b c GRCh38: Ensembl release 89: ... Myoglobin is a sensitive marker for muscle injury, making it a potential marker for heart attack in patients with chest pain.[ ... In humans, myoglobin is only found in the bloodstream after muscle injury. It is an abnormal finding, and can be diagnostically ... released myoglobin is filtered by the kidneys but is toxic to the renal tubular epithelium and so may cause acute kidney injury ...
Endothelial injury: Injury to the endothelium (interior surface of blood vessel), causing platelet activation and aggregation; ... Main articles: Thrombolysis, Thrombosis prophylaxis, and Reperfusion therapy. Anticoagulants are drugs used to prevent the ... A thrombus is a healthy response to injury intended to prevent bleeding, but can be harmful in thrombosis, when clots obstruct ... If rapid blood circulation (e.g., because of tachycardia) occurs within vessels that have endothelial injuries, that creates ...
Most notably, SOD1 is pivotal in reactive oxygen species (ROS) release during oxidative stress by ischemia-reperfusion injury, ... "Past and present course of cardioprotection against ischemia-reperfusion injury". Journal of Applied Physiology. 103 (6): 2129- ... SOD1 has been implicated in cardioprotection against ischemia-reperfusion injury, such as during ischemic preconditioning of ... response to axon injury. • relaxation of vascular smooth muscle. • ovarian follicle development. • cellular response to ATP. • ...
"Effect of low-level laser therapy on lung injury induced by hindlimb ischemia/reperfusion in rats". Lasers in Medical Science ... "Low-level laser irradiation improves functional recovery and nerve regeneration in sciatic nerve crush rat injury model". PloS ...
"Reversible blockade of electron transport with amobarbital at the onset of reperfusion attenuates cardiac injury". ... mitochondrial electron transport in the rat heart in an attempt to preserve mitochondrial function following reperfusion.[2] ...
The deletion of p66SHC also protects from ischemia/reperfusion brain injuries through blunted production of free radicals.[14] ...
Reperfusion injury. *Machine perfusion. *Perfusionist. *Myocardial perfusion imaging. *rCBF. *Cerebral edema. References[edit] ...
thrombus aspiration as reperfusion strategy. *platelet P2Y12 receptor inhibitors: The CURE trial in 2001 determined that the ... Also applicable is the Virchow's triad of blood stasis, endothelial injury, and hypercoagulable state. Atherosclerosis ... contributes to coronary thrombosis formation by facilitating blood stasis as well as causing local endothelial injury.[citation ...
It is a reperfusion injury that appears after the release of the crushing pressure. The mechanism is believed to be the release ... Acute kidney injury[edit]. Main article: Acute kidney injury. Acute kidney injury (AKI), previously called acute renal failure ... Acute kidney injury[edit]. Acute kidney injury (previously known as acute renal failure) - or AKI - usually occurs when the ... Causes of acute kidney injury include accidents, injuries, or complications from surgeries in which the kidneys are deprived of ...
It is a reperfusion injury that appears after the release of the crushing pressure. The mechanism is believed to be the release ... Acute kidney injuryEdit. Acute kidney injury (previously known as acute renal failure) - or AKI - usually occurs when the blood ... Main article: Acute kidney injury. Acute kidney injury (AKI), previously called acute renal failure (ARF),[10][11] is a rapidly ... Causes of acute kidney injury include accidents, injuries, or complications from surgeries in which the kidneys are deprived of ...
doi:10.1016/j.injury.2007.03.028. PMID 17640641.. *^ "What Does a Super Paramedic Do? (BBC News website)". 30 June 2005. ... "Applying the new STEMI guidelines: 1. Reperfusion in acute ST-segment elevation myocardial infarction". CMAJ. 171 (9): 1039-41 ... They have a particular advantage for major trauma injuries. The well-established theory of the golden hour suggests that major ... BS Roudsari (2007). "International comparison of prehospital trauma care systems". Injury. 38 (9): 993-1000. ...
"eMedicine - Reperfusion Injury in Stroke : Article by Wayne M Clark, MD". Retrieved 2007-08-05.. ... is necessary but also contributes to reperfusion injury.[7] Other comorbidities may also be the root cause of venous ulcers.[8] ...
Ischemia-reperfusion injury of the appendicular musculoskeletal system. *Vascular occlusion training. References[edit]. *^ ... Ischemic injuries can also result from prolonged tourniquet time periods. The majority of such injuries may be transient, and ... Complications and injuries related to the use of a surgical tourniquet include: nerve injury, post-tourniquet syndrome, ... "Tourniquet Injuries: Mechanisms and Prevention". Retrieved 2017-10-03.. *^ McEwen, JA (2009). "Surgical ...
Potential mechanism for brain ischemia reperfusion injury". Journal of Cerebral Blood Flow and Metabolism. 37 (12): 3649-3658. ... Defects in this enzyme are responsible for the development of several pathological processes such as ischemia/reperfusion ... "Krebs cycle metabolites and preferential succinate oxidation following neonatal hypoxic-ischemic brain injury in mice" ...
Cannabinoid-2 receptor agonist HU-308 protects against hepatic ischemia/reperfusion injury by attenuating oxidative stress, ...
Reperfusion injury, sometimes called ischemia-reperfusion injury (IRI) or reoxygenation injury, is the tissue damage caused ... Reperfusion injury plays a major part in the biochemistry of hypoxic brain injury in stroke. Similar failure processes are ... or what is termed reperfusion injuries. In fact an individual suffering from an ischemic insult continues suffering injuries ... Reperfusion injury is a primary concern in liver transplantation surgery. A study of aortic cross-clamping, a common procedure ...
... enhancing the survivability of platelets during storage or transfusion and to attenuate ischemia-reperfusion injury (IPI), are ... The modified annexin decreases the binding of leukocytes and platelets during post-ischemic reperfusion, thereby restoring ... myocytes are viable before reperfusion then progress to irreversible injury during reperfusion. Apoptosis can contribute to ... up to at least about 3 hours prior to reperfusion, up to at least about 1 hour prior to reperfusion, during reperfusion, and/or ...
In fact, this damage properly constitutes a partial diastolic depolarization or injury, i.e., a moderate reduction of the rest ... Ischemia-reperfusion myocardial injury] Arch Cardiol Mex. Oct-Dec 2003;73(4):284-90. ... In fact, this damage properly constitutes a partial diastolic depolarization or injury, i.e., a moderate reduction of the rest ... During the initial ischemia phase, as well as during reperfusion, metabolic therapy can be very useful as, for example, glucose ...
Levosimendan protects human hepatocytes from ischemia-reperfusion injury.. Brunner SN1, Bogert NV2, Schnitzbauer AA3, Juengel E ... Ischemia-reperfusion injury (IRI) is a major challenge in liver transplantation. The mitochondrial pathway plays a pivotal role ... B) After a 48 hour treatment with levosimendan after I/R injury, the metabolic activity is increased but there is no dependency ... A) The metabolic activity of human hepatocytes increased after 24 hour treatment with levosimendan after I/R injury in a dose- ...
Blue light reduces organ injury from ischemia and reperfusion. Du Yuan, Richard D. Collage, Hai Huang, Xianghong Zhang, ... Blue light reduces organ injury from I/R. Du Yuan, Richard D. Collage, Hai Huang, Xianghong Zhang, Benjamin C. Kautza, Anthony ... Blue light reduces organ injury from I/R. Du Yuan, Richard D. Collage, Hai Huang, Xianghong Zhang, Benjamin C. Kautza, Anthony ... light prior to ischemia/reperfusion (I/R) significantly attenuates the degree of organ injury. Our characterization of the ...
... Peter Schemmer,1 John J. Lemasters,2 and Pierre-Alain Clavien ... Peter Schemmer, John J. Lemasters, and Pierre-Alain Clavien, "Ischemia/Reperfusion Injury in Liver Surgery and Transplantation ... 2Center for Cell Death, Injury and Regeneration, Departments of Drug Discovery and Biomedical Sciences and Biochemistry and ...
... and improves energy metabolism against cerebral ischemia-reperfusion injuries. Dr. Wei Lu and his team from the Second Xiangya ... Hospital, Central South University, China found that administration of salvianolate during reperfusion after ischemia appears ... Salvianolate increases heat shock protein expression in a cerebral ischemia-reperfusion injury model. Neural Regen Res. 2013;8( ... Salvianolate for treatment of cerebral ischemia-reperfusion injuries. Neural Regeneration Research. Journal. Neural ...
Lethal myocardial reperfusion injury. Reperfusion-induced death of cardiomyocytes that were viable at the end of the index ... Lethal myocardial reperfusion injury attenuates the full benefits of myocardial reperfusion in terms of MI size reduction and ... Reduction of infarct size by gentle reperfusion without activation of reperfusion injury salvage kinases in pigs. Cardiovasc ... This figure illustrates the individual contributions of acute myocardial ischemic injury and myocardial reperfusion injury to ...
The mouse model of cerebral artery ischemia/reperfusion injury was established to test the anticerebral ischemia-reperfusion ... Anticerebral Ischemia-Reperfusion Injury Activity of Synthesized Puerarin Derivatives. Yubin Ji,1 Pei Jiang,2 and Xinjia Yan3 ... When cerebral ischemia-reperfusion injury happened in patients, multiple pathological processes occur, such as leukocyte ... derivatives of puerarin may serve as promising approach to improve neuron function in ischemia-reperfusion brain injury-related ...
Reperfusion Injury After Stroke Study Official Title Reperfusion Injury After Cerebral Ischemia: an in Vivo Study Using Neuro ... Reperfusion Injury After Stroke Study (RISKS). The safety and scientific validity of this study is the responsibility of the ... The aim of this study is to evaluate the effects of circulating and imaging biomarkers in relation to reperfusion injury. ... contribute to reperfusion brain injury. Preliminary data show that BBB disruption can be traced in vivo by Computed Tomography ...
However, reperfusion can itself amplify cell injury and death; this is known as myocardial ischemia-reperfusion injury (I/R). ... Review highlights calcium handling mechanisms involved in reperfusion injury. *Download PDF Copy ... These treatments have been known to reduce acute myocardial ischemic injury and to limit MI size when experiments and were done ... Several studies have uncovered complex mechanisms of cardiomyocyte damage after the process of reperfusion, and efforts are ...
... at the beginning of reperfusion attenuated tissue injury and inflammatory responses in a rat model of gut I/R induced by ... attenuates organ injury and inflammation responses, and reduces mortality following gut I/R injury. The primary aim of this ... Although we have shown that administration of rat AM plus human AMBP-1 at the beginning of reperfusion is protective, it ... As such, the development of effective strategies for preventing and treating circulatory collapse and organ injury after gut I/ ...
Reperfusion injury Reperfusion therapy Eltzschig, H.K. & T. Eckle (2011). "Ischemia and reperfusion-from mechanism to ... Ischemia-reperfusion (IR) tissue injury is the resultant pathology from a combination of factors, including tissue hypoxia, ... The ischemia-reperfusion injury associated with surgical tourniquets is typically not clinically apparent when used for less ... Alam, M.R.; D. Baetz; M. Ovize (2015). "Cyclophilin D and myocardial ischemia-reperfusion injury: a fresh perspective". J Mol ...
Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS.. Chouchani ET#1,2, Pell VR#2, Gaude ... Ischaemia-reperfusion injury occurs when the blood supply to an organ is disrupted and then restored, and underlies many ... Succinate: A Promising Therapeutic Target for Reperfusion Injury. [Neurosurgery. 2015]. *Biochemistry: succinate strikes. [ ... Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS. Nature. 2014 Nov 20;515(7527):431- ...
Inflammation and oxidative stress exert important roles in intestinal ischemia-reperfusion injury (IRI). Lycium barbarum ... Lycium barbarum polysaccharides reduce intestinal ischemia/reperfusion injuries in rats Chem Biol Interact. 2013 Aug 25;204(3): ... Inflammation and oxidative stress exert important roles in intestinal ischemia-reperfusion injury (IRI). Lycium barbarum ... Keywords: Inflammation; Ischemia-reperfusion injury; Lycium barbarum polysaccharides; Oxidative stress; Small intestine. ...
In their mouse model of this ischemia/reperfusion injury of the heart, theyve found they can reduce heart muscle death 40 ... Study shows microRNA can protect the heart from reperfusion injury. *Download PDF Copy ... 2019) MiR322 mediates cardioprotection against ischemia/reperfusion injury via FBXW7/notch pathway. Journal of Molecular and ... it protects the heart from reperfusion injury.. Dr. Yaoliang Tang, cardiovascular researcher in the Vascular Biology Center ...
TLR4 is implicated in the pathogenesis of ischemia-reperfusion injury of multiple organs including heart, liver, kidney and ... we hypothesized that lung ischemia-reperfusion injury was mediated by MyD88-dependent signaling. To test this hypothesis, we ... implicating other MyD88-dependent pathways in lung injury following ischemia-reperfusion. We also found that left lung ischemia ... We found that Myd88-/- mice had significantly less MCP-1/CCL2 in the left lung following ischemia-reperfusion as compared with ...
Reperfusion injury induces apoptosis in rabbit cardiomyocytes. J Clin Invest. 1994; 94: 1621-1628. ... Smad1 Protects Cardiomyocytes From Ischemia-Reperfusion Injury. Mitsuru Masaki, Masahiro Izumi, Yuichi Oshima, Yoshikazu ... Nakamura T, Mizuno S, Matsumoto K, Sawa Y, Matsuda H. Myocardial protection from ischemia/reperfusion injury by endogenous and ... Smad1 Protects Cardiomyocytes From Ischemia-Reperfusion Injury. Mitsuru Masaki, Masahiro Izumi, Yuichi Oshima, Yoshikazu ...
After 4 months, the resulting scar mass was reduced by 37%, suggesting that a reduction of reperfusion injury indeed may lead ... Cardiology »F.I.R.E. »FX06 »Fibrin-Derived »PCI »Reperfusion »STEMI »Thrombolysis »blood flow »blood vessel »myocardial ... Further reports about: , Cardiology , F.I.R.E. , FX06 , Fibrin-Derived , PCI , Reperfusion , STEMI , Thrombolysis , blood flow ... "reperfusion injury". FX06 is a novel compound intended to prevent that damage. ...
Diseases : Liver Injury: Ischemia/reperfusion : CK(19) : AC(10). Pharmacological Actions : Anti-Apoptotic : CK(1620) : AC(932) ... Diseases : Liver Injury: Ischemia/reperfusion : CK(19) : AC(10). Pharmacological Actions : Anti-Inflammatory Agents : CK(12461 ... Additional Keywords : Anti-Apoptotic, Autophagy Inhibitors : CK(5) : AC(4), Hepatoprotective, Liver Injury: Ischemia/ ...
... warm ischemia and reperfusion injury with emphasis on cryonics technology ... ISCHEMIC INJURY IN BRAIN AND ELSEWHERE *REPERFUSION INJURY AND NO REFLOW *STROKE THERAPY *HIBERNATION AND ESTIVATION *ORGAN ... BRAIN DAMAGE DUE TO ISCHEMIA/REPERFUSION *PREVENTING ISCHEMIC/REPERFUSION INJURY IN CRYONICS *PRE-TREATMENT FOR CRYONICS ... and can thereby worsen damage from reperfusion injury if given in delayed reperfusion. Treatment with tPA is generally deemed ...
... injury. Peroxynitrite (ONOO−), a representative reactive nitrogen species, mediates excessive mitophagy... ... Excessive autophagy/mitophagy plays important roles during cerebral ischemia-reperfusion (I/R) ... Winquist RJ, Kerr S (1997) Cerebral ischemia-reperfusion injury and adhesion. Neurology 49(5 Suppl 4):S23-S26CrossRefPubMed ... Cerebral ischemia-reperfusion injury Mitophagy Naringin Nitrative stress Peroxynitrite Electronic supplementary material. The ...
... including myocardial ischemia-reperfusion injury (IRI), but the molecular basis of UPS impairment remains poorly understood. ... When subject to regional myocardial ischemia-reperfusion, young Ubqln1-CKO mice showed substantially exacerbated cardiac ...
Reperfusion injury and reactive oxygen species: The evolution of a concept. Redox Biol. 2015;6:524-551.. View this article via ... Inadequate ubiquitination-proteasome coupling contributes to myocardial ischemia-reperfusion injury. Chengjun Hu,1,2 Yihao Tian ... Endoplasmic reticulum stress gene induction and protection from ischemia/reperfusion injury in the hearts of transgenic mice ... Impaired autophagosome clearance contributes to cardiomyocyte death in ischemia/reperfusion injury. Circulation. 2012;125(25): ...
Ischemia Reperfusion Injury - Pipeline Review, H2 2015, provides an... ... Ischemia Reperfusion Injury - Pipeline Review, H2 2015 Summary Global Markets Direct s, ... Ischemia Reperfusion Injury - Pipeline Review, H2 2015 Summary Global Markets Direct s, Ischemia Reperfusion Injury - Pipeline ... Ischemia Reperfusion Injury - Therapeutics under Development by Companies 11. Ischemia Reperfusion Injury - Therapeutics under ...
We investigated whether necroptosis is involved in myocardial ischemia-reperfusion... ... Yaoita H, Ogawa K, Maehara K, Maruyama Y. Attenuation of ischemia/reperfusion injury in rats by a caspase inhibitor. ... We investigated whether necroptosis is involved in myocardial ischemia-reperfusion injury in isolated guinea pig hearts and, if ... Caspase inhibition and limitation of myocardial infarct size: protection against lethal reperfusion injury. Br J Pharmacol. ...
... severe injury takes place. Ischemia/reperfusion (I/R) injury affects patient outcome after transplants, states of shock or ... A research group in Mexico investigated patterns of response to I/R injury arise after venous, arterial or total interruption ... Arterial, venous or total mesenteric ischemia/reperfusion causes different types of injury?. World Journal of Gastroenterology ... Arterial, venous or total mesenteric ischemia/reperfusion causes different types of injury? ...
Single-dose radiotherapy disables tumor cell homologous recombination via ischemia/reperfusion injury. Sahra Bodo,1 Cécile ... I/R injury, not endothelial apoptosis, impairs DSB repair. To assess whether SDRT-induced I/R injury (termed SDRT-I/R), ... showed that rapid ceramide-mediated ischemia/reperfusion (I/R) injury preceding endothelial apoptosis dysregulates DDR via ... linking tumor microvascular injury mediated by acid sphingomyelinase (ASMase)/ceramide-mediated tumor microvascular injury in ...
... the reperfusion of acute MI which includes modulation of coronary blood flow or oxygen delivery following the reperfusion of ... A method and apparatus for the prevention and treatment of reperfusion injury following ... One hallmark of reperfusion injury is that it may be attenuated by interventions initiated before or during the reperfusion. ... This invention relates to a method for reducing reperfusion injury after therapeutic reperfusion of an infarct of a heart or ...
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  • Abstract P600: Conditional Knockout of AT1a Receptors Selectively in The Proximal Tubules Attenuates Renal Ischemia-Reperfusion Injury in Mice. (
  • A common IRI model was used to induce intestinal injury by clamping and unclamping the superior mesenteric artery in rats. (
  • Different patterns of intestinal response to injury fter arterial, venous or arteriovenous occlusion in rats. (
  • Methods and Results -Sprague-Dawley rats were subjected to a 30-minute coronary occlusion followed by a 24-hour reperfusion. (
  • Rats were subjected to 30min of cardiac ischemia followed by 2h of reperfusion, with or without prior OzoneOP (100μg/kg/day) for 5 days. (
  • The present results have shown that GAS pretreatment significantly compensated for neurological behavior defects in rats with I/R-induced injury, reduced brain infarction size, reversed BBB impairment, and attenuated inflammation. (
  • 11 used the concentration of creatinine in ischemia/reperfusion models in rats and showed that parecoxib increases renal dysfunction and injury associated with this form of renal stress. (
  • Sprague Dawley rats were pretreated with QSYQ or saline for 7 days and subjected to ischemia (30 minutes occlusion of the left anterior descending coronary artery) and reperfusion (120 minutes). (
  • Pretreatment of QSYQ in Sprague Dawley rats improves ventricular function and energy metabolism and reduces oxidative stress via ameliorating multiple mitochondrial dysfunctions during I/R injury. (
  • SD rats were subjected to a total hepatic ischemia for 30 min after pretreatment with either vehicle or butyrate, followed by 6 h and 24 h of reperfusion. (
  • We conclude that butyrate inhibition of endotoxin translocation, macrophages activation, inflammatory factors production, and neutrophil infiltration is involved in the alleviation of total hepatic I/R liver injury in rats. (
  • Male Wistar rats were submitted to muscle ischemic and reperfusion injury (4h of the left common iliac artery occlusion followed by 1h of reperfusion). (
  • Effects of propofol pretreatment on myocardial cell apoptosis and SERCA2 expression in rats with hepatic ischemia/reperfusion. (
  • Ischemic postconditioning modified renal oxidative stress and lipid peroxidation caused by ischemic reperfusion injury in rats. (
  • 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. (
  • A total of 60 rats were randomly divided into the normal group (N), the sham operation group (S), the dimethyl sulfoxide control group (D) and the curcumin treatment group (C). For group D and C, 12 (T1), 24 (T2) and 72 h (T3) of reperfusion were performed after 2 h ischemia. (
  • For the rats in groups D and C, 12 (T1), 24 (T2) and 72 h (T3) of reperfusion were performed after 2-h ischemia (n=9 in each subgroup). (
  • Male Sprague-Dawley rats underwent a 45-min transient left coronary artery occlusion, followed by reperfusion. (
  • To investigate whether emulsified isoflurane preconditioning could reduce lung injury induced by hepatic I/R in rats and its mechanism. (
  • 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. (
  • 2) The peak apoptotic rate of pneumocytes occurred 2 hours after reperfusion in rats with single lung transplantation. (
  • Zhang P, Lv J, Li Y, Zhang L, Xiao D. Neonatal Lipopolysaccharide Exposure Gender-Dependently Increases Heart Susceptibility to Ischemia/Reperfusion Injury in Male Rats. (
  • To identify the potential target proteins of XST, two-dimensional gel electrophoresis (2-DE)-based proteomics was utilized to analyze the protein profile of myocardium in rats with myocardial ischemia/reperfusion (I/R) injury. (
  • AMBP-1), at the beginning of reperfusion attenuated tissue injury and inflammatory responses in a rat model of gut I/R induced by superior mesenteric artery occlusion (SMAO). (
  • For these studies, they caused an occlusion in the left coronary artery of mice for about 45 minutes, then enabled reperfusion to reflect what happens when a human has a heart attack, then gets treatment. (
  • group 1, n=8) or ZVAD-fmk, at a total dose of 3.3 mg/kg (group 2, n=8), was administered intravenously every 6 hours starting at 30 minutes before coronary occlusion until 24 hours of reperfusion. (
  • Ischemia-reperfusion injury was produced by a 90-min occlusion of the right middle cerebral artery followed by a 4-day reperfusion. (
  • Ischemia-reperfusion (IR) injury is the inevitable result of liver resection performed using vascular inflow occlusion (VIO), which entails clamping of the afferent hepatic blood supply. (
  • Timely reperfusion of an infarct-related artery within a reasonable time-frame after acute coronary occlusion continues to be the most effective intervention in patients to reduce morbidity and mortality. (
  • Background and Purpose- Most experimental models of cerebral ischemia use mechanical methods of occlusion and reperfusion. (
  • The majority of experimental cerebral ischemia studies utilize mechanical methods of arterial occlusion and reperfusion. (
  • Reperfusion injury in the heart can occur either as a result of transient arterial occlusion (eg, due to vasospasm or thrombus formation with spontaneous lysis) or as an iatrogenic consequence of thrombolytic or angioplastic therapy. (
  • Furthermore, treatment with miR‑187‑3p inhibitor could decrease the infarction volume in a rat model of middle cerebral artery occlusion/reperfusion. (
  • However solutions, including cardiac bypass surgery and angioplasty to reopen blocked coronary arteries, can result in a second period of adjustment and injury that can be responsible for as much as half of the size of the damage done to the heart muscle, called the infarct size. (
  • When subject to regional myocardial ischemia-reperfusion, young Ubqln1-CKO mice showed substantially exacerbated cardiac malfunction and enlarged infarct size, and conversely, mice with transgenic Ubqln1 overexpression displayed attenuated IRI. (
  • By contrast a competing strategy using nicorandil, a nicotinamide nitrate that activates potassium channels, did not reduce infarct size or reduce reperfusion injury. (
  • The J-WIND trial was actually two parallel trials of different strategies to reduce infarct size, improve ejection fraction, and reduce revascularization injury. (
  • Dr. Harrington, who served as discussant for the J-WIND trial, noted that about a dozen drugs that were tested for reduction of infarct size and reperfusion injury "all reported early, positive results. (
  • The resultant ROS served as a second messenger and was responsible for the STAT3 dimerization and, hence, the activation of antiapoptotic signaling, which eventually significantly suppressed the superoxide burst and decreased the infarct size during the ischemia-reperfusion process. (
  • In a rat model for myocardial reperfusion injury, infarct size and the appearance of presumed apoptotic cardiomyocytes were assessed in two groups that were or were not administered this protease inhibitor. (
  • Methods Mini swine (25-30 kg) were subjected to in situ left anterior descending (LAD) coronary artery ischaemia (60 min) followed by myocardial reperfusion (180 min) at the end of which myocardial infarct size was determined using tetrazolium staining. (
  • Arimura T, Saku K, Kakino T, Nishikawa T, Tohyama T, Sakamoto T, Sakamoto K, Kishi T, Ide T, Sunagawa K (2017) Intravenous electrical vagal nerve stimulation prior to coronary reperfusion in a canine ischemia-reperfusion model markedly reduces infarct size and prevents subsequent heart failure. (
  • In conclusion, EMPA can trigger AMPK signaling pathways and modulate myocardial contractility and reduce myocardial infarct size caused by ischemia and reperfusion independent of hypoglycemic effect. (
  • Valsartan inhibited Toll-like receptor 4 (TLR-4) and nuclear factor-kappa B (NF-B) expressions concomitant with an improvement in myocardial injury, such as smaller infarct size, reduced release of myocardial enzymes, and proinflammatory mediators. (
  • Shikonin attenuated hepatic ischemia/reperfusion injury by inhibiting apoptosis and autophagy. (
  • Biochemical analysis showed that the amounts of lactate dehydrogenase, alanine aminotransfrase and aspartate aminotransfrase, creatinine and urea were significantly increased in the serums obtained from the animals exposed to hepatic ischemia-reperfusion. (
  • Butyrate protects rat liver against total hepatic ischemia reperfusion injury with bowel congestion. (
  • Hepatic ischemia/reperfusion (I/R) injury is an unavoidable consequence of major liver surgery, especially in liver transplantation with bowel congestion, during which endotoxemia is often evident. (
  • Hepatic ischemia-reperfusion injury is a common pathophysiological process in liver surgery. (
  • To examine the biological relevance of 1, a hepatic ischemia/reperfusion model was chosen as a widely accepted model of oxidative stress generation. (
  • Ischaemia-reperfusion injury occurs when the blood supply to an organ is disrupted and then restored, and underlies many disorders, notably heart attack and stroke. (
  • After reperfusion, the accumulated succinate is rapidly re-oxidized by succinate dehydrogenase, driving extensive ROS generation by reverse electron transport at mitochondrial complex I. Decreasing ischaemic succinate accumulation by pharmacological inhibition is sufficient to ameliorate in vivo ischaemia-reperfusion injury in murine models of heart attack and stroke. (
  • Thus, we have identified a conserved metabolic response of tissues to ischaemia and reperfusion that unifies many hitherto unconnected aspects of ischaemia-reperfusion injury. (
  • Furthermore, these findings reveal a new pathway for metabolic control of ROS production in vivo, while demonstrating that inhibition of ischaemic succinate accumulation and its oxidation after subsequent reperfusion is a potential therapeutic target to decrease ischaemia-reperfusion injury in a range of pathologies. (
  • Which pathways trigger the role of complement in ischaemia/reperfusion injury? (
  • This is the first study to show that the anticancer drug Doxorubicin exacerbates myocardial ischaemia reperfusion injury. (
  • Rationale Primary graft dysfunction in lung transplant recipients derives from the initial, largely leukocyte-dependent, ischaemia-reperfusion injury. (
  • 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. (
  • Conclusions These results indicate that lung-marginated intravascular monocytes are retained as a 'passenger' leukocyte population during lung transplantation, and play a key role in the development of transplant-associated ischaemia-reperfusion injury. (
  • 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. (
  • Ischaemia-reperfusion injury of the lung is a major cause of morbidity and mortality, particularly following lung transplantation, the mainstay treatment for patients with end-stage pulmonary disease. (
  • The N-terminal lectin-like domain (LLD) of TM has no direct effects on coagulation, but has distinct anti-inflammatory properties, interfering with leukocyte adhesion, complement activation and cytokine generation, all of which are hallmarks of ischaemia-reperfusion injury. (
  • Using a murine model of lung ischaemia-reperfusion injury (90 min ischaemia, 4 h reperfusion), the present study shows that mice lacking the LLD of TM respond with increased extravasation of neutrophils and macrophages into the lung parenchyma and bronchoalveolar fluid (BALF), with augmented BALF levels of cytokines interleukin (IL)-1β and granulocyte-monocytic colony-stimulating factor (GM-CSF). (
  • In spite of major surgical advances, better organ preservation techniques, and the development of safer and more effective immunosuppressive approaches, lung transplantation continues to be complicated by ischaemia-reperfusion injury, which significantly impacts on short- and long-term outcomes 1 , 2 . (
  • The cellular and molecular mechanisms underlying ischaemia-reperfusion injury are complex and remain incompletely understood. (
  • Thus, ischaemia-reperfusion injury remains a highly relevant but largely unsolved problem, and novel therapeutic and/or preventative measures are urgently needed. (
  • Our findings suggest that treatment with levosimendan during reperfusion attenuates apoptosis of human hepatocytes by influencing BAX and Bcl-2 levels. (
  • Dr. Wei Lu and his team from the Second Xiangya Hospital, Central South University, China found that administration of salvianolate during reperfusion after ischemia appears to attenuate brain tissue damage and inhibit neuronal apoptosis by increasing heat shock protein 22 and phosphorylated protein kinase B expression. (
  • We investigated whether necroptosis is involved in myocardial ischemia-reperfusion injury in isolated guinea pig hearts and, if so, whether simultaneous inhibition of necroptosis and apoptosis confers enhanced cardioprotection. (
  • Necroptosis is involved in myocardial ischemia-reperfusion injury, and simultaneous inhibition of necroptosis and apoptosis enhances the cardioprotective effect. (
  • Apoptosis in myocardial ischemia-reperfusion. (
  • Necrostatin-1 suppresses autophagy and apoptosis in mice traumatic brain injury model. (
  • In the present study, we generated cardiac-specific tamoxifen-inducible NDUFA13 knockout mice and demonstrated that cardiac-specific heterozygous knockout (cHet) mice exhibited normal cardiac morphology and function in the basal state but were more resistant to apoptosis when exposed to ischemia-reperfusion (I/R) injury. (
  • Background -Z-Val-Ala-Asp(OMe)-CH 2 F (ZVAD-fmk), a tripeptide inhibitor of the caspase interleukin-1β-converting enzyme family of cysteine proteases, may reduce myocardial reperfusion injury in vivo by attenuating cardiomyocyte apoptosis within the ischemic area at risk. (
  • Conclusions -ZVAD-fmk was effective in reducing myocardial reperfusion injury, which could at least be partially attributed to the attenuation of cardiomyocyte apoptosis. (
  • 6 7 8 9 10 It has been reported that apoptosis is a significant contributor to myocardial cell death as a result of reperfusion injury. (
  • As opposed to reducing the exposure of cardiomyocytes to injurious stimuli, apoptosis of these cells is attenuated through modulation of the caspase-related proapoptotic process, and this may allow ischemic myocardium to survive even after receiving significant injury. (
  • 6 In the present study, we investigated whether ZVAD-fmk lowers the extent of experimental myocardial reperfusion injury in vivo by attenuating cardiomyocyte apoptosis. (
  • However, during reperfusion not only some changes including bleb formation was reduced, but some other alterations including portal hepatitis, inflammation and the induction of apoptosis, were occurred. (
  • The results of this study indicate that the occurrence of inflammation and the subsequent cell death by apoptosis are the most important changes in the early stage of hepatic reperfusion injury and the presence of apoptotic bodies were augmented as the time of reperfusion was increased. (
  • Antioxidant capacity, myocardial apoptosis and mitochondrial damage were evaluated and compared at the end of reperfusion. (
  • However, the impact of rapamycin via modulating mitophagy and apoptosis after spinal cord ischemia-reperfusion injury remains unclear. (
  • This study was undertaken to investigate the potential role of rapamycin in modulating mitophagy and mitochondria-dependent apoptosis using the spinal cord ischemia-reperfusion injury (SCIRI) mouse model. (
  • Our results therefore demonstrate that rapamycin can improve the locomotor function by promoting mitophagy and attenuating SCIRI -induced apoptosis, indicating its potential therapeutic application in a spinal cord injury. (
  • articles concerning reperfusion injury (lethal and otherwise), ischemia-reperfusion injury, apoptosis, microvascular injury, ischemic conditioning and different combinations thereof were consulted. (
  • Cellular injury was subsequently determined by measurement of live/death ratio and apoptosis using flow cytometry. (
  • The results reported by Hernandez et al 3 in this issue of Circulation Research are in agreement with a previous study linking both oxygen/glucose deprivation in cardiac myocytes and ischemia/reperfusion in the intact heart with increased ceramide production and apoptosis. (
  • We conclude that local anesthetics potentiated renal injury after I/R by increasing necrosis, apoptosis, and inflammation. (
  • 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. (
  • 9) Pulmonary reperfusion injury after lung transplantation is also mediated by oxidative stress-dependent mechanisms involving nicotinamide adenine dinucleotide phosphate oxidase and by apoptosis, (10) and the central role of nuclear factor-κB in the induction of lung inflammatory injury is now emerging. (
  • The major mechanisms of ischaemic reperfusion injury are oxidative stress (mainly oxygen-free radicals), apoptosis, neutrophil-endothelium interactions, and hypercontracture (i.e. myocyte Ca2+ over loading), endothelial cell activation with microvascular dysfunction, and altered myocardial metabolism. (
  • FX06 was administered intravenously to patients during reperfusion treatment, and the effect on heart muscle preservation was then assessed using the most advanced imaging technology: cardiac magnetic resonance imaging (CMR). (
  • Ischemia and reperfusion can cause serious brain damage in stroke or cardiac arrest. (
  • In this article I attempt to evaluate the nature & extent of ischemic & reperfusion injury -- primarily focused on the impact for cryonics (although certainly relevant to stroke and cardiac arrest). (
  • More importantly, impaired UPS performance plays a major role in cardiac pathogenesis, including myocardial ischemia-reperfusion injury (IRI), but the molecular basis of UPS impairment remains poorly understood. (
  • Ischemia-reperfusion injury (IRI) is a major cause of cardiac dysfunction during cardiovascular surgery, heart transplantation and cardiopulmonary bypass procedures. (
  • We hypothesized pulmonary exposure to Ag core AgNP induces a measureable increase in circulating cytokines, expansion of cardiac ischemia-reperfusion (I/R) injury and is associated with depressed coronary constrictor and relaxation responses. (
  • cardiac I/R injury and coronary artery reactivity were assessed. (
  • However, restoration of blood flow to reversibly injured cardiocytes (and other cardiac cell types) within the under-perfused region may also provoke additional damage-commonly referred to as lethal reperfusion injury. (
  • This review examines evidence from basic science and clinical studies that support the premise of cardiac injury caused by reperfusion. (
  • Although issues relating to Doxorubicin and cardiac safety have been well established in normal conditions, the effects of this drug on the myocardium during ischaemia-reperfusion have not been investigated in detail to date. (
  • Sympathetic regeneration is well documented after chronic cardiac ischemia, so we were surprised that the cardiac infarct remained denervated following ischemia-reperfusion (I-R). We used mice to ask if the lack of sympathetic regeneration into the scar was due to blockade by inhibitory extracellular matrix within the infarct. (
  • Cardiac infarcts in ptprs −/− mice were hyperinnervated, while infarcts in ptprs +/− littermates were denervated, confirming that CSPGs prevent sympathetic reinnervation of the cardiac scar after I-R. This is the first example of CSPGs preventing sympathetic reinnervation of an autonomic target following injury, and may have important consequences for cardiac function and arrhythmia susceptibility after myocardial infarction. (
  • Pretreatment with QSYQ protected against I/R-induced myocardial structural injury and improved cardiac hemodynamics, as demonstrated by normalized serum creatine kinase and suppressed oxidative stress. (
  • Cardiac MRI analysis revealed a significant relationship between postCreperfusion effector T cell kinetics and microvascular obstruction (MVO), a component of I/R injury, raising the possibility of a mechanistic link. (
  • Regardless of how gracefully we age, our ability to recover from injury, including ischemic cardiac and skeletal muscle injury, substantially reduces as we grow old. (
  • A recent study by Quan and colleagues demonstrates that modulation of glucose metabolism improves cardiac tolerance to ischemia-reperfusion (IR) injury. (
  • It is known that 5′ adenosine monophosphate -activated protein kinase (AMPK) activation stimulates glucose transport and that AMPK is central to activating glucose uptake after ischemic cardiac injury. (
  • Hearts from Sesn2 KO mice after cardiac IR had decreased contractile function and more severe myocardial injury than age-matched wild-type hearts. (
  • Such reperfusion injury is a major problem during cardiac surgery and in the treatment of coronary thrombosis and stroke. (
  • COPENHAGEN, Denmark I March 2, 2016 I Zealand announces top-line results from its clinical Phase II Proof-of-Concept trial with danegaptide for the protection against cardiac reperfusion injuries in patients with an acute myocardial infarction (blood clot in the heart). (
  • Results show no effect of danegaptide on the primary endpoint of saving cardiac tissue from ischemic reperfusion injuries as measured on the Myocardial Salvage Index (MSI). (
  • The compound has demonstrated cell protective and anti-arrhythmic properties and shown significant effect in established preclinical models of cardiac ischemic reperfusion injuries. (
  • Cardiac denervation protected myocyte against ischemia - reperfusion injury through decreasing direct NE toxicity, but not through decreasing NE-derived free radicals. (
  • We recently reported chronic neuropathic pain attenuates cardiac IR injury in mice. (
  • Direct activation of PVA neurons also provides cardioprotection against cardiac IR injury. (
  • This review summarizes the potential interaction of chronic pain and cardiac IR injury. (
  • The cerebral damage after cardiac arrest is thought to arise both from the ischemia during the cardiac arrest but also during reperfusion. (
  • The cardioprotective effects of XST were further validated in H9c2 cardiac muscle cells with hypoxia/reoxygenation injury. (
  • Renal ischemia-reperfusion (I/R) injury is a primary cause of acute renal failure that results in high mortality. (
  • The complement system has been shown to mediate renal ischemia-reperfusion (I/R) injury. (
  • Recent data have demonstrated a role for CD4 + cells in the pathogenesis of renal ischemia reperfusion injury (IRI). (
  • Renal ischemia reperfusion injury (IRI) 4 is a major cause of acute renal failure (ARF) and is associated with a high mortality rate in native kidneys and increased allograft rejection in the transplanted kidney. (
  • To better understand the dynamics of intraoperative renal ischemia and recovery of renal oxygenation during reperfusion, a visible reflectance imaging system (VRIS) was developed to measure renal oxygenation during renal artery clamping in both cooled and warm porcine kidneys. (
  • The activation of the intrarenal renin-angiotensin system plays an important role in the pathogenesis of renal ischemia-reperfusion injury, but the underlying cellular and signaling mechanisms remain incompletely understood. (
  • In the present study, we tested the hypothesis that conditional knockout of AT1a receptors selectively in the proximal tubules attenuates renal ischemia-reperfusion injury in mice. (
  • Systolic blood pressure, 24 h urine and urinary sodium excretion were not significantly altered in all strains 24 h or 7 days after renal ischemia-reperfusion. (
  • Renal ischemia-reperfusion injury was assessed by Masson Trichrome staining and compared between WT, AT1a-KO and PT-AT1a-KO mice. (
  • Our results suggest that AT1a receptors in the proximal tubule play an important role in the pathogenesis of renal ischemia-reperfusion injury, and thus may represent a therapeutic target in the future. (
  • Reperfusion injury, sometimes called ischemia-reperfusion injury (IRI) or reoxygenation injury, is the tissue damage caused when blood supply returns to tissue (re- + perfusion) after a period of ischemia or lack of oxygen (anoxia or hypoxia). (
  • Ischemic tissue would have decreased function of these scavengers because of cell injury. (
  • While reperfusion of ischaemic tissue is essential for survival, it also initiates oxidative damage, cell death and aberrant immune responses through the generation of mitochondrial reactive oxygen species (ROS). (
  • When the organ is ready for the transplantation, the reperfusion of the organ induces an increase of the oxidative stress, endoplasmic reticulum stress, and inflammation which causes tissue damage, resulting in a decrease of the transplantation success. (
  • After 4 months, the resulting scar mass was reduced by 37%, suggesting that a reduction of reperfusion injury indeed may lead to decrease in scar tissue formation. (
  • Reperfusion injury refers to the tissue damage inflicted when blood flow is restored after an ischemic period of more than about ten minutes. (
  • Tissue samples were obtained after 4 h reperfusion to determine expression of receptor-interacting protein 1 (RIP1) and activated caspase 3 by Western blot analysis. (
  • 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. (
  • citation needed] "Reperfusion": the restoration of blood flow to an organ or tissue after having been blocked. (
  • citation needed] While some investigations suggest a possible beneficial effect of mesenchymal stem cells on heart and kidney reperfusion injury, to date, none have explored the role of stem cells in muscle tissue exposed to ischemia-reperfusion injury. (
  • citation needed] Systemic effects of IR injury During periods of ischemia, cellular break down products accumulate in the local tissue. (
  • citation needed] Tissue swelling and fasciotomy Following ischemia, reperfusion induces local tissue swelling. (
  • Reperfusion of a previously ischemic tissue is associated with additional injury leading to structural and functional alterations in many organs including the liver. (
  • In summary, the study showed that GLN reduced the gene expressions of inflammatory mediator in muscle tissue and decreased blood macrophage percentage and plasma IL-6 concentrations at the early or late phase of reperfusion. (
  • Silver within lung tissue was persistent at 7 days post IT instillation and was associated with an elevation in cytokines: IL-2, IL-13, and TNFα and expansion of I/R injury. (
  • In this review we discuss how the principal mechanisms underlying tissue protection against IR injury and the associated immediate elevation of O-GlcNAc may involve attenuation of calcium overload, attenuation of mitochondrial permeability transition pore opening, reduction of endoplasmic reticulum stress, modification of inflammatory and heat shock responses, and interference with established cardioprotective pathways. (
  • The protective action of cilostazol in IR injury has been demonstrated in the central nervous system, 14 , 15 renal tissue 6 , heart 17 and in chronic arterial disease 16 . (
  • Thrombolytic reperfusion was achieved by administering tissue plasminogen activator at 2 hours after embolic focal ischemia. (
  • 8-12 ⇓ ⇓ ⇓ ⇓ In the context of reperfusion injury, profiles of tissue damage after clot thrombolysis may differ from those that occur after mechanical reperfusion. (
  • Complement activation plays an important role in local and remote tissue injury associated with gastrointestinal ischemia-reperfusion (GI/R). The role of the classical and lectin complement pathways in GI/R injury was evaluated using C1q-deficient (C1q KO), MBL-A/C-deficient (MBL-null), complement factor 2- and factor B-deficient (C2/fB KO), and wild-type (WT) mice. (
  • tissue injury following ischemia/reperfusion (I/R) may occur in multiple clinical situations such as shock, trauma, sepsis, and surgery. (
  • Tissue ischemia can induce local hypoxic changes that increase tissue susceptibility to injury following reperfusion. (
  • NF-κB activity was reduced in vitro as well as in hepatic tissue after ischemia/reperfusion upon pretreatment with 1. (
  • Moreover, hepatic tissue damage as well as TNF-R levels increased in xanthohumol-pretreated liver tissue after ischemia/reperfusion. (
  • These novel findings support further evaluation of recombinant lectin-like domain of thrombomodulin to protect the lung against tissue-damaging pro-inflammatory responses following ischaemia-reperfusion. (
  • Porcine laparotomies, as part of an animal protocol approved by National Institutes of Health, National Cancer Institute, the Institutional Animal Care and Use Committee, were used to assess the extent of ischemic injury (i.e., decreased tissue oxygenation) incurred during surgery. (
  • Cerebral ischemic reperfusion injury (CIRI) is defined as deterioration of brain tissue suffered from ischemia that concomitantly reverses the benefits of re-establishing cerebral blood flow following mechanical or chemical therapies for acute ischemic stroke. (
  • Systemic manifestations are caused by a traumatic rhabdomyolysis due to muscle reperfusion injury when compressive forces on the tissues are released.This can cause local tissue injury, organ dysfunction, and metabolic abnormalities, including acidosis, hyperkalemia, and hypocalcemia. (
  • 11) In lung tissue biopsies obtained from 20 consecutive human lungs for transplantation, apoptotic cells increased in number after graft reperfusion in a time-dependent manner. (
  • Although restoration of blood flow to an ischaemic organ is essential to prevent irreversible cellular injury, reperfusion may enhance tissue injury in excess of that produced by ischaemia alone [1]. (
  • In both models, blue light reduced neutrophil influx, as evidenced by reduced myeloperoxidase (MPO) within each organ, and reduced the release of high-mobility group box 1 (HMGB1), a neutrophil chemotactant and key mediator in the pathogenesis of I/R injury. (
  • Several mechanisms have been proposed for the pathogenesis of cerebral reperfusion injury. (
  • Pathogenesis of post-ischemic cellular injury is discussed along with potential interventions (pharmacologic and non-pharmacologic) currently being used to improve clinical outcomes. (
  • These data provide evidence that C5a is crucially involved in the pathogenesis of renal I/R injury by modulation of neutrophil-dependent as well as neutrophil-independent pathways, which include the regulation of CXC chemokines but not TNF-alpha or apoptotic pathways. (
  • 8) However, the exact pathogenesis of pulmonary reperfusion injury remains uncertain. (
  • The study, published today in the OnlineFirst version of the Journal of Parenteral and Enteral Nutrition ( JPEN ), the research journal of the American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.), used a mice model to compare the effects of GLN on hind limb ischemia reperfusion (IR) injury. (
  • The study subjected three groups of mice to 90 minutes of ischemia followed by a variable period of reperfusion. (
  • AQP4 Knockout Aggravates Ischemia/Reperfusion Injury in Mice. (
  • An established model of renal IRI was used: 30 min of renal pedicle clamping was followed by reperfusion in B cell-deficient (μMT) and wild-type mice. (
  • μMT mice also had significantly reduced tubular injury. (
  • To identify a possible mechanism involved in the protection from renal injury seen in the μMT mice, transfer experiments of B cells or serum from wild-type mice were investigated. (
  • Serum transfer, but not B cell transfer, restored the injury phenotype, indicating that a circulating factor mediates the protection seen in B cell-deficient mice. (
  • Sulfatide-mediated activation of type II natural killer T cells prevents hepatic ischemic reperfusion injury in mice. (
  • Gastrointestinal ischemia (20 min), followed by 3-h reperfusion, induced intestinal and lung injury in C1q KO and WT mice, but not in C2/fB KO mice. (
  • Addition of human C2 to C2/fB KO mice significantly restored GI/R injury, demonstrating that GI/R injury is mediated via the lectin and/or classical pathway. (
  • Germ-free mice were reported to have less local and remote injury following M I/R ( 59 ). (
  • 63 ) demonstrated that disruption of the TLR/MyD88 pathway in mice attenuated acute intestinal and lung injury, inflammation, and endothelial damage and improved survival after M I/R. Signals from gut commensal bacteria are mediated through TLRs, and depletion of gut commensals is expected to decrease the expression of TLRs in the intestine. (
  • 2 They also used Langendorff-perfused hearts from wild-type and p53-knockout mice to provide compelling evidence that cell death induced by ischemia-reperfusion did not require p53 expression. (
  • Furthermore, mice in which a component of the MPTP, CyP-D (cyclophilin D), has been knocked out are protected against heart and brain ischaemia/reperfusion. (
  • Three groups (n=5-8/per group) of adult male C57BL/6J (WT), global AT1a receptor-deficient (AT1a-KO), and conditional proximal tubule-specific AT1a-KO mice (PT-AT1a-KO) were subjected to sham surgery or 30 min unilateral left kidney ischemia, followed by reperfusion for 24 h or 7 days, respectively. (
  • Continuous pressure limits blood supply and causes ischemia, and the inflammation occurs during reperfusion. (
  • We therefore hypothesize that administration of human AM/AMBP-1, even after reperfusion, improves cardiovascular function, attenuates organ injury and inflammation responses, and reduces mortality following gut I/R injury. (
  • Inflammation and oxidative stress exert important roles in intestinal ischemia-reperfusion injury (IRI). (
  • Brain damage, including blood-brain barrier (BBB) dysfunction, neurological behavior deficit, cerebral infarction and inflammation, is commonly caused by ischemic-reperfusion (I/R) injury. (
  • Several studies have demonstrated that the blockade of leukocyte adhesion molecules (CD11/CD18, ICAM-1, selectins) protect the kidney in renal IRI, evidence of an important role of inflammation in the injury process ( 5 , 6 , 7 ). (
  • However, reperfusion itself induces more cellular alterations, likely through mitochondrial dysfunction, increased reactive oxygen species production, and inflammation 3 , 4 , 5 . (
  • These results suggest that depletion of gut commensal bacteria decreases B cells, Igs, and TLR expression in the intestine, inhibits complement activation, and attenuates intestinal inflammation and injury following M I/R. (
  • However, the role of gut microbiota in acute intestinal inflammation and injury is still undetermined and controversial. (
  • Monocyte retention, activation phenotype and the effects of their depletion by intravenous clodronate-liposome treatment on lung inflammation and injury were determined. (
  • suggested that valsartan plays an essential role in the protective effects on myocardial ischemic reperfusion injury, and the possible protection mechanism is due to its anti-inflammation function via TLR-4/NF-B signalling pathway [5]. (
  • In contrast, early decompression led to resolution of reperfusion-mediated inflammation, neurological improvement, and reduced hyperalgesia. (
  • 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). (
  • 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). (
  • Implementation of reperfusion modalities, including percutaneous coronary intervention and thrombolytic therapy, has significantly improved mortality and morbidity over the last 20 years [ 3 , 4 ]. (
  • Treatment of STCelevation MI (STEMI) has improved enormously with the advent of primary percutaneous coronary intervention (PPCI), but ischaemia/reperfusion (I/R) injury remains an important complication. (
  • We have reported that NFkB activation is increased in the heart following I/R. We have also observed that modulation of TLR signaling pathways was induce cardioprotection in I/R. Our long-term goals are to elucidate the immunoregulatory and pro-inflammatory signaling mechanisms associated with myocardial I/R injury. (
  • this is known as myocardial ischemia-reperfusion injury (I/R). Several studies have uncovered complex mechanisms of cardiomyocyte damage after the process of reperfusion, and efforts are ongoing to search for therapeutic targets to reduce I/R. One of the most observations is is the elevation of Ca2+ ions that takes place at intracellular and mitochondrial levels during reperfusion. (
  • The current review outlines the multifocal mechanisms of reperfusion injury and focuses on understanding the potential role of each element and its contribution to the injury pattern inflicted upon the myocardium. (
  • However, the detailed mechanisms of cell death and the structural alterations induced during different stages of reperfusion injury i.e. the early stage, are not completely determined yet. (
  • Investigations into the role of complement in ischemia/reperfusion (I/R) injury have identified common effector mechanisms that depend on the production of C5a and C5b-9 through the cleavage of C3. (
  • Less clear however is the mechanism of complement activation that leads to the cleavage of C3 in ischemic tissues and to what extent the potential trigger mechanisms are organ dependent - an important question which informs the development of therapies that are more selective in their ability to limit the injury, yet preserve the other functions of complement where possible. (
  • The purpose of the present study was to investigate the protective effect of butyrate, a naturally occurring four-carbon fatty acid in the body and a dietary component of foods such as cheese and butter, on hepatic injury complicated by enterogenous endotoxin, as well as to examine the underlying mechanisms involved. (
  • The goal of my PhD was to investigate this phenomenon in human patients treated with PPCI, with particular emphasis on T cell kinetics, their relationship to I/R injury, and the potential mechanisms involved. (
  • Pharmaceutical agents, including inhaled nitric oxide, soluble complement receptor type 1, prostaglandin E 1 and exogenous surfactant, attenuate pulmonary reperfusion injury through distinct mechanisms. (
  • Mechanisms of pulmonary reperfusion injury have been extensively studied. (
  • However, unlike APN, CTRP9 protects diabetic heart against IR injury [14], but with partially understood mechanisms. (
  • A growing body of evidence suggests that inflammatory pathways initiated by the innate immune system are involved in the pathophysiology of myocardial I/R injury and congestive heart failure. (
  • Most studies have so far concentrated on arterial ischemia, implicating molecules such as tumor necrosis factor-alpha (TNF-alpha) and adhesion molecules in the pathophysiology of the response to injury. (
  • One of the most important factors in the pathophysiology of liver dysfunction after hepatic surgery is the cellular damage derived from the interruption of blood flood with reperfusion of the organ. (
  • Finally, we explore promising innovative strategies targeting novel reperfusion injury pathways to protect ischemic myocardium during reperfusion. (
  • Damage to the MYOCARDIUM resulting from MYOCARDIAL REPERFUSION (restoration of blood flow to ischemic areas of the HEART. (
  • Taurine and calcium interaction in protection of myocardium exposed to ischemic reperfusion injury. (
  • Restored blood flow quickly rescues myocardium but also causes ischemia-reperfusion (IR) injury. (
  • This is the first study on the proteomic expression of XST-treated myocardium with I/R injury to reveal that the cardioprotective effects of XST may be attributed to the PDH-mediated restoration of aerobic glucose oxidation. (
  • The modified annexin decreases the binding of leukocytes and platelets during post-ischemic reperfusion, thereby restoring microvascular blood flow and decreasing organ damage. (
  • We show that an acute and short (24 h) exposure to high-illuminance (1,400 lx) blue spectrum (peak 442 nm) light prior to ischemia/reperfusion (I/R) significantly attenuates the degree of organ injury. (
  • Here, we show that acute exposure to bright blue spectrum light reduces organ injury by comparison with bright red spectrum or ambient white fluorescent light in two murine models of sterile insult: warm liver ischemia/reperfusion (I/R) and unilateral renal I/R. Exposure to bright blue light before I/R reduced hepatocellular injury and necrosis and reduced acute kidney injury and necrosis. (
  • As such, the development of effective strategies for preventing and treating circulatory collapse and organ injury after gut I/R is critical for the improvement of patient outcome under such conditions. (
  • this may offer local and distant organ protection in hind limb IR injury. (
  • Here we consider recent evidence for each of the three major pathways of complement activation (classical, lectin, and alternative) as mediators of I/R injury, and in particular highlight the role of lectin molecules that increasingly seem to underpin the injury in different organ models and in addition reveal unusual routes of complement activation that contribute to organ damage. (
  • Ischemia-reperfusion injury manifests itself in strokes, heart attacks, organ transplantations and during long surgical procedures. (
  • Attention should also be focused on the possibility of concomitant injury (fractures, organ damage, spinal injury and obvious hemorrhage). (
  • The Food and Drug Administration (FDA) has granted Orphan Drug designation for cannabidiol (CBD) to prevent ischemia and reperfusion injury resulting from solid organ transplantation. (
  • The Company believes that the immunosuppressant and antiinflammatory effects of cannabidiol may attenuate the damage caused by ischemia and reperfusion during organ transplantation and could potentially be an alternative to more expensive strategies (ie, ischemic preconditioning, ischemic postconditiong, machine perfusion). (
  • Intestinal ischemia and reperfusion (I/R) is not infrequent in the clinical situation and the intestinal barrier plays an important role in gut barrier function, preventing not at least septic complications and potentially the development of the multiple organ dysfunction syndrome. (
  • Brief episodes of ischemia at a distant organ could reduce the myocardial reperfusion injury. (
  • Attempts to reduce the extent of myocardial reperfusion injury have included lowering the risk posed by certain injurious factors and potentiating various aspects of cardioprotection relating to ischemic duration, 1 oxygen free radicals, 2 3 proinflammatory cytokines, 4 5 and preconditioning. (
  • Damage introduced by ischemia reperfusion injury (IR injury) is pivotal in diseases such as coronary heart disease (CHD) and stroke, causing substantial mortality and morbidity [ 1 , 2 ]. (
  • Ozone protects rat heart against ischemia-reperfusion injury: A role for oxidative preconditioning in attenuating mitochondrial injury. (
  • Clq/TNF-Related Protein 9 Protects Diabetic Rat Heart against Ischemia Reperfusion Injury: Role of Endoplasmic Reticulum Stress. (
  • Does a Seven Day Treatment With Dipyridamole Induce Protection Against Ischemia-Reperfusion Injury? (
  • Does Caffeine Reduce Dipyridamole-Induced Protection Against Ischemia-Reperfusion Injury? (
  • It is thought that reactive oxygen species formation during reperfusion induces a cascade of series of cellular events that eventually leads to hepatocellur injury. (
  • Activation of peripheral nociception also induces cardioprotection against IR injury via neurogenic pathway. (
  • These data suggest that modifying the spectrum of light may offer therapeutic utility in sterile forms of cellular 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. (
  • In this respect, myocardial reperfusion injury remains a neglected therapeutic target for cardioprotection in PPCI patients. (
  • Succinate: A Promising Therapeutic Target for Reperfusion Injury. (
  • Taken together, naringin could be a potential therapeutic agent to prevent the brain from I/R injury via attenuating ONOO − -mediated excessive mitophagy. (
  • Ischemia Reperfusion Injury - Pipeline Review, H2 2015 Summary Global Markets Direct s, Ischemia Reperfusion Injury - Pipeline Review, H2 2015, provides an overview of the Ischemia Reperfusion Injurys therapeutic pipeline. (
  • This report provides comprehensive information on the therapeutic development for Ischemia Reperfusion Injury, complete with comparative analysis at various stages, therapeutics assessment by drug target, mechanism of action (MoA), route of administration (RoA) and molecule type, along with latest updates, and featured news and press releases. (
  • It also reviews key players involved in the therapeutic development for Ischemia Reperfusion Injury and special features on late-stage and discontinued projects. (
  • These findings identify a possible therapeutic target in I/R injury postCPPCI, opening up a new avenue for further research and future treatment development. (
  • Such clinical studies have clearly pushed the boundary of our understanding about reperfusion injury and therapeutic time window. (
  • A solid scientific foundation is needed for expanding therapeutic window way beyond reperfusion injury. (
  • 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. (
  • When given at therapeutic immunosuppressive doses, SRL compromises renal function after ischemia-reperfusion injury in a rat kidney transplant model. (
  • Methods for their use, such as to prevent thrombosis without increasing hemorrhage, enhancing the survivability of platelets during storage or transfusion and to attenuate ischemia-reperfusion injury (IPI), are also provided. (
  • In the present study, we tested the hypothesis that naringin, a natural antioxidant, could inhibit ONOO − -mediated mitophagy activation and attenuate cerebral I/R injury. (
  • However, mitochondria can become the major sites of reactive oxygen species (ROS) generation in the pathological process, causing significant cell damage, for example, in the process of ischemia-reperfusion (I/R) injury ( 2 ). (
  • 0.05) enhanced mitophagy by increasing the translocation of p62 and Parkin to the damaged mitochondria in the mouse spinal cord injury model. (
  • Mitochondria have been proposed to be the principal subcellular target of a ischemia-reperfusion injury. (
  • Myocardial mitochondria were obtained to evaluate changes in mitochondrial structure and function, immediately after 120 minutes reperfusion. (
  • We believe a therapy for treating ischemia-reperfusion injury must be able to address the mitochondria dysfunction, which is induced during ischemia. (
  • With the mitochondria disabled, the cell can no longer process oxygen, which is re-introduced during reperfusion into energy, ultimately leading to cell death. (
  • Tsivgoulis G, Katsanos AH, Alexandrov AV (2014) Reperfusion therapies of acute ischemic stroke: potentials and failures. (
  • Gomis M, Dávalos A (2014) Recanalization and reperfusion therapies of acute ischemic stroke: what have we learned, what are the major research questions, and where are we headed? (
  • The proximal portion of the left coronary artery was surgically occluded for 30 minutes through ligation with a suture (size 6.0) followed by coronary reperfusion through release of the tie. (
  • After coronary reperfusion, the tie was left loose on the surface of the heart, the chest was closed, and the intratracheal tube and ECG electrodes were removed. (
  • Reperfusion injury is a primary concern in liver transplantation surgery. (
  • Ischemia-reperfusion injury (IRI) is a major challenge in liver transplantation. (
  • Hepatic injury caused by ischemia/reperfusion (I/R) has been proposed as a key clinical problem associated with liver transplantation and major liver surgery. (
  • cellvie , a company based in Houston, Texas, is developing a mitochondrial transplantation therapy to help reduce the damage caused by ischemia-reperfusion injury. (
  • In kidney transplantation, the incidence of delayed graft function, which may be as high as 50%, has been closely tied to ischemia-reperfusion injury. (
  • Sirolimus (SRL) seems to impair renal recovery from ischemic injury in animal models and delayed graft function after clinical renal transplantation. (
  • Pulmonary reperfusion injury is a common clinical problem secondary to severe shock, cardiopulmonary bypass (CPB) and lung transplantation, etc . (1) It is a major cause of morbidity, predominantly primary graft dysfunction (PGD) and mortality following lung transplantation. (
  • In a porcine transplantation model, nuclear factor-κB played a central role in triggering the pathways for lung inflammatory injury. (
  • Salvianolic acid B exerts strong resistance to oxidative stress and inflammatory reaction, and improves energy metabolism against cerebral ischemia-reperfusion injuries. (
  • LBPs increased the levels of antioxidant enzymes and reduced intestinal oxidative injury in animal models of intestinal IRI. (
  • Hepatocellular oxidative stress forms a pivotal aspect of IR injury, predominantly during the early (0-30 min) phase of reperfusion. (
  • Prevention of MPTP opening either directly, using agents such as cyclosporin A, or indirectly by reducing oxidative stress or Ca 2+ overload, provides a protective strategy against reperfusion injury. (
  • Our DIEP-operation is actually a clinical model of ischemia-reperfusion. (
  • A mechanical model of ischemia/reperfusion is compared with an embolic model with tPA-induced thrombolysis. (
  • Levosimendan protects human hepatocytes from ischemia-reperfusion injury. (
  • We still need to see how and if it can protect the heart long term, but we find in the short term when we give enough of this microRNA, it protects the heart from reperfusion injury. (
  • PGD(2) DP1 receptor protects brain from ischemia-reperfusion injury. (
  • Activation of the adenosine receptor protects against ischemia-reperfusion injury (pharmacologic preconditioning). (
  • Splenectomy protects the kidneys against ischemic reperfusion injury in the rat. (
  • Melatonin scavenges hydroxyl radical and protects isolated rat hearts from ischemic reperfusion injury. (
  • The aim of this study was to determine whether C1INH protects against myocardial cell injury via an anti-apoptotic activity or anti-inflammatory effect. (
  • Studies have revealed that APN protects against myocardial IR injury, while the cardioprotective effect is attenuated in diabetic condition [4-6]. (
  • Using a definite protocol, a prospective collection of data, and an adequate number of patients assuring statistically powered data, this study will integrate clinical information with imaging and biological factors involved in reperfusion injury after cerebral ischemia. (
  • Professor Dan Atar, the Coordinating Investigator of the F.I.R.E. (FX06 In ischemia and REperfusion) trial, a Phase II clinical study of FX06, will present the results of the trial at: 12-noon on September 2nd in the Hot Line III Session at the European Society of Cardiology Congress in Munich, Germany. (
  • The Phase II clinical trial of FX06 (F.I.R.E. study) was completed in March 2008, with data indicating a statistically significant reduction in myocardial necrosis following intravenous application of FX06 concurrent with reperfusion. (
  • Carperitide also reduced reperfusion injury by 25.9% compared with placebo ( P =0.019), said Dr. Kitakaze, reporting the results of the 65-center J-WIND trial (Japan-Working Groups of Acute Myocardial Infarction for the Reduction of Necrotic Damage by ANP or Nicorandil) at a late-breaking clinical trials session at the American Heart Association meeting. (
  • Clinical perspectives on reperfusion injury in acute myocardial infarction. (
  • Prompt reperfusion therapy in acute myocardial infarction enhances clinical outcome. (
  • and infusion of 50 mg/kg, from 30 minutes before the ischemia up to 60 minutes later to the reperfusion) or placebo in a phase IV clinical trial. (
  • Reperfusion therapy has been one of the major breakthroughs in clinical medicine. (
  • acute renal failure (ARF) secondary to ischemia-reperfusion (I/R) injury continues to be a significant clinical problem ( 2 , 17 , 26 ). (
  • Glucagonlike peptide (GLP-1) and its receptor (GLP-1R) exhibit cardioprotective effects after myocardial ischemia and reperfusion (MI/R) in both animal studies and clinical trials. (
  • Pulmonary reperfusion injury is a clinical syndrome with no single and recognized pathophysiologic mechanism. (
  • During the initial ischemia phase, as well as during reperfusion, metabolic therapy can be very useful as, for example, glucose-insulin-potassium solutions (G-I-K). These could act as scavengers of the free radicals derived from oxygen and avoid or reduce the myocardial damage due to reperfused myocytes. (
  • Myocardial 'reperfusion injury' has been partly attributed to the production of free radicals which are cytotoxic towards cells. (
  • During postischemic reperfusion, free radicals are produced and have deleterious effects in isolated rat hearts. (
  • Norepinephrine (NE)-derived free radicals may contribute to myocyte injury after ischemia -reperfusion, so the influence of sympathetic denervation on myocardial ischemia - reperfusion injury was investigated in the present study. (
  • In their mouse model of this ischemia/reperfusion injury of the heart, they've found they can reduce heart muscle death 40 percent by giving a manmade version of the microRNA miR322, they report in the Journal of Molecular and Cellular Cardiology . (
  • Once reperfusion occurs, these cellular products are returned to the systemic circulation, and are exposed to other organs. (
  • Organs involved in filtration (e.g., the kidneys and the liver), may be overwhelmed by the high load of cellular break down products, and face injury themselves (e.g., acute kidney injury). (
  • The notion of lethal reperfusion injury in the heart implies that injury ensues to viable myocytes at the time of reperfusion, over and above, the cellular damage normally attributed to the initial ischemic event. (
  • Timely reperfusion of the infarct-related artery continues to be the most effective means to limit development of cellular necrosis. (
  • Further studies are being undertaken to determine the cellular mechanism via which Doxorubicin mediates increased myocardial injury in conditions of ischaemia-reperfusion. (
  • Experimental cellular and animal models, and also human studies, have demonstrated that protection against IR injury by ischemic preconditioning, and the more clinically applicable remote ischemic preconditioning, is associated with increases in O-GlcNAc levels. (
  • IP in skeletal muscle has showed a protective effect in vascular reperfusion, cellular membrane structure and function, muscle preservation, decreasing inflammatory infiltrate and vascular stasis 8 - 12 . (
  • In fact, this damage properly constitutes a partial diastolic depolarization or injury, i.e., a moderate reduction of the rest transmembrane potential. (
  • The inflammatory response is partially responsible for the damage of reperfusion injury. (
  • Studies indicate that reperfusion injury is involved directly in the potentiation of stroke damage. (
  • Damage to the blood-brain barrier (BBB), an important factor in reperfusion injury, is seen in the image below. (
  • Debate concerning prevalence of reperfusion injury continues but no true experimental model is presently available to distinguish damage caused by restoration of flow to the perfusion bed of the infarct related artery compared to that present at the end of ischemia. (
  • With about 800,000 heart attacks in the U.S. alone, and 1 out of 3 hearts offered for donation being discarded, there is ample need for a therapy ameliorating the damage of ischemia and reperfusion. (
  • Treating select accessories to the disease, such as the excessive calcium accumulation in the cells, has not been successful in ameliorating the damage of ischemia and reperfusion. (
  • 4) Pulmonary reperfusion injury is characterized by non-specific alveolar damage, lung edema and hypoxemia occurring within 72 hours. (
  • MicroRNAs (miRNAs/miRs) have been reported to affect ischemia/reperfusion (I/R)‑induced cerebral damage. (
  • Our hypothesis is that complement activation and the TLRs are triggered by the stress of ischemia and reperfusion and that this leads to activation of inflammatory cells (leucocytes and endothelial cells), production of inflammatory mediators and direct damage to the kidney. (
  • The occurrence of reperfusion injury may be inevitable but restoration of blood flow to the infarct-related artery is critical to ensure salvage of reversibly injured myocytes within the area at risk. (
  • Objective To define the role of donor intravascular monocytes in lung transplant-related acute lung injury and primary graft dysfunction. (
  • We questioned whether local anesthetics potentiate renal dysfunction after ischemia-reperfusion (I/R) injury in vivo. (
  • Continuous local anesthetic infusion with renal I/R injury resulted in an increased magnitude and duration of renal dysfunction compared with the saline-infused I/R group. (
  • Activated endothelial cells produce more reactive oxygen species but less nitric oxide following reperfusion, and the imbalance results in a subsequent inflammatory response. (
  • Some theorize that this delayed reaction derives from the various inflammatory immune responses that occur during reperfusion. (
  • These inflammatory responses cause intracranial pressure, pressure which leads to cell injury and in some situations cell death. (
  • Osthole treatment ameliorates renal I/R injury by inhibiting inflammatory responses in kidneys. (
  • June 9, 2015, Silver Spring, MD -- A single dose of intravenous glutamine (GLN) administered immediately after a non-lethal lower limb ischemia reduces the reperfusion inflammatory reaction locally and systemically according to a new study. (
  • In this study, we investigated the impact of blocking the C5aR pathway on the inflammatory response and on the renal function in a murine model of I/R injury. (
  • Several methods, such as thrombolytic agents, hyperbaric oxygen treatment, and anti-inflammatory agents have been tested to prevent or lessen the harmful effects of IR injury 6 . (
  • Therefore, we hypothesized that depletion of gut commensal bacteria would lead to a reduction in the acute intestinal inflammatory response after mesenteric I/R (M I/R) injury. (
  • In the setting of reperfusion therapy in an acute myocardial infarction using primary percutaneous intervention (PCI), the body's own inflammatory system involving the complement cascade m. (
  • Lung inflammatory injury induced by lipopolysaccharide, characterized by rapid sequestration of neutrophils in response to inflammatory chemokines and cytokines released in the lungs is an acceptable theory. (
  • A transplanted kidney is exposed to episodes of ischemia (during explantation, transportation and implantation) and reperfusion (in the recipient) which mediate deleterious inflammatory responses and reduce the lifetime of the kidney graft. (
  • We are interested in the role of Toll-like receptor (TLR) mediated signaling pathways in myocardial ischemia/reperfusion injury. (
  • Here we develop a comparative in vivo metabolomic analysis, and unexpectedly identify widely conserved metabolic pathways responsible for mitochondrial ROS production during ischaemia reperfusion. (
  • Debate has gone on, and continues regarding the existence of reperfusion injury and the pathways that are solicited. (
  • 6) What other apoptotic pathways are induced by reoxygenation or other aspects of reperfusion? (
  • The lectin pathway is one of the three activation pathways of the complement activation cascade that can recognise and respond to structures on oxygen deprived cells and contribute to ischaemia and reperfusion injury (IRI). (
  • We describe in detail a clinically relevant colorectal cancer liver metastases (CRLM) tumor model and the influence of liver ischemia reperfusion (I/R) in tumor growth and metastasis. (
  • However, the addition of proteasome inhibitor in the preservation solution alleviated the injuries due to the ischemia-reperfusion process. (
  • However, the role of gut commensals in intestinal ischemia/reperfusion (I/R) injury is unclear. (
  • To determine the roles of gut commensal bacteria in intestinal IR injury, we depleted gut microbiota with a broad-spectrum antibiotic cocktail and performed mesenteric I/R (M I/R). First, we confirmed that antibiotic treatment completely depleted gut commensal bacteria and diminished the size of secondary lymphoid tissues such as the Peyer's patches. (
  • We next found that antibiotic treatment attenuated intestinal injury following M I/R. Depletion of gut commensal bacteria reduced the expression of Toll-like receptor (TLR)2 and TLR4 in the intestine. (
  • Intestinal I/R injury is initiated when natural antibodies recognize neo-antigens that are revealed on ischemic cells and activate the complement pathway. (
  • Gut decontamination with antibiotics reduced intestinal ischemia-induced lung injury ( 58 ). (
  • However, another group had reported that depletion of gut commensal bacteria with antibiotics increased intestinal I/R injury ( 15 ). (
  • To determine the role of gut commensal bacteria in acute intestinal injury, we depleted gut flora with a broad-spectrum antibiotic cocktail and evaluated the effects on intestinal I/R injury. (
  • A short period of intestinal ischemia (20 min) was followed by an early epithelial barrier recovery as compared to longer (40 min) ischemia and same time period of reperfusion, though without obvious recovery of endothelial barrier. (
  • However, the process of reperfusion can itself induce cardiomyocyte death, known as myocardial reperfusion injury, for which there is still no effective therapy. (
  • Expression of RIP1 was preserved in Z-VAD and Nec + Z-VAD compared with CTL, suggesting RIP1-mediated necrosis is involved in myocardial ischemia-reperfusion injury. (
  • Introduction The Reperfusion Injury Salvage Kinase (RISK) pathway is the term given to prosurvival kinases such as the phosphatidylinositol-3 kinase (PI3K)-Akt cascade, which confer cardioprotection when specifically activated at the onset of myocardial reperfusion following an infarct. (
  • The aim of the present study was to investigate the role of ERS in CTRP9 induced cardioprotection against IR injury in HFD induced type 2 diabetic heart and the underlying mechanism. (
  • Recognizing this, surgeons frequently prophylactically release (i.e., incise) fascia of arm and leg fascial compartments after repair of a proximal vascular injury. (
  • Conclusions: Based on these data, IT instillation of AgNP increases circulating levels of several key cytokines, which may contribute to persistent expansion of I/R injury possibly through an impaired vascular responsiveness. (
  • Various forms of reperfusion injury can include myocardial and vascular stunning, microvascular injury and no-reflow, arrhythmias, etc. (
  • Reperfusion takes place when there is spontaneous thrombolysis, THROMBOLYTIC THERAPY, collateral flow from other coronary vascular beds, or reversal of vasospasm. (
  • 2,5,6 ⇓ ⇓ These vascular complications of reperfusion injury pose a serious limitation for thrombolytic stroke therapy. (
  • This study suggests that vascular monocytes play a key role in lung injury following ischaemia-reperfusion. (
  • Ischaemic reperfusion injury prompts a release of cytokines and other proinflammatory mediators that activate both the neutrophils and the coronary vascular endothelium. (
  • If it seems odd that reestablishing blood rich in oxygen and nutrients back to heart cells that are screaming for both and dying without them, would also cause injury, Tang explains that it's a fragile transition period. (
  • A method and apparatus for the prevention and treatment of reperfusion injury following the reperfusion of acute MI which includes modulation of coronary blood flow or oxygen delivery following the reperfusion of the infarct with a catheter placed in the coronary artery or vein. (
  • The production of reactive oxygen species (ROS), including superoxide, hydrogen peroxide, and hydroxyl radical, has been demonstrated in reperfusion injury. (
  • IR injury happens when ,during ischemia, blood flow interruption creates local lesions in proportion to oxygen and nutriment privation time, urging reperfusion to be performed as soon as possible. (
  • Morphological analysis of cells showed that 4 hours of ischemia followed by reperfusion produced blebbing cells within 2 hours of restoring oxygen to the chip. (
  • Ren Z, Xie P, Lv J, Hu Y, Guan Z, Chen L and Yu W: miR‑187‑3p inhibitor attenuates cerebral ischemia/reperfusion injury by regulating Seipin‑mediated autophagic flux. (
  • Reperfusion of ischemic tissues is often associated with microvascular injury, particularly due to increased permeability of capillaries and arterioles that lead to an increase of diffusion and fluid filtration across the tissues. (

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