Inhibiting mitochondrial permeability transition pore opening at reperfusion protects against ischaemia-reperfusion injury

Cardiovascular Research

Volumn 60, Issue 3, 2003, Pages 617-625

  Hausenloy, Derek J ^a   Duchen, Michael R ^b   Yellon, Derek M ^a  

^a UNIVERSITY COLLEGE HOSPITAL   (United Kingdom)

^b UNIVERSITY COLLEGE LONDON   (United Kingdom)

Author keywords

Infarction; Ischaemia; Membrane permeability; Membrane potential; Reperfusion

Indexed keywords

DIMETHYL SULFOXIDE; REACTIVE OXYGEN METABOLITE; SANGLIFEHRIN A;

ANIMAL TISSUE; ARTICLE; CELL DEATH; CELL MEMBRANE DEPOLARIZATION; CELL PROTECTION; CHANNEL GATING; CONTROLLED STUDY; DRUG EFFECT; DRUG MECHANISM; HEART INFARCTION SIZE; HEART MUSCLE; HEART MUSCLE ISCHEMIA; HEART MUSCLE PERFUSION; HYPOTHESIS; ISOLATED HEART; LASER; MALE; MEMBRANE PERMEABILITY; MEMBRANE POTENTIAL; MITOCHONDRIAL MEMBRANE; MUSCLE CELL; NONHUMAN; OXIDATIVE STRESS; PRIORITY JOURNAL; RAT; REPERFUSION INJURY; RISK FACTOR;

ANIMALS; INTRACELLULAR MEMBRANES; ION CHANNELS; LACTONES; MALE; MICROSCOPY, CONFOCAL; MITOCHONDRIA, HEART; MITOCHONDRIAL MEMBRANE TRANSPORT PROTEINS; MYOCARDIAL INFARCTION; MYOCARDIAL REPERFUSION; MYOCARDIAL REPERFUSION INJURY; RATS; RATS, SPRAGUE-DAWLEY; SPIRO COMPOUNDS;

EID: 0345490687     PISSN: 00086363     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.cardiores.2003.09.025     Document Type: Article

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