Brief hypoxia before normoxic reperfusion (postconditioning) protects the heart against ischemia-reperfusion injury by preventing mitochondria peroxyde production and glutathione depletion

FASEB Journal

Volumn 19, Issue 3, 2005, Pages 354-361

  Serviddio, Gaetano ^a   Di Venosa, Nicola ^b   Federici, Antonio ^b   D'Agostino, Donate ^b   Rollo, Tiziana ^a   Prigigallo, Filomena ^a   Altomare, Emanuele ^a   Fiore, Tommaso ^b   Vendemiale, Gianluigi ^a  

^a UNIVERSITY OF FOGGIA   (Italy)

^b UNIVERSITY OF BARI   (Italy)

Author keywords

Hypoxic reperfusion; Ischemia reperfusion; Mitochondria; Oxidative stress

Indexed keywords

CARBONYL DERIVATIVE; GLUTATHIONE; GLUTATHIONE DISULFIDE; PEROXIDE;

ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; DEPLETION; HEART LEFT VENTRICLE ENDDIASTOLIC PRESSURE; HEART LEFT VENTRICLE FILLING; HEART MUSCLE ISCHEMIA; HEART MUSCLE REPERFUSION; HEART PROTECTION; HEMODYNAMICS; HYPOXIA; MALE; MITOCHONDRION; NONHUMAN; OXIDATIVE STRESS; PRIORITY JOURNAL; RAT; REPERFUSION INJURY; UREA CYCLE;

ANIMALS; ANOXIA; DIASTOLE; GLUTATHIONE; HEMODYNAMIC PROCESSES; KINETICS; MALE; MITOCHONDRIA, HEART; MITOCHONDRIAL PROTEINS; MYOCARDIAL REPERFUSION; MYOCARDIAL REPERFUSION INJURY; OXIDATION-REDUCTION; PEROXIDES; RATS; RATS, WISTAR; SYSTOLE;

EID: 14644412783     PISSN: 08926638     EISSN: None     Source Type: Journal    
DOI: 10.1096/fj.04-2338com     Document Type: Article

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