Xanthine oxidase contributes to mitochondrial ROS generation in an experimental model of cocaine-induced diastolic dysfunction

Journal of Cardiovascular Pharmacology

Volumn 60, Issue 6, 2012, Pages 538-543

  Vergeade, Aurélia ^a   Mulder, Paul ^a   Vendeville, Cathy ^a   Ventura Clapier, Renée ^b   Thuillez, Christian ^a   Monteil, Christelle ^a  

^a UNIVERSITÉ DE ROUEN   (France)

^b INSERM   (France)

Author keywords

cardiac dysfunction; cocaine; heart; mitochondria; oxidative stress; reactive oxygen species

Indexed keywords

ADENOSINE TRIPHOSPHATE; ALLOPURINOL; COCAINE; REACTIVE OXYGEN METABOLITE; XANTHINE OXIDASE;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CONTROLLED STUDY; DIASTOLIC DYSFUNCTION; DRUG EFFECT; ENZYME ACTIVATION; HEART LEFT VENTRICLE ENDDIASTOLIC PRESSURE; HEART LEFT VENTRICLE RELAXATION; IN VIVO STUDY; MALE; MITOCHONDRION; NONHUMAN; OXYGEN CONSUMPTION; PRIORITY JOURNAL; RAT;

ADENOSINE TRIPHOSPHATE; ALLOPURINOL; ANIMALS; ANTIOXIDANTS; COCAINE; DIASTOLE; DISEASE MODELS, ANIMAL; ELECTRON TRANSPORT COMPLEX I; ELECTRON TRANSPORT COMPLEX III; ENERGY METABOLISM; ENZYME INHIBITORS; HEMODYNAMICS; MALE; MITOCHONDRIA, HEART; OXIDATIVE STRESS; RATS; RATS, WISTAR; REACTIVE OXYGEN SPECIES; SUPEROXIDES; VENTRICULAR DYSFUNCTION, LEFT; VENTRICULAR FUNCTION, LEFT; XANTHINE OXIDASE;

EID: 84871607234     PISSN: 01602446     EISSN: 15334023     Source Type: Journal    
DOI: 10.1097/FJC.0b013e318271223c     Document Type: Article

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