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Titolo:
Heat stress protects against electrophysiological damages induced by acutedoxorubicin exposure in isolated rat hearts
Autore:
Joyeux, M; Godin-Ribuot, D; Faure, P; Demenge, P; Ribuot, C;
Indirizzi:
Univ Grenoble 1, UFR Pharm, Lab Stress Cardiovasc & Pathol Associees, Grenoble, France Univ Grenoble 1 Grenoble France sc & Pathol Associees, Grenoble, France
Titolo Testata:
CARDIOVASCULAR DRUGS AND THERAPY
fascicolo: 3, volume: 15, anno: 2001,
pagine: 219 - 224
SICI:
0920-3206(200105)15:3<219:HSPAED>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
ANTHRACYCLINE CARDIOTOXICITY; HISTAMINE-RELEASE; ADRIAMYCIN; CARDIOMYOPATHY; CATALASE; TOXICITY; FAILURE; ARRHYTHMOGENESIS; HYPERTHERMIA; PROTEINS;
Keywords:
heat stress; anthracycline; doxorubicin toxicity; isolated rat heart;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Ribuot, C Fac Pharm, Lab LSCPA, Domaine Merci, F-38706 La Tronche, France Fac Pharm Domaine Merci La Tronche France F-38706 onche, France
Citazione:
M. Joyeux et al., "Heat stress protects against electrophysiological damages induced by acutedoxorubicin exposure in isolated rat hearts", CARDIO DRUG, 15(3), 2001, pp. 219-224

Abstract

The use of anthracycline antibiotics as anticancer agents is limited by their cardiac toxicity. Heat stress (HS) is known to confer protection against various myocardial injuries such as ischemia-reperfusion induced damage. This cardioprotective mechanism is associated with an increase in endogenous antioxidative defenses and heat stress proteins (HSPs) synthesis. The aimof this study was thus to investigate whether HS could protect against acute doxorubicin cardiotoxicity using the isolated rat heart model. Rats were either heat stressed (42 degreesC for 15 min) or sham anesthetized. 24 h later, their hearts were isolated and retrogradely perfused at constant flow. Following 30-min of stabilization, hearts were perfused during 70 min with modified-Krebs solution containing 6 mg/1 doxorubicin. Control hearts were perfused under identical conditions but without doxorubicin. Different hemodynamic and electrophysiological parameters were assessed in hearts from the four experimental groups. Doxorubicin exposure decreased left ventricular developed pressure (approximately -60% of baseline) and increased coronary perfusion pressure (approximately +230% of baseline). Prior HS did not modify these effects. Incidence of ventricular fibrillation (VF) was significantly enhanced by doxorubicin exposure (66% vs 0% in control group). Moreover, the ventricular action potential duration (APD) was significantly shortened in the presence of doxorubicin. Prior HS prevented both increase in VF incidence and shortening ofAPD. We conclude that prior heat stress protects myocardium against electrophysiological injury, but not against hemodynamic damage, induced by acute doxorubicine exposure. Further investigations are required to elucidate the precise mechanisms involved in this effect.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 00:00:30