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Titolo:
Urodilatin limits acute reperfusion injury in the isolated rat heart
Autore:
Inserte, J; Garcia-Dorado, D; Agullo, L; Paniagua, A; Soler-Soler, J;
Indirizzi:
Hosp Gen Univ Valle Hebron, Serv Cardiol, Barcelona 08035, Spain Hosp Gen Univ Valle Hebron Barcelona Spain 08035 Barcelona 08035, Spain
Titolo Testata:
CARDIOVASCULAR RESEARCH
fascicolo: 2, volume: 45, anno: 2000,
pagine: 351 - 359
SICI:
0008-6363(20000114)45:2<351:ULARII>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE; CONTRACTION BAND; OXYGEN PARADOX; HYPERTROPHIED MYOCYTES; PEPTIDE INFUSION; INTRACELLULAR PH; CARDIAC MYOCYTES; INFARCT SIZE; ISCHEMIA; FAILURE;
Keywords:
ischemia; natriuretic peptide; necrosis; reperfusion; second messengers;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Garcia-Dorado, D Hosp Gen Univ Valle Hebron, Serv Cardiol, Passeig Vall Hebron 119-129, Barcelona 08035, Spain Hosp Gen Univ Valle Hebron Passeig Vall Hebron 119-129 Barcelona Spain 08035
Citazione:
J. Inserte et al., "Urodilatin limits acute reperfusion injury in the isolated rat heart", CARDIO RES, 45(2), 2000, pp. 351-359

Abstract

Objectives: Hypercontracture is an important mechanism of myocyte death during reperfusion. cGMP modulates the sensitivity of contractile myofilaments to Ca2+, and increasing cGMP concentration during the last minutes of anoxia prevents reoxygenation-induced hypercontracture in isolated cardiomyocytes. The purpose of this study was to determine whether stimulation of particulate guanylyl cyclase with the natriuretic peptide urodilatin, given at the time of reperfusion, reduces myocardial necrosis in the rat heart submitted to transient ischemia. Methods: Isolated rat hearts (n=38) were submitted to either 40 or 60 min of no-flow ischemia and 2 h of reperfusion, and were allocated to receive or not receive 0.05 mu M urodilatin during the first 15 min of reperfusion or non-reperfusion treatment. Results: A marked reduction in myocardial cGMP concentration was observed in control hearts during reperfusion after 40 or 60 min of ischemia. Urodilatin significantly attenuated cGMP depletion during initial reperfusion, markedly improved contractile recovery after 40 min of ischemia (P<0.0309), and reduced reperfusion-induced increase in left ventricular end-diastolic pressure (P=0.0139), LDH release (P=0.0263), and contraction band necrosis (P=0.0179) after 60 min of ischemia. The beneficial effect of urodilatin was reproduced by the membrane permeable cGMP analog 8-Bromo-cGMP. Conclusions: These results indicate that reduced cGMP concentration may impair myocyte survival during reperfusion. Stimulation of particulate guanylyl cyclase may appear as a new strategy to prevent immediate lethal reperfusion injury. (C) 2000 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/07/20 alle ore 18:23:25