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Titolo:
Endothelin-1 increases susceptibility of isolated rat hearts to ischemia/reperfusion injury by reducing coronary flow
Autore:
de Groot, MCH; Illing, B; Horn, M; Urban, B; Haase, A; Schnackerz, K; Neubauer, S;
Indirizzi:
Univ Wurzburg, Med Klin, D-97080 Wurzburg, Germany Univ Wurzburg Wurzburg Germany D-97080 d Klin, D-97080 Wurzburg, Germany Univ Wurzburg, Inst Phys, EPV, D-97080 Wurzburg, Germany Univ Wurzburg Wurzburg Germany D-97080 s, EPV, D-97080 Wurzburg, Germany Univ Wurzburg, Theodor Boveri Inst Biowissensch, D-97080 Wurzburg, GermanyUniv Wurzburg Wurzburg Germany D-97080 sensch, D-97080 Wurzburg, Germany
Titolo Testata:
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
fascicolo: 12, volume: 30, anno: 1998,
pagine: 2657 - 2668
SICI:
0022-2828(199812)30:12<2657:EISOIR>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
MAGNETIC-RESONANCE SPECTROSCOPY; ISCHEMIA-REPERFUSION INJURY; ENDOGENOUS ENDOTHELIN; NITRIC-OXIDE; MYOCARDIAL-INFARCTION; ENERGY-METABOLISM; CARDIAC MYOCYTES; CONTRACTILE FUNCTION; ANESTHETIZED RAT; CA2+ CURRENT;
Keywords:
ischemia/reperfusion injury; rat; endothelins; NMR spectroscopy; coronary circulation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
48
Recensione:
Indirizzi per estratti:
Indirizzo: Neubauer, S Univ Wurzburg, Med Klin, Josef Schneider Str 2, D-97080 Wurzburg, Germany Univ Wurzburg Josef Schneider Str 2 Wurzburg Germany D-97080
Citazione:
M.C.H. de Groot et al., "Endothelin-1 increases susceptibility of isolated rat hearts to ischemia/reperfusion injury by reducing coronary flow", J MOL CEL C, 30(12), 1998, pp. 2657-2668

Abstract

Endothelin-1 (ET-1) is the most potent vasoconstrictor known to date, and it was proposed that this peptide plays a major role in myocardial ischemia/reperfusion injury. ET-1 could increase myocardial susceptibility to ischemia by two mechanisms:via coronary flow reduction and/or via direct, metabolic effects on the heart. In isolated, buffer-perfused rat hearts, function was measured with a leftventricular balloon, and energy metabolism (ATP, phosphocreatine, inorganic phosphate, intracellular pH) was estimated by (NMR)-N-31-spectroscopy. Under constant pressure perfusion, hearts were subjected to 15 min of controlperfusion, 15 ("moderate injury") or 30 ("severe injury") min of global ischemia, followed by 30 min of reperfusion. Hearts were pre-treated with ET-1 (boluses of 0, 0.4, 4, 40 of 400 pmol) 5 min prior to ischemia. In the control period, ET-1 reduced coronary flow ventricular function, phosphocreatine and intracellular pH dose-dependently; during ischemia/reperfusion, coronary now, functional recovery and high-energy phosphate metabolism were adversely affected by ET-1 in a dose-related manner. To study effects of ET-1 not related to coronary now reduction, additional hearts were perfused under constant flow conditions (ET-1 0 or 400 pmol) during 15 min ofcontrol, 15 min of ischemia and 30 min of reperfusion. When coronary flow was held constant, functional and energetic parameters were similar for untreated and ET-1 treated hearts during the entire protocol, i.e, the adverseeffects of ET-1 on function and energy metabolism during ischemia/reperfusion were completely abolished. In both constant pressure and constant flow protocols, 400 pmol ET-1 reduced the extent of ischemic intracellular acidosis, The authors conclude that ET-1 increases the susceptibility of isolated hearts to ischemia/reperfusion injury via reduction of coronary flow. (C)1998 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/09/20 alle ore 01:00:49