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Titolo:
Enalaprilat attenuates ischemic rises in intracellular sodium in the isolated rat heart via the bradykinin receptor
Autore:
Whang, J; Ramasamy, R; Dizon, JM; Bergmann, SR;
Indirizzi:
Inst Heart & Vasc, MAC, Morristown, NJ 07960 USA Inst Heart & Vasc Morristown NJ USA 07960 , MAC, Morristown, NJ 07960 USA Columbia Univ Coll Phys & Surg, Div Cardiol, New York, NY 10032 USA Columbia Univ Coll Phys & Surg New York NY USA 10032 w York, NY 10032 USA
Titolo Testata:
JOURNAL OF CARDIOVASCULAR MAGNETIC RESONANCE
fascicolo: 1, volume: 3, anno: 2001,
pagine: 27 - 34
SICI:
1097-6647(2001)3:1<27:EAIRII>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
CONVERTING ENZYME-INHIBITION; NA+-H+ EXCHANGE; VENTRICULAR-FIBRILLATION; POSTISCHEMIC RECOVERY; MYOCARDIAL-INFARCTION; MAGNETIC-RESONANCE; CA-2+ OVERLOAD; RABBIT HEART; REPERFUSION; CALCIUM;
Keywords:
ACE inhibitors; experimental; heart; ischemia; NMR; reperfusion;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
27
Recensione:
Indirizzi per estratti:
Indirizzo: Whang, J Inst Heart & Vasc, MAC, 299 Madison Ave, Morristown, NJ 07960 USAInst Heart & Vasc 299 Madison Ave Morristown NJ USA 07960 960 USA
Citazione:
J. Whang et al., "Enalaprilat attenuates ischemic rises in intracellular sodium in the isolated rat heart via the bradykinin receptor", J CARD M RE, 3(1), 2001, pp. 27-34

Abstract

Purpose: Angiotensin-converting enzyme (ACE) inhibitors have been shown tohave beneficial effects on ischemic myocardium. We examined whether rite ACE inhibitor: enalaprilat (EN), improves intracellular sodium homeostasis during myocardial ischemia and the relationship of this effect to bradykinin. Methods: EN (3.2 nM) was administered to isolated rat hearts that were subjected to ischemia and reperfusion. Intracellular sodium and pH were monitored using magnetic resonance spectroscopy? (MRS). The specific bradykinin B2 receptor antagonist, HOE 140 (10 nM), was administered with EN in some hearts to determine the effects of bradykinin blockade on EN-mediated effects. Results: EN blunted the rise in ischemic intracellular sodium, measured using MRS. With reperfusion, EN-treated hearts recovered 80% of their preischemic ventricular function, compared with negligible recovery in controls. These beneficial effects of EN were blocked when the bradykinin receptor antagonist, HOE 140, was coadministered with EN. HOE 140 also blocked EN-mediated attenuation of ischemic intracellular acidosis. Conclusions: These results suggest that EN exerts beneficial effects on ischemic intracellular sodium and pH homeostasis via the bradykinin receptor These effects of EN may provide a mechanism for the beneficial actions of this agent during isc hemin.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/01/20 alle ore 06:30:34