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Titolo:
HOE-642 (cariporide) alters pH(i) and diastolic function after ischemia during reperfusion in pig hearts in situ
Autore:
Portman, MA; Panos, AL; Xiao, Y; Anderson, DL; Ning, XH;
Indirizzi:
Childrens Hosp & Reg Med Ctr, Div Cardiol, Seattle, WA 98105 USA ChildrensHosp & Reg Med Ctr Seattle WA USA 98105 , Seattle, WA 98105 USA Univ Washington, Dept Pediat, Div Cardiol, Seattle, WA 98195 USA Univ Washington Seattle WA USA 98195 , Div Cardiol, Seattle, WA 98195 USA Univ Washington, Dept Surg, Div Cardiothorac Surg, Seattle, WA 98195 USA Univ Washington Seattle WA USA 98195 iothorac Surg, Seattle, WA 98195 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
fascicolo: 2, volume: 280, anno: 2001,
pagine: H830 - H834
SICI:
0363-6135(200102)280:2<H830:H(APAD>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
NA+-H+ EXCHANGE; PORCINE HEART; RAT HEARTS; INHIBITOR; SODIUM; REOXYGENATION; ARRHYTHMIAS; PROTECTION; METABOLISM; OVERLOAD;
Keywords:
magnetic resonance spectroscopy; metabolism; phosphates; intracellular pH;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
21
Recensione:
Indirizzi per estratti:
Indirizzo: Portman, MA Childrens Hosp & Reg Med Ctr, Div Cardiol, CH11, Seattle, WA 98105 USA Childrens Hosp & Reg Med Ctr CH11 Seattle WA USA 98105 105 USA
Citazione:
M.A. Portman et al., "HOE-642 (cariporide) alters pH(i) and diastolic function after ischemia during reperfusion in pig hearts in situ", AM J P-HEAR, 280(2), 2001, pp. H830-H834

Abstract

The specific Na+/H+ exchange inhibitor HOE-642 prevents ischemic and reperfusion injury in the myocardium. Although this inhibitor alters H+ ion fluxduring reperfusion in vitro, this action has not been confirmed during complex conditions in situ. Myocardial intracellular pH (pH(i)) and high-energy phosphates were monitored using P-31 magnetic resonance spectroscopy in open-chest pigs supported by cardiopulmonary bypass during 10 min of ischemia and reperfusion. Intravenous HOE-642 (2 mg/kg; n = 8) administered beforeischemia prevented the increases in diastolic stiffness noted in control pigs (n = 8), although it did not alter the postischemic peak-elastance or pressure-rate product measured using a distensible balloon within the left ventricle. HOE-642 induced no change in pHi during ischemia but caused significant delays in intracellular realkalinization during reperfusion. HOE-642did not alter phosphocreatine depletion and repletion but did improve ATP preservation. Na+/H+ exchange inhibition through HOE-642 delays intracellular alkalinization in the myocardium in situ during reperfusion in association with improved diastolic function and high-energy phosphate preservation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/01/20 alle ore 12:02:01