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Titolo:
Changes in intracellular Na+ and pH in rat heart during ischemia: role of Na+/H+ exchanger
Autore:
Park, CO; Xiao, XH; Allen, DG;
Indirizzi:
Univ Sydney F13, Inst Biomed Res, Sydney, NSW 2006, Australia Univ Sydney F13 Sydney NSW Australia 2006 es, Sydney, NSW 2006, Australia Univ Sydney F13, Dept Physiol, Sydney, NSW 2006, Australia Univ Sydney F13 Sydney NSW Australia 2006 ol, Sydney, NSW 2006, Australia
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
fascicolo: 5, volume: 45, anno: 1999,
pagine: H1581 - H1590
SICI:
0363-6135(199905)45:5<H1581:CIINAP>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
FREE CALCIUM-CONCENTRATION; CARDIAC PURKINJE-FIBER; ISOLATED FERRET HEARTS; CYTOSOLIC FREE CALCIUM; H+ EXCHANGE; CONTRACTILE FAILURE; MYOCARDIAL-ISCHEMIA; GLOBAL-ISCHEMIA; CA-2+ OVERLOAD; SODIUM;
Keywords:
ischemia-reperfusion; methylisobutyl amiloride;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Park, CO Univ Sydney F13, Inst Biomed Res, Sydney, NSW 2006, Australia Univ Sydney F13 Sydney NSW Australia 2006 y, NSW 2006, Australia
Citazione:
C.O. Park et al., "Changes in intracellular Na+ and pH in rat heart during ischemia: role of Na+/H+ exchanger", AM J P-HEAR, 45(5), 1999, pp. H1581-H1590

Abstract

The role of the Na+/H+ exchanger in rat hearts during ischemia and reperfusion was investigated by measurements of intracellular Na+ concentration ([Na+](i)) and intracellular and extracellular pH. Under our standard conditions (2-Hz stimulation), 10 min of ischemia caused no significant rise in [Na+](i) but an acidosis of 1.0 pH unit, suggesting that the Na+/H+ exchangerwas inactive during ischemia. This was confirmed by showing that the Na+/H exchange inhibitor methylisobutyl amiloride (MIA) had no effect on [Na+](i) or on intracellular pH during ischemia. However, there was a short-livedincrease in [Na+](i) of 8.2 +/- 0.6 mM on reperfusion, which was reduced by MIA, showing that the Na+/H+ exchanger became active on reperfusion. To investigate the role of metabolic changes, we measured [Na+](i) during anoxia. The [Na+](i) did not change during 10 min of anoxia, but there was a small, transient rise of [Na+](i) on reoxygenation, which was inhibited by MIA. In addition, we show that the Na+/H+ exchanger, tested by sodium lactate exposure, was inhibited during anoxia. These results show that the Na+/H+ exchanger is inhibited during ischemia and anoxia, probably by an intracellular metabolic mechanism. The exchanger activates rapidly on reperfusion andcan cause a rapid rise in [Na+](i).

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 18:56:53