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Titolo:
MECHANISMS OF PH(I) RECOVERY AFTER GLOBAL-ISCHEMIA IN THE PERFUSED HEART
Autore:
VANDENBERG JI; METCALFE JC; GRACE AA;
Indirizzi:
UNIV CAMBRIDGE,DEPT BIOCHEM,TENNIS COURT RD CAMBRIDGE CB2 1QW ENGLAND
Titolo Testata:
Circulation research
fascicolo: 5, volume: 72, anno: 1993,
pagine: 993 - 1003
SICI:
0009-7330(1993)72:5<993:MOPRAG>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
NUCLEAR MAGNETIC-RESONANCE; MYOCARDIAL-ISCHEMIA; CONTRACTILE FAILURE; INTRACELLULAR PH; FERRET HEART; EXCHANGE; TRANSPORT; ERYTHROCYTES; INHIBITION; AMILORIDE;
Keywords:
PH(I); ISCHEMIA; REPERFUSION; NUCLEAR MAGNETIC RESONANCE SPECTROSCOPY;
Tipo documento:
Article
Natura:
Periodico
Citazioni:
48
Recensione:
Indirizzi per estratti:
Citazione:
J.I. Vandenberg et al., "MECHANISMS OF PH(I) RECOVERY AFTER GLOBAL-ISCHEMIA IN THE PERFUSED HEART", Circulation research, 72(5), 1993, pp. 993-1003

Abstract

A Na+-HCO3- coinflux carrier and the Na+-H+ antiport have both been shown to contribute to recovery from intracellular acidosis in cardiac tissue. We have investigated the participation of these mechanisms as well as metabolite (lactate and CO2) washout in the recovery of pH(i) after myocardial ischemia. Isovolumic ferret hearts were Langendorff-perfused with either HCO3--buffered or nominally HCO3--free (HEPES-buffered) medium at 30-degrees-C. pH(i) was estimated from the chemical shift of the P-31-nuclear magnetic resonance signal of intracellular PO4-, and net H+ efflux rates were calculated at pH(i) 6.80. The H+ efflux rate during reperfusion, after 10 minutes of global ischemia, was 15.5+/-1.9 mmol.l-1.min-1 (n=10) in hearts perfused with HCO3--buffered medium and 8.2+/-1.5 mmol.l-1.min-1 (n=9, p<0.01) in hearts perfused with HEPES-buffered medium. HCO3- influx, assessed either by inhibitionby 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (20 muM) or by initially perfusing hearts with HEPES-buffered medium but reperfusing with HCO3--buffered medium, accounted for 3.5-4.9 mmol.l-1.min-1, and CO2 efflux accounted for 3.8-6.2 mmol.l-1.min-1 of the additional H+ efflux in HCO3--buffered medium. H+-coupled lactate efflux, measured by NAD+-linked spectrophotometric assay and inhibited by the sarcolemmal monocarboxylate transport inhibitor 4,4'-dibenzamidostilbene-2,2'-disulfonate (0.25 mM), contributed 3.7-6.2 mmol.l-1.min-1. H+ efflux via the 5-(N-ethyl-N-isopropyl)amiloride-sensitive Na+-H+ antiport was 1.0-2.9 mmol.l-1.min-1. pH(i) recovery after ischemia is therefore principally mediated by metabolite (lactate and CO2) washout. Na+-coupled acidextrusion contributed approximately 35% of total H+ efflux in this system. However, the associated Na+ entry (almost-equal-to 5 mmol.l-1.min-1) may contribute to Ca2+ overload after reperfusion.

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Documento generato il 01/12/20 alle ore 10:58:19