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Titolo:
ACUTE SIMULATED ISCHEMIA PRODUCES BOTH INHIBITION AND ACTIVATION OF K+ CURRENTS IN ISOLATED VENTRICULAR MYOCYTES
Autore:
HENRY P; POPESCU A; PUCEAT M; HINESCU ME; ESCANDE D;
Indirizzi:
HOP BROUSSAIS,DEPT CARDIOL F-75014 PARIS FRANCE HOP BROUSSAIS,DEPT CARDIOL F-75014 PARIS FRANCE HOP G&R LAENNEC,LAB PHYSIOPATHOL & PHARMACOL CELLULAIRES & MOL F-44035 NANTES FRANCE HOP ARNAUD VILLENEUVE,INSERM CJF 961 F-34295 MONTPELLIER FRANCE
Titolo Testata:
Cardiovascular Research
fascicolo: 5, volume: 32, anno: 1996,
pagine: 930 - 939
SICI:
0008-6363(1996)32:5<930:ASIPBI>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
GUINEA-PIG; CARDIAC-CELLS; INTRACELLULAR PROTONS; METABOLIC INHIBITION; MYOCARDIAL-ISCHEMIA; CONTRACTILE FAILURE; POTASSIUM CHANNELS; OUTWARD CURRENT; ATP; MEMBRANE;
Keywords:
MYOCARDIAL ISCHEMIA; PH, INTRACELLULAR; PATCH-CLAMP; POTASSIUM FLUXES; PRECONDITIONING; RAT, VENTRICULAR MYOCYTES; POTASSIUM CHANNELS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
36
Recensione:
Indirizzi per estratti:
Citazione:
P. Henry et al., "ACUTE SIMULATED ISCHEMIA PRODUCES BOTH INHIBITION AND ACTIVATION OF K+ CURRENTS IN ISOLATED VENTRICULAR MYOCYTES", Cardiovascular Research, 32(5), 1996, pp. 930-939

Abstract

Objective: The aim was to investigate the effects of acute ischaemia on cardiac repolarizing K+ currents. Methods: We developed a model of acute ischaemia in isolated rat ventricular myocytes transiently surrounded with a mineral oil droplet. During ischaemic challenges, we recorded intracellular pH using the fluorescent probe seminaphthorhodafluor-1 (SNARF-1) and whole-cell K+ currents using the patch-damp technique. Results: Decrease in intracellular pH (pH(i)) during simulated ischaemia was dependent upon the extracellular proton buffer used (pH, decreased from 7.44 +/- 0.02 to 7.16 +/- 0.04 in a Hepes-buffered medium and from 7.08 +/- 0.04 to 6.56 +/- 0.07 with bicarbonate buffer). In Hepes, action potential duration initially lengthened and then shortened under the effects of ischaemia. Initial action potential duration lengthening was concomitant with a block of the inward rectifier K+ current, whereas late shortening corresponded with the activation of the ATP-sensitive K+ current. Similar changes occurred in bicarbonate buffer although with different amplitudes and kinetics. Patch-clamp experiments also showed inhibition of the transient outward K+ current. Brieftransient episodes of ischaemia activated ATP-sensitive K+ current inonly 20% of control cells (n = 21) but in 100% of cells treated with 15 mu M cromakalim (n = 9). Conclusions: (i) Simulated ischaemia produces complex effects on repolarizing K+ currents including both inhibition and activation; (ii) cromakalim accelerates activation of ATP-sensitive K+ current during simulated ischaemia.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 20:05:52