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• W2087686988 startingPage "930" @default.
• W2087686988 abstract "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-clamp technique. Results: Decrease in intracellular pH (pHi) during simulated ischaemia was dependent upon the extracellular proton buffer used (pHi 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. Brief transient episodes of ischaemia activated ATP-sensitive K+ current in only 20% of control cells (n = 21) but in 100% of cells treated with 15 μM 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." @default.
• W2087686988 created "2016-06-24" @default.
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• W2087686988 date "1996-11-01" @default.
• W2087686988 modified "2023-10-14" @default.
• W2087686988 title "Acute simulated ischaemia produces both inhibition and activation of K+ currents in isolated ventricular myocytes" @default.
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• W2087686988 doi "https://doi.org/10.1016/s0008-6363(96)00124-1" @default.
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