Proarrhythmic effects of aldosterone during myocardial ischemia-reperfusion: implication of the sarcolemmal-KATP channels.

摘要: OBJECTIVE To assess the electrophysiological impact of aldosterone during myocardial ischemia-reperfusion. METHODS We used an in vitro model "border zone" using rabbit right ventricle and standard microelectrodes. RESULTS Aldosterone (10 100 nmol/L) shortened ischemic action potential [action duration at 90% repolarization (APD90), from 55 ± 3 to 39 1 ms 36 ms, respectively, P < 0.05] induced resting membrane (RMP) hyperpolarization nonischemic zone (from -83 -93 7 mV -94 mV, 0.05) reperfusion -81 2 -88 -91 0.05). Bimakalim, ATP-sensitive potassium (K(ATP)) channel opener, also RMP APD90 shortening. increased dispersion between zones 96 117 5 131 6 reperfusion-induced severe premature ventricular contraction occurrence 18% 67% 75%, Adding glibenclamide, a nonspecific K(ATP) antagonist, superfusion abolished these effects different sodium 5-hydroxydecanoate, mitochondrial-K(ATP) antagonist. CONCLUSIONS In this border zone, decreased evoking modulation K currents. Glibenclamide prevented suggesting that sarcolemmal-K(ATP) channels may be involved context.