Shortening of monophasic action potential duration during hyperkalemia and myocardial ischemia in anesthetized dogs.
The elevation of the myocardial extracellular potassium concentration ([K+]o) is known to shorten action potential duration, which may lead to the occurrence of arrhythmias. The aim of this study was to compare the mechanisms responsible for the shortening of monophasic action potential duration (MAPD) in hyperkalemic and myocardial ischemic hearts in anesthetized dogs. During a venous infusion of KCl for 5 min, [K+]o was increased and MAPD was significantly shortened. The ATP-sensitive K+ (K[ATP]) channel blocker glibenclamide did not affect the shortening of MAPD during KCl-infusion, indicating that K(ATP) channels are not involved in this mechanism. During 5-min occlusion of the left anterior descending coronary artery, [K+]o was increased, myocardial pH was decreased and MAPD was shortened. Glibenclamide completely abolished the shortening of MAPD, while partial elevation of [K+]o remained even in the presence of glibenclamide. This suggests that the shortening of MAPD is dependent mainly on the activation of K(ATP) channels. Both models in the present study demonstrate that different types of potassium channels are involved in the regulation of action potential duration.
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