Abstract

Abstract The effects of verapamil on the conduction delay and potassium efflux induced by global ischemia were evaluated in 40 isolated Langendorff-perfused rabbit hearts under constant ventricular pacing. Global ischemia of 7 min duration, which was produced by stopping the perfusion flow, prolonged the intramyocardial conduction time by 86.5 ± 9.6% of the pre-ischemic values in 10 non-treated control hearts. Verapamil, when perfused in various concentratiins (10–1000 ng/ml) in Tyrode solution for 15 min prior to the global ischemia, significantly and concentration-dependently reduced the ischemia-induced conduction delay. However, the increased potassium content of the coronary effluents collected during ischemia and 1 min after reperfusion, which was assumed to reflect the extracellularly accumulated potassium during ischemia, was not significantly reduced by verapamil. These results suggest that the favorable effect of verapamil on the ischemia-induced conduction delay is a direct action on the ischemic myocardial cells, being independent of its vasodilating action. It also seems unlikely to be mediated by reduction of extracellular potassium accumulation in the ischemic myocardium.

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