维拉帕米对离体兔心全心缺血诱导的传导延迟和钾外流的影响。

Effects of verapamil on conduction delay and potassium efflux induced by global ischemia in isolated rabbit hearts.

作者信息

Nakaya H, Kanno M

出版信息

Eur J Pharmacol. 1982 Apr 23;79(3-4):185-92. doi: 10.1016/0014-2999(82)90624-0.

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 concentrations (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.

摘要

在40个经Langendorff法离体灌注的兔心脏上，在心室持续起搏条件下，评估了维拉帕米对整体缺血诱导的传导延迟和钾外流的影响。通过停止灌注血流产生持续7分钟的整体缺血，在10个未处理的对照心脏中，心肌内传导时间比缺血前值延长了86.5±9.6%。在整体缺血前，将不同浓度（10 - 1000 ng/ml）的维拉帕米在台氏液中灌注15分钟，可显著且呈浓度依赖性地减少缺血诱导的传导延迟。然而，缺血期间及再灌注后1分钟收集的冠脉流出液中增加的钾含量（假定其反映了缺血期间细胞外积聚的钾），并未被维拉帕米显著降低。这些结果表明，维拉帕米对缺血诱导的传导延迟的有益作用是对缺血心肌细胞的直接作用，与其血管舒张作用无关。它似乎也不太可能通过减少缺血心肌细胞外钾的积聚来介导。