Effects of verapamil and lidocaine on changes in action potential characteristics and conduction time induced by combined hypoxia, hyperkalemia, and acidosis in canine ventricular myocardium.

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We examined the effects of verapamil and lidocaine on changes in action potential characteristics and conduction time in the isolated right ventricular myocardium of canine hearts during superfusion with altered Tyrode's solution imitating some of metabolic alterations that occur in acute myocardial ischemia (Po2 less than 50 mm Hg, KCl 8 mM, pH 6.80). Altered Tyrode's solution produced loss of resting membrane potential (RMP), action potential amplitude (APA), action potential duration, and upstroke velocity of action potential (Vmax), and prolonged conduction time (CT). In the presence of lidocaine (5 mg/L), altered Tyrode's solution aggravated the reductions of APA and Vmax and the prolongation of CT in both endocardial and epicardial muscle cells. On the other hand, in the presence of verapamil (1 mg/L), the degree of the reductions of APA and Vmax and of the prolongation of CT induced by altered Tyrode's solution was reduced in epicardial muscle cells, but not in endocardial ones. Neither verapamil nor lidocaine affected change in RMP. These results suggest that the improving effect of verapamil on ischemia-induced conduction delay can be partly explained by its salutary effect on the depressed fast channel.