[Mechanism of actions involved in improved effects of calcium channel blockers on ischemic myocardial conduction delay].

The effects of calcium channel blockers and lidocaine on changes in action potential characteristics and conduction time during exposure to altered Tyrode's solution imitating some of metabolic alterations that occur in acute myocardial ischemia (pO2 less than 50 mmHg, KCl 8 mM, pH 6.80) were examined in the isolated right ventricular epicardium of canine heart. The superfusion with altered Tyrode's solution produced loss of resting membrane potential (RMP), action potential amplitude (APA), action potential duration (APD), 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 of the prolongation of CT. On the other hand, in the presence of either verapamil (1 mg/l), diltiazem (3 mg/l), nifedipine (1 mg/l), or Ni2+ (1 mM), the degree of the reductions of APA and Vmax and of the prolongation of CT induced by altered Tyrode's solution was reduced. However, neither lidocaine nor calcium channel blockers affected change in RMP. These results suggest that decreasing calcium influx during ischemia improves depressed sodium channel, and this effect can partly explain the improvement of ischemia-induced conduction delay by calcium channel blockers.