A comparison of the effects of bethanidine, meobentine and quinidine on the electrical activity of rat hearts in vivo and in vitro.

Glass microelectrodes were used to record transmembrane electrical activity from cells located just beneath the endocardial surface of segments of the right ventricular free wall of the rat heart during superfusion and electrical stimulation in vitro at 37 degrees C. The sulphates of bethanidine, meobentine or quinidine (4 to 20 microM) applied in vitro caused a prolongation of action potential duration and a delayed and slowed return of electrical excitability following an action potential. Intracardiac electrical stimulation of the urethane-anaesthetized rat heart in situ was used to measure ventricular refractory periods from the electrocardiogram. Intravenous administration of bethanidine, meobentine or quinidine (10 to 20 mg kg-1) caused a prolongation of ventricular refractory periods. Quinidine had a briefer duration of action than either of the other two drugs tested. Urethane-anaesthetized open-chested rats which were subjected to left coronary artery occlusion displayed ventricular tachyarrhythmias in their electrocardiogram. These arrhythmias occurred during the period of occlusion and even more prominently after release of the occlusion. Intravenous administration of bethanidine, meobentine or quinidine (1 to 20 mg kg-1) protected rats against these arrhythmias. The protective effect of quinidine was briefer than that of either of the other two drugs tested.