The effects of N-acetyl procainamide (NAPA) was studied on isolated canine cardiac tissues by using standard microelectrode techniques. NAPA (10-40 mg/l) does not suppress the rate of phase 4 depolarization of Purkinje fibers and does not change resting membrane potential, action potential amplitude or maximum upstroke velocity of phase O of the action potentials of Purkinje fibers or ventricular muscle cells. Action potential duration of both types of cells is significantly prolonged by NAPA in a dose-dependent manner. In toxic concentrations (80-240 mg/l), NAPA can produce a secondary plateau at about -55 mV during phase 3 of the action potential of Purkinje fibers driven at cycle lengths of 2000-4000 ms. Early afterdepolarizations and single or multiple spontaneous action potentials were often triggered during the secondary plateau. When NAPA is given to conscious or anesthetized dogs (50-100 mg/kg i.v.), ventricular extrasystoles occur at constant coupling intervals if the basic rate of ventricular activation is slow (60/min or slower). Single extrasystoles or the 1st extrasystole in a salvo, appear at coupling intervals of 400-600 ms. The single and multiple extrasystoles induced by NAPA may be caused by action potentials triggered during the secondary plateau and may degenerate into ventricular fibrillation. In doses of up to 100 mg/kg i.v., NAPA exerts slight antiarrhythmic effects in dogs with 24 h myocardial infarcts.