Flecainide acetate is a new antiarrhythmic drug which suppresses different kinds of experimental arrhythmias. We studied the efficacy of flecainide acetate on reperfusion- and barium-induced ventricular tachyarrhythmias in the isolated perfused rat heart by monitoring heart rate, coronary flow rate, left ventricular systolic pressure, dp/dtmax, and the voltage of the epicardial electrogram. Seventy-five male rats were randomized into 5 groups. In group I, after a 15 min period of stabilization, hearts were perfused by ischemic perfusion and then reperfused. In group II, flecainide acetate (10(-6) M) was given after stabilization and before ischaemic perfusion. In group III, barium chloride (10(-3) M) was given after stabilization. In group IV, flecainide acetate was given after stabilization and before barium chloride administration. In group V, acetylcholine chloride (10(-6) M) was given after stabilization and before barium chloride administration. In group I, we noted during ischemia a reduction in heart rate, coronary flow rate, left ventricular systolic pressure and dp/dtmax and an increase in the voltage of the epicardial electrogram. In group II, after administration of flecainide acetate, we observed a reduction in heart rate, left ventricular systolic pressure and dp/dtmax; during the ischaemic period there was no difference in these parameters with respect to group I. Reperfusion induced ventricular arrhythmias in 12 out of 15 hearts in group I and in only 3 out of 15 in group II (p less than 0.005). Barium induced ventricular arrhythmias in the 15 hearts studied in group III as well as in group IV. On the contrary, acetylcholine chloride in group V prevented the occurrence of barium-induced ventricular arrhythmias (p less than 0.005 vs group III and IV). Thus, flecainide acetate is able to reduce reperfusion-induced ventricular arrhythmias, but is unable to reduce barium-induced ventricular arrhythmias, presumably because of a different mechanism of these two types of arrhythmias.