Effects of procainamide on automatic and triggered impulse initiation in isolated preparations of canine cardiac Purkinje fibers.

The effects of procainamide (40 mg/L) were studied on automatic and triggered impulse initiation in isolated preparations of canine cardiac Purkinje fibers using standard microelectrode techniques. Procainamide decreased normal automaticity by 48% in Purkinje fibers superfused with standard (KCl 4 mM) Tyrode's solution. In contrast, procainamide decreased the rate of normal Purkinje fibers that had been treated with isoproterenol (1 microM) by only 6% (NS). For comparison, the effects of lidocaine (4 mg/L) and quinidine (5 mg/L) were studied on isoproterenol-treated fibers. Lidocaine and quinidine both significantly decreased the isoproterenol-enhanced rate of normal automaticity (by 45 and 10%, respectively). In studies of the effects of procainamide on Purkinje fibers with abnormal automaticity (i.e., the pacemakers had maximal diastolic potentials less than -60 mV), it was found that drug treatment decreased the rate of 24 h infarct zone Purkinje fibers by 22% and barium chloride (250 microM) treated Purkinje fibers by 51%. In studies of another five infarct zone preparations, the Purkinje fibers had maximal diastolic potentials greater than -75 mV and showed triggered activity with delayed afterdepolarizations. Procainamide decreased the triggered activity in only one of these preparations. Ventricular tachycardias that respond to procainamide may be caused by abnormal automaticity, whereas procainamide refractory tachycardias may result from triggered activity or from catecholamine-enhanced normal automaticity.