Electrophysiologic and Antiarrhythmic Actions of Pirmenol on Rabbit and Guinea Pig Cardiac Preparations

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Abstract
The electrophysiological and antiarrhythmic effects of pirmenol HCl were examined using the microelectrode technique applied to multicellular preparations and the suction-pipette whole-cell clamp method applied to ventricular myocytes from rabbit and guinea pig hearts. Pirmenol at 5 .mu.M and higher doses suppressed the sinus node automaticity by depressing the slow diastolic depolarization without changing the maximum diastolic potential. Pirmenol at 1 .mu.M and higher doses depressed the maximum upstroke velocity (.ovrhdot.Vmax) of action potentials and prolonged the action of potential duration at 90% repolarization in atrial muscles and Purkinje fibers without affecting resting membrane potentials. Pirmenol at 5 .mu.M depressed the early part of the plateau and lengthened the final repolarization of the action potentials of ventricular myocytes, of which effects were attributed to the depression of the calcium current and the delayed outward K+ current. Triggered tachyarrhythmias arising from delayed afterdepolarization in papillary muscles and ventricular myocytes were markedly inhibited by 1-5 .mu.M pirmenol. The drug changed the amplitude and appearance of the transient inward current in ventricular myocytes. These results suggest that pirmenol has electrophysiologic properties that could provide an antiarrhythmic action on various types of arrhythmias.