Kotake H, Hirai S, Kinugawa T, Ito T, Yamasaki J, Hasegawa J, Mashiba H
First Department of Internal Medicine, Tottori University, Nishimachi, Japan.
J Electrocardiol. 1988 Nov;21(4):355-9. doi: 10.1016/0022-0736(88)90112-4.
The electrophysiologic effects of pirmenol hydrochloride on rabbit sinoatrial node cells were examined and compared with those of several class I antiarrhythmic agents. At 1 microM, pirmenol decreased the heart rate and the rate of diastolic depolarization and increased the action potential duration at half-amplitude. Above 10 microM, the agent also decreased the maximum rate of rise (Vmax) and the action potential amplitude significantly. The order of the inhibitory potency on Vmax was apridine greater than 711389-S greater than pirmenol greater than mexiletine greater than tocainide. With respect to the current systems, pirmenol decreased the slow inward current (Isi) and the time-dependent potassium outward current (IK). The agent also prolonged the recovery time constant of Isi without any changes in the decay process of the tail current (IK). These findings suggest that pirmenol depresses the spontaneous discharge of the sinoatrial node through a decrease in Isi and Ik.
