Antiarrhythmic-like actions of the smooth muscle spasmolytic agent, cinnamedrine, on action potentials of mammalian ventricular tissue.

Abstract

Cinnamedrine is an active ingredient in preparations used to relieve dysmenorrhea. It has been reported to have local anesthetic properties in nerve. This property prompted us to evaluate the effects of cinnamedrine on the cardiac action potential. Cinnamedrine (10-35 microM) significantly reduced the overshoot and maximum rate of rise, and also prolonged the duration of action potentials recorded from rat and guinea pig ventricular tissues. The action of cinnamedrine to depress upstroke velocity in guinea pig papillary muscle was dependent on the rate of stimulation. In addition, the refractory period of rat ventricular muscle was prolonged markedly. Finally, cinnamedrine (10 microM) significantly reduced, or totally abolished, epinephrine-induced automatic activity in both dog and rat myocardium in vitro. Prolongation of action potential duration and refractory period, and depression of upstroke velocity are characteristics which cinnamedrine shares with antiarrhythmic drugs.