The electrophysiologic effects of ethmozin on canine myocardium were studied in anesthetized open-chest animals and in superfused Purkinje fibers. On selective injection into the sinus node artery and the posterior septal artery the drug caused no changes in the sinus node length and atrioventricular conduction, respectively. Intravenous infusion of 4 mg/kg ethmozin led to an increase of right and left ventricular diastolic excitability threshold and refractory period. Intravenous administration of 3--5 mg/kg ethmozin caused marked increase in conduction delay in which the ischemic zone of the left ventricle during acute coronary artery occlusion, which was associated with ventricular fibrillation in 50% of the dogs. In vitro, 1 x 10(-6) g/ml ethmozin shortened the Purkinje fibers' action potential duration whereas a dose of 1 x 10(-5) g/ml reduced the rate of phase 0 rise and slightly reduced the action potential amplitude. Ethmozin in a dose of 1 x 10(-7) g/ml increased transiently the isometric developed tension of false-tendon preparations. Higher concentrations caused marked depression of contractility. These observations suggest depression of the fast current by ethmozin. However, further studies are needed to elucidate its effect on action potential duration and false-tendor contractility.