Experiments on anesthetized cats and rats showed that 2-mercaptobenzimidazole derivatives, known as SM-266 and SM-345, induced marked and long-term bradycardia, increased the stroke output, and reduced the requirements of the heart of oxygen. The drugs had practically no effect on systemic arterial pressure, cardiac output, and heart contractility. Studies on isolated frog venous sinuses disclosed that bradycardia induced by the drugs under study was related to the decrease caused by them in the velocity of slow diastolic depolarization directly in the pacemaker cells on the sinus node. On grounds of the obtained results it is concluded that the drugs under study may be related to a new group of specific bradycardiac agents.

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