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Journal of Pharmacology And Experimental Therapeutics, Vol. 164, Issue 2, 326-332, 1968
Copyright © 1968 by American Society for Pharmacology and Experimental Therapeutics

PREVENTION OF VENTRICULAR FIBRILLATION INDUCED BY CORONARY LIGATION

A. J. KAUMANN 1 and P. ARAMENDIA 2

1 Centro de Investigaciones Cardiológicas, Universidad de Buenos Aires, Buenos Aires, Argentina
2 Centro de Investigaciones Cardiolgicas, Universidad de Buenos Aires, Buenos Aires, Argentina

Ligation of the left descending coronary artery at its origin produced ventricular fibrillation in anesthetized dogs. This situation held true in untreated controls (10 dogs of 11 died between 0.8 and 19 mm after the ligature), reserpine-treated dogs (five of five) or animals pretreated with 0.5 mg/kg i.v. of 4-(2-isopropylamino-1-hydroxyethyl) methanesulfonanilide hydrochloride (MJ 1999) (five of five). On the other hand, i.v. administration of 10 mg/kg of MJ 1999 or 0.79 mg/kg of iproveratril 10 min before the coronary ligation prevented ventricular fibrillation whether or not the animals had been pretreated with reserpine. Neither macroscopic examination of the heart nor the electrocardiogram infarction pattern showed differences between control experiments and experiments with MJ 1999 and iproveratril. Dogs injected with iproveratril survived more than 10 months. Animals pretreated with 10 mg/kg i.v. of MJ 1999 died within 24 hr after coronary ligation (except one dog that lived several months). The evidence supports the conclusion that the incidence of ventricular fibrillation induced by coronary occlusion is not related to the content of norepinephrine of the heart. Furthermore, the ability of these compounds to prevent ventricular fibrillation does not depend on a beta adrenergic blocking action.

Submitted on February 1, 1968
Accepted on August 16, 1968




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Copyright © 1968 by the American Society for Pharmacology and Experimental Therapeutics.