The termination of auricular fibrillation in dogs with procaine amide hydrochloride

Abstract

Meek, Hathaway, and Orth demonstrated that small amounts of intravenous epinephrine may cause a ventricular fibrillation in dogs given cyclopropane. 1 Burstein and associates, by utilizing this method of investigation, established the effectiveness of procaine and its derivatives, both intravenously and topically, in the termination and prevention of epinephrine-induced ventricular fibrillation and tachycardia. 2,3 In the human being there are several reports on the successful treatment of the ventricular arrhythmias with procaine and its derivatives when used both orally and intravenously. 4–7 These early investigators stressed that the procaines were ineffectual in the therapy of arrhythmias of auricular origin. However, Schaffer and associates have shown that procaine will slow the “F” waves in auricular flutter and that procaine amide will terminate the auricular arrhythmias in the human being. 8,9 Burstein reported one case of auricular tachycardia and one of atrioventricular nodal tachycardia occurring during cardiac surgery which he believed were reverted to normal sinus rhythm by the intravenous injection of procaine. 4 Beck and Mautz were able to terminate auricular fibrillation by applying procaine directly to the auricles. 10 Rosenberg and co-workers have shown that ethylaminoethanol, a metabolized product of procaine, is more effective and less toxic in the treatment of the ventricular arrhythmias although larger doses are required. 5 It is the purpose of this communication to demonstrate the successful termination of drug-induced auricular fibrillation in dogs by both the intravenous injection and local topical application of p-amino-N-(2-diethylaminoethyl) benzamide hydrochloride. ∗ ∗ Pronestyl was kindly supplied by Dr. L. B. Hobson of E. R. Squibb & Sons, New York, N. Y.