ACTION OF QUINIDINE, PROCAINE AMIDE AND OTHER COMPOUNDS ON EXPERIMENTAL ATRIAL AND VENTRICULAR ARRHYTHMIAS IN THE DOG

¹ Division of Biological Research, G. D. Searle & Co., Chicago 80, Illinois

The action of quinidine, procaine amide and five SC-compounds on experimental atrial and ventricular arrhythmias was investigated. The SC-compounds are hydrochlorides of the following bases: SC-3920,N-(-isopropylaminopropyl)- ,-diphenylacetamide; SC-3323, -diisopropylaminoethyl-4-phenyl-4- tetrahydropyrancarboxylate; SC-3755, o-(4-chlorobenzyl)phenoxyacetamidine; SC-2919, N,N,N'-triphenyl-N'-(-diethylaminoethyl)urea; and SC-3412, -diethylaminoethyl-2, 6-dimethyl-5, 6-dihydro-4H-pyran-3-carboxylate. Atrial flutter was produced in dogs by injury and electrical stimulation of the atrium; atrial fibrillation was produced by direct application of aconitine. Ventricular arrhythmias were studied in unanesthetized dogs twenty-four hours after a two-step coronary ligation.

The activity spectrum of the compounds differed and the compounds could be classified as follows: (a) active on atrial and ventricular arrhythmias (quinidine, procaine amide, SC-3920, SC-2919 and SC-3412; (b) active primarily on the atrium (SC-3323); and (c) active primarily on the ventricle (SC-3755). All of the compounds increased the “effective refractory period” of the isolated papillary muscle.