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July 14, 1951


Author Affiliations

Los Angeles

Fellow of the National Heart Institute (Dr. Miller).; From the Division of Medicine (Cardiology), School of Medicine, University of Southern California, the Los Angeles County Hospital and the Medical Service, Cedars of Lebanon Hospital.

JAMA. 1951;146(11):1004-1007. doi:10.1001/jama.1951.03670110024007

It has been demonstrated that procaine applied locally to the heart reduces cardiac irritability as indicated by the added intensity of stimulation necessary to induce extrasystoles or ventricular fibrillation.1 It has also been shown that after procaine administration a larger dose of epinephrine is required to produce ventricular fibrillation during chloroform anesthesia.2 Since the administration of procaine in man may be followed by untoward reactions, Burstein and others3 studied the effect of less toxic substances chemically related to procaine. They found that several related compounds protected dogs from epinephrine-cyclopropane ventricular fibrillation. Brodie, Lief and Poet4 demonstrated that procaine administered intravenously in man is hydrolyzed rapidly to paraaminobenzoic acid and diethylaminoethanol. Because of the high concentration and relative persistence of diethylaminoethanol in the plasma, Rosenberg and others5 studied the effect of this compound on cardiac arrhythmias. The drug prevented the development of ventricular ectopic beats in