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
Miller H, Nathanson MH, Griffith GC. THE ACTION OF PROCAINE AMIDE IN CARDIAC ARRHYTHMIAS. JAMA. 1951;146(11):1004–1007. doi:10.1001/jama.1951.03670110024007
Customize your JAMA Network experience by selecting one or more topics from the list below.
Create a personal account or sign in to: