Abstract
PROCAINE amide hydrochloride (p-amino-N-(2-diethylaminoethyl) benzamide hydrochloride1) has recently been introduced as an effective therapeutic means of controlling ventricular arrhythmias and premature contractions because of its ability to depress the irritability of the ventricular muscle.2 Unlike procaine hydrochloride, procaine amide is only partially, if at all, hydrolyzed by plasma esterase to p-aminobenzoic acid and diethylaminoethanol; hence its effect is more prolonged.1 , 2 It is now being used also in arrhythmias and premature contractions of auricular origin.3 4 5 Thus far, the main toxic effect noted on intravenous administration of the drug is hypotension; toxic effects following its oral use have been described as . . .

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