Abstract
Abstract
While many antiarrhythmic drugs depress myocardial function, N-acetylprocainamide, the major metabolite of procainamide, appears to improve myocardial performance in vivo. The present study compared the effect of procainamide with N-acetylprocainamide on the isolated, perfused, globally ischemic rabbit heart. Procainamide depressed dPldt at infusion rates of 2 mg/min or greater. N-Acetylprocainamide depressed dP/dt at infusion rates of 40 mg/min or greater and may have increased dP/dt at low rates of around 1 mg/min. Pretreatment of the rabbits with reserpine abolished any increase in dPldt produced by N-acetylprocainamide. We conclude that N-acetylprocainamide does not have intrinsic direct positive inotropic activity in this model.
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