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  • Title: Effects of therapeutic concentrations of procainamide on transmembrane action potentials of normal and infarct zone Purkinje fibers and ventricular muscle cells.
    Author: Dangman KH, Miura DS.
    Journal: J Cardiovasc Pharmacol; 1989 Jun; 13(6):846-52. PubMed ID: 2484078.
    Abstract:
    Procainamide is a class I antiarrhythmic drug. Most studies of the cellular electrophysiologic effects of procainamide have been done with concentrations well above the therapeutic range. We studied the effects of therapeutic concentrations (10 mg/L) of the drug on transmembrane action potentials recorded from isolated canine cardiac tissues. In normal false tendon Purkinje fibers with maximal diastolic potentials (MDPs) of -93 +/- 1 mV, procainamide decreased action potential duration (APD)-20mV and slightly prolonged APD100%. The dV/dtmax was not decreased. In normal subendocardial Purkinje fibers with MDPs of -92 +/- 1 mV, procainamide 10 mg/L significantly decreased dV/dtmax but did not affect APD-20mV. In normal muscle cells from left ventricular endocardium, procainamide 10 mg/L increased only APD100%. The effects of procainamide on partially depolarized Purkinje fibers varied. In normal subendocardial Purkinje fiber preparations superfused with 7.5 mM KCl-Tyrode's solution, the mean maximal diastolic potentials were -73 +/- 2 mV, and procainamide 10 mg/L slightly decreased action potential amplitude (APA) and increased APD-60mV. In contrast, in 24-h infarct zone Purkinje fibers with MDPs of -75 +/- 4 mV, procainamide 10 mg/L decreased APA and dV/dtmax and prolonged APD100%. In one experiment on an infarct preparation, procainamide also induced 2:1 block at cycle lengths shorter than approximately 400 ms. The results of these experiments indicate that therapeutic concentrations of procainamide exert selective effects on action potentials in partially depolarized zones of infarcted hearts. This action may explain why procainamide can abolish some reentrant arrhythmias.
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