The electrophysiological actions of lidocaine on ischemic ventricular muscle as compared with procainamide.

For the purpose to evaluate the effects of lidocaine on the ventricular arrhythmias occurring as complications of acute myocardial ischemia or infarction, the electrophysiological actions of lidocaine were estimated, as compared with those of procainamide, on the right ventricular papillary muscle of the rabbit heart superfused with hypoxic, hyperkalemic and/or acidic Krebs-Ringer solution. Lidocaine (1 to 5 x 10(-5)M) and procainamide (1.7 to 3.4 x 10(-5)M) depressed the maximum rate of action potential upstroke (Vmax) and prolonged both of the effective refractory period (ERP) and the diastolic interval needed for the premature Vmax to recover to 98% in magnitude of the basic Vmax (98% recovery time) dose-dependently, without decreasing the resting potential. Among the ischemic components, low pH (pH 6.9) and high potassium (10 mM) extracellular environments potentiated the depressant actions of lidocaine in synergic manner, but no significant enhancement of the actions of procainamide were observed under exposure to any components of ischemia. Mechanisms underlying the difference of the depressant actions on ischemic myocardium between lidocaine and procainamide were discussed in the light of recent concepts of actions of local anesthetics, and came to the conclusion that lidocaine is the most preferable antiarrhythmic agent for the management of ventricular arrhythmias during acute ischemia or infarction.