This study examines the electrophysiologic effects of an intravenous bolus of lidocaine in the normal canine ventricle. In 14 open-chest dogs, left ventricular effective refractory period, ventricular repolarization time, and activation time were measured continuously during ventricular pacing (150/min) before, during, and after intravenous lidocaine given over 4 minutes. Lidocaine doses of 1.25, 2.5, and 5.0 mg/kg transiently prolonged the ventricular effective refractory period from 177 +/- 4 (X +/- standard error of the mean) to 185 +/- 5 msec (p less than 0.05), 176 +/- 3 to 188 +/- 6 msec (p less than 0.05), and 176 +/- 5 to 197 +/- 5 msec, (p less than 0.05), respectively, at 6 +/- 1.5 minutes from the onset of the bolus. Serum lidocaine levels obtained at the peak of the effective refractory period prolongation averaged 4.3 +/- 1.0, 9.0 +/- 3.0, and 22.3 +/- 4.7 micrograms/ml, respectively. Ventricular repolarization time was not prolonged. Activation time also transiently increased from 43 to 45 msec (p less than 0.05) and from 47 to 52 msec with the 2.5 mg/kg and 5.0 mg/kg doses, respectively. Cardiac denervation and administration of propranolol, 1 mg/kg intravenously, did not influence these responses to lidocaine. We conclude that a bolus of lidocaine transiently prolongs the effective refractory period and activation time in the normal canine ventricle because of its direct membrane rather than autonomic effects.