We compared the effects of lidocaine, 2 X 10(-5) M, on transmembrane resting and action potentials of Purkinje fibers on the endocardial surface of 24- to 72-hour-old myocardial infarcts in dogs with its actions and subendocardial Purkinje fibers in normal hearts. At both proximal (near the tip of the papillary muscle) and distal (toward the apex) recording sites in noninfarcted hearts, lidocaine had no significant effect on maximum diastolic potential (MDP) or Vmax. It shortened action potential duration (APD) only at the proximal site. In infarcted hearts, we arbitrarily divided Purkinje fibers at the infarcted distal site into two groups. Group I consisted of fibers which did not have a severely depressed MDP or Vmax but in which APD was markedly prolonged. Lidocaine had no effect on MDP of these fibers, significantly depressed Vmax, and shortened APD. Group II consisted of fibers in which MDP and Vmax were markedly reduced. Lidocaine also reduced Vmax of these fibers further (by 60%) without altering resting potential. In addition, lidocaine depressed pacemaker activity of Purkinje fibers in infarcts. The drug did not alter conduction of premature impulses in the subendocardial Purkinje network in normal hearts but increased the maximum delay of early premature impulses in Purkinje fibers in infarcted hearts and sometimes resulted in nondriven repetitive activity. Therefore, the effects of lidocaine on transmembrane potentials of Purkinje fibers in infarcts are different from its effects on fibers in normal hearts.