Effects of epinephrine on the electrophysiologic properties of Purkinje fibers surviving myocardial infarction.

The electrophysiologic effects of epinephrine on canine subendocardial Purkinje fibers were examined 24 hours after two-stage ligation of the left anterior descending coronary artery. Transmembrane action potential were monitored simultaneously in noninfarcted (NZ) and infarcted (IZ) zones during epinephrine superfusion at 37 degrees C. Epinephrine (10(-8) M to 10(-5) M) induced dose-dependent increases in maximum rate of phase O depolarization (Vmax), action potential amplitude (APA), and maximum diastolic potential (MDP) in both NZ and IZ. Epinephrine consistently shortened effective refractory period (ERP) in both regions No significant change in action potential duration (APD) was noted at either 50% or 90% repolarization. Impulse conduction through the NZ and into the IZ was significantly improved, as indicated by an increased maximum follow-rate in each region at 10(-6) and 10(-5) M epinephrine. The IZ fibers showed a marked hypersensitivity to this agent, in that responses were particularly pronounced in the IZ vs the NZ in terms of both absolute and percentage changes. The effects of epinephrine on Vmax, MDP, APA, and ERP were generally reversed by propranolol, while remaining relatively unaffected by phentolamine, suggesting a beta-adrenergic mechanism. Increased stimulation of ventricular beta-adrenoceptors in the period 16 to 72 hours after myocardial infarction may influence ventricular vulnerability to "late-phase" arrhythmias through nonuniform effects in Purkinje fibers.