Effects of epinephrine on automaticity and the incidence of arrhythmias in Purkinje fibers surviving myocardial infarction.

The role of the sympathetic nervous system in the development of late-phase ventricular arrhythmias occurring 24 hr after myocardial infarction was investigated using canine ventricular preparations in vitro. One day after two-stage ligation of the left anterior descending coronary artery, transmembrane action potentials from subendocardial Purkinje fibers were monitored in noninfarcted (NZ) and infarcted (IZ) zones during Tyrode's superfusion at 37 degrees C. In combined preparations incorporating both NZ and IZ, epinephrine (10(-7)-10(-5)M) produced dose-dependent increases in spontaneous rates of depolarization, slope of phase 4 depolarization and incidence of spontaneous and induced arrhythmias. In particular, premature electrical stimulation induced increased numbers of unstimulated responses or rapid, repetitive depolarizations. These responses to the drug were antagonized by propranolol (10(-6)M) but not phentolamine (10(-7)M). Epinephrine appeared to promote the functional dissociation of conducted impulses often observed in the IZ of combined preparations. In preparations excised from either NZ or IZ alone, epinephrine induced elevated spontaneous firing rates, particularly in the IZ, but no increase in arrhythmias. These data suggest that elevated levels of beta adrenergic receptor stimulation 24 hr after myocardial infarction may increase ventricular vulnerability to arrhythmias arising through enhanced automaticity or reentry.