In contrast to previous opinions, recent investigations have suggested that increasing heart rate (HR) with atropine when moderate sinus bradycardia accompanies acute myocardial infarction is not necessarily beneficial. To further characterize the influence of vagally mediated changes in HR during ischemia, the authors evaluated the effects of atropine and of electric stimulation of the vagus nerves on the incidence of ventricular arrhythmias during acute coronary occlusion in closed chest dogs. Protection from occlusion induced arrhythmia was not observed when 28 dogs receiving atropine were compared with 27 control dogs. Rather, the total incidence of ventricular arrhythmias was significantly higher (P<0.05) and ventricular fibrillation tended to occur more frequently in the atropine treated group. Moreover, fewer ventricular arrhythmias (and total absence of ventricular fibrillation or close coupled premature beats) were noted in 12 control animals with spontaneous bradycardia (HR<60 beats/min) compared with 15 nonbradycardic animals. When vagal stimulation produced bradycardia (HR = 40-60 beats/min) during coronary occlusion, occurrence and character of ventricular arrhythmias were the same as in dogs with normal rates (HR = 80-100 beats/min). Although these results may not necessarily apply to man, further studies are needed before it can be assumed that all individuals with moderate bradycardia during acute myocardial infarction should receive vagolytic agents.