The induction of arrhythmias by sympathetic activity before and after occlusion of a coronary artery in the canine heart

Stimulation of the left ansa subclavia before and after occlusion of the anterior descending artery of the dog's heart has produced significantly greater ventricular arrhythmia responses in the post-occlusion trials than in trials before occlusion. Data are presented from two series of acute experiments, Series 1 and Series 2 which include findings from 11 and 16 dogs, respectively. The experiments of the two series differed in types of electrical stimuli used and in elapsed time between occlusion of the artery and the first post-occlusion stimulation. All stimulations were applied when sinus rhythm was complete and no premature beats had occurred within a specified preceding duration. The arrhythmia responses in Series 1 were more intense (except that ventricular fibrillations were equal) and more prolonged than in Series 2. Reasons are discussed but not yet clear. The increased ventricular arrhythmia response persists strongly 5 days after occlusion. Propranolol, 0.5 mg/kg, blocked the arrhythmia response to sympathetic nerve stimulation completely during a period of 45–60 min after injection, but no blockade was apparent after 80 min. Possible mechanisms of origin of the induced arrhythmias were considered and evidence presented to indicate that individually generated discharges in ectopic pacemakers produced the arrhythmia in parts of the records and that reentry was the mechanism in other parts, particularly during approach to onset of ventricular fibrillation. The demonstration that brief periods of stimulation of sympathetic nerve strands to dog's hearts after coronary occlusion can produce ventricular arrhythmias of all degrees of severity including ventricular fibrillation suggests that emotional excitation of a myocardial infarction patient may induce similar ventricular arrhythmias and thereby place life in jeopardy.