Role of the vagus nerves in the cardiovascular changes induced by coronary occlusion.

Abstract

The importance of vagus nerves to the heart rate, contractile force, blood pressure, and incidence of fatal arrhythmias produced by occlusion of the anterior descending branch of the left coronary artery was studied in chloralose-anesthetized cats. Occlusion performed in 20 animals with intact vagus nerves produced significant decreases in heart rate (23 ± 5.3 beats/min), contractile force (23 ± 6.6%), and blood pressure (20 ± 2.7 mm Hg). Time to onset of arrhythmias was 2.6 ± 0.4 minutes and death due to ventricular fibrillation occurred in four of 20 animals. Occlusion performed in 20 animals with bilateral vagotomy and 20 animals with intact vagus nerves but pretreated with atropine did not decrease heart rate and resulted in significantly more deaths. Time to onset of the arrhythmia was significantly less in both cases. Occlusion produced the usual decrease in contractile force and blood pressure. In addition, a delayed (i.e., after sinus rhythm was restored) decrease in blood pressure and contractile force occurred in animals with vagus nerves sectioned. Pacing hearts of animals with intact and functional vagus nerves to rates comparable to those seen in vagotomized and atropinized cats resulted in a mortality rate identical to that seen in controls. On the other hand, time to onset of the arrhythmia was significantly less than controls and equivalent to the onset times of the vagotomized and atropinized groups. These results suggest that 1) efferent vagus nerves mediate sinus bradyeardia that occurs after coronary occlusion, 2) presence of efferent vagus tone per se reduces the incidence of death, 3) rate effect of efferent vagal tone increases the time to onset of arrhythmias, and 4) presence of afferent vagal tone counteracts the late decline in arterial pressure and contractile force.