The effect of vagus nerve stimulation upon vulnerability of the canine ventricle. Role of sympathetic parasympathetic interactions

Abstract

The effect of vagus nerve stimulation (VNS) upon ventricular vulnerability was studied in 30 mongrel dogs subjected to varying levels of adrenergic stimulation. Vulnerability was assessed both by determining the minimum current required to produce ventricular fibrillation (VF threshold) and by plotting VF threshold throughout the vulnerable period (VF zone). Chloralose anesthetized animals were studied by means of sequential pulses applied to the apex of the right ventricular endocardium. Testing was carried out in closed chest dogs, in open chest dogs with and without left stellate ganglion stimulation (LSGS), and in open and slowed chest dogs pretreated with propranolol. In the absence of adrenergic stimulation, VNS was without significant effect on either the VF threshold or the VF zone under closed or open chest conditions. During LSGS, however, VNS was associated with a 93 ± 22% (mean ± SE) increase in VF threshold (P < 0.01) and constriction of the VR zone. Vagus nerve stimulation combined with LSGS raised VF threshold to the control value, but not beyond. After beta adrenergic blockade with propranolol, VNS was without effect on VF threshold in either open or closed chest animals. It is concluded that augmented sympathetic tone is a precondition for a VNS induced elevation in VF threshold. The vagal effect is indirect and is expressed by opposing the effects of heightened adrenergic tone on ventricular vulnerability.