Circulation, Vol 52, 578-585, Copyright © 1975 by American Heart Association
BS Kolman, RL Verrier and B Lown
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 closed-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 less
than 0.01) and constriction of the VF 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.
ARTICLES
The effect of vagus nerve stimulation upon vulnerability of the canine ventricle: role of sympathetic-parasympathetic interactions
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