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SUMMARY The precise mechanism of the vagus in opposing adrenergic influences on cardiac vulnerability has not been defined. In the present investigation, cholinergic stimulation was produced by administering the selective muscarinic agent methacholine (MCh) and ventricular vulnerability was assessed by measuring the repetitive extrasystole (RE) threshold. MCh produced a sustained 98 ± 12% (P < 0.0001) increase in the RE threshold; the increase was abolished by concurrent infusion of atropine (0.2 mg/kg). When MCh was administered during beta-adrenergic blockade with pro-THE INFLUENCE OF THE VAGOSYMPATHETIC TRUNK on the occurrence of ventricular arrhythmias has been studied for over 100 years. In 1859, Einbrodt' employed an inductorium to provoke ventricular fibrillation (VF) in dogs. He measured VF threshold by changing the distance between inductorium coils. The delivered current was increased by approximating these coils. In the control state, VF was provoked at a distance between the coils of 90 cm. During vagal stimulation, the spacing could be narrowed to 30 cm before VF occurred. Einbrodt concluded that the vagus was protective against VF. Later investigators extended these observations to other ventricular arrhythmias. It has been demonstrated that vagosympathetic trunk stimulation,2`6 as well as vagomimetic drugs,7'-3 protect against, while vagotomy' 31'-11 and vagolytic drugs7' 1-19 predispose to ventricular arrhythmias. Contrary observations, in which vagal stimulation provoked ventricular arrhythmias, have also been recorded. [20][21][22] Recently, attention has been refocused on the action of the vagus on ventricular vulnerability to VF. Vagal stimulation has been shown to increase the vulnerable period threshold, as well as protect the acutely ischemic canine heart against arrhythmias.23-26 Kent et al.27 have demonstrated anatomic cholinergic pathways in the ventricular conduction system by which this presumed effect is mediated. However, Kolman et al.28 failed to observe a rise in vulnerable period threshold for VF in the absence of enhanced sympathetic activity. These workers ascribed vagal protection in the acutely ischemic heart to antagonism of the well known enhancement of both sympathetic neural as well as humoral activity which follows coronary artery (VS). It is concluded that VS affects ventricular vulnerability through its muscarinic action and that the protection against VF is in part due to modulation of neural and humoral betaadrenergic inputs.occlusion.29 Thus, two diametrically opposed views are currently being entertained; namely, that the vagus exerts a direct effect on ventricular vulnerability, and conversely, that this action is indirect and only operates with increasing levels of sympathetic tone. These disparate interpretations require clarification. Resolution of this problem is complicated by the fact that testing for cardiac vulnerability by repeatedly provoking VF and defibrillating is associated with enhanced sympathetic neural and humoral activity. This may thereby pred...

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