The Effects of Autonomic Denervation on Ventricular Tachyarrhythmia in the Ischemia and the Reperfusion of Canine Heart

ABSTRACT

BACKGROUND: little is known about the mechanisms responsible for ventricular tachycardia during myocardial ischemia and reperfusion. The purpose of this study was to evaluate the effects of the autonomic nervous system on ventricular tachycardia in dogs. METHODS: Four groups of eight dogs were studied. The control group had intact autonomic neural innervation:the stellectomy group had bilateral transection of stellate ganglia:the vagotomy group had bilateral transection of cervical vagi; and the autonomic denervation group underwent bilateral transection of stellate ganglia and cervical vagi. Open-chest dogs anesthetized with ketamine were studied in 3 sequential steps: denervation, ischemia, and reperfusion stage. At the end of each step, we estimated effective refractory period (ERP) at four sites : the apex of non-ischemic area, the base of non-ischemic area, the apex of ischemic area, and the base of ischemic area. We observed early afterdepolarization (EAD) through recording monophasic action potential on the ischemic epicardium during ischemia and reperfusion stages. RESULTS: In ischemia stage, deltaERPs(ERPmax.-ERPmin.) were significantly prolonged, compared to deltaERPs at denervation stage, and deltaERPs of the vagotomy group tended to be prolonged to 60 minutes after myocardial ischemia, as compared to those of the stellectomy group and the autonomic denervation group. The incidence of ventricular tachycardia during ischemia presented a significant increase in the vagotomy group, compared to the control group. However, there was no difference in incidence of ventricular tachycardia between the stellectomy group and the control group. deltaERP at the group with the occurrence of ventricular tachycardia were significantly prolonged , compared to the other group without the occurrence of ventricular tachycardia. In terms of the incidence of EAD, there was no difference between the groups and it was not associated with ventricular tachycardia. deltaERP was significantly decreased to 30 minutes after reperfusion, at which point there was no significant difference between the groups. There was no correlation between EAD and ventricular tachycardia. However, deltaERP with ventricular tachycardia indicated much more significant increase than deltaERP without ventricular tachycardia. CONCLUSIONS: Sympathetic nerve may be related to prolongation of deltaERP and incidence of ventricular tachycardia in the ischemic period. However, EAD is not related to ventricular tachycardia during ischemia and reperfusion. These findings suggest that the major mechanism of ventricular tachycardia may be a reentry in ischemia and reperfusion period.