Chemical cardiac sympathetic denervation hampers defibrillation in the dog

Cardiac defibrillation is influenced by several physical and nonphysical factors. Previous animal studies have shown that beta-adrenergic stimulation facilitates the process of defibrillation. The purpose of this study was to examine the effects of chemical sympathetic denervation on the ability to defibrillate the canine heart.

Twelve chronically instrumented dogs underwent serial measurements of the energy required to defibrillate the heart, ten before and after treatment with 50 mg/kg 6-hydroxydopamine (6-OHDA). Two of the animals received 1% ascorbic acid in 0.9% saline solution (the vehicle) only, and three dogs received the vehicle followed several weeks later by 6-OHDA. Following treatment with 6-OHDA, the energy to defibrillate the heart rose from 11.9 +/- 7.4 J (baseline 1) and 14.3 +/- 8.7 J (baseline 2) to 23.3 +/- 10.8 J (P < 0.01 and < 0.05, respectively). In contrast, following saline administration, no significant change was measured in the energy required to defibrillate the heart. After 6-OHDA, 5 of the 10 animals could not be defibrillated versus none of 5 after saline treatment (Chi square 3.750, P = 0.053). In surviving animals, a return of measurements to, or toward, baseline was measured after active treatment.

In this chronically instrumented, closed chest animal model, chemical sympathetic denervation with 6-OHDA hampered the process of cardiac defibrillation. These results support previous observations of a modulating effect of this process by adrenergic activity.