CHEMICAL CARDIAC SYMPATHETIC DENERVATION HAMPERS DEFIBRILLATION IN THE DOG

Cardiac Sympathetic Denervation and Defibrillation, Introduction: Card iac defibrillation is influenced by several physical and nonphysical f actors, Previous animal studies have shown that beta-adrenergic stimul ation facilitates the process of defibrillation. The purpose of this s tudy was to examine the effects of chemical sympathetic denervation on the ability to defibrillate the canine heart, Methods and Results: Tw elve chronically instrumented dogs underwent serial measurements of th e energy required to defibrillate the heart, ten before and after trea tment with 50 mg/kg 6-hydroxydopamine (6-OHDA), Two of the animals rec eived 1% ascorbic acid in 0.9% saline solution (the vehicle) only, and three dogs received the vehicle followed several weeks later by 6-OHD A, Following treatment with 6-OHDA, the energy to defibrillate the hea rt rose from 11.9 +/- 7.4 J (baseline I) and 14.3 +/- 8.7 J (baseline 2) to 23.3 +/- 10.8 d (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 t he 10 animals could not be defibrillated versus none of 5 after saline treatment (Chi square 3.750, P = 0.053), In surviving animals, a retu rn of measurements to, or toward, baseline was measured after active t reatment, Conclusions: In this chronically instrumented closed chest a nimal model, chemical sympathetic denervation with 6-OHDA hampered the process of cardiac defibrillation, These results support previous obs ervations of a modulating effect of this process by adrenergic activit y.