DEFIBRILLATING SHOCKS DELIVERED TO THE HEART IMPAIR EFFERENT SYMPATHETIC RESPONSIVENESS

Citation
M. Ito et al., DEFIBRILLATING SHOCKS DELIVERED TO THE HEART IMPAIR EFFERENT SYMPATHETIC RESPONSIVENESS, Circulation, 88(6), 1993, pp. 2661-2673
Citations number
52
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiac & Cardiovascular System",Hematology
Journal title
ISSN journal
0009-7322
Volume
88
Issue
6
Year of publication
1993
Pages
2661 - 2673
Database
ISI
SICI code
0009-7322(1993)88:6<2661:DSDTTH>2.0.ZU;2-0
Abstract
Background. Functional studies indicate that sympathetic efferents are located in the superficial subepicardium and vagal efferents are loca ted in the subendocardium. It is possible that electrical shocks appli ed directly to the heart might affect the function of these autonomic nerves. Methods and Results. Low- (less than or equal to 1 J), medium- (6 to 16 J), or high- (30 to 35 J) energy truncated monophasic expone ntial shocks, synchronized to the R wave during sinus rhythm, were del ivered over implantable patches sutured inside the pericardium in anes thetized open-chest dogs. Shortening of ventricular effective refracto ry period (ERP), produced by bilateral ansae subclaviae stimulation (S S), was measured before and after shock delivery. High-energy shocks s hifted the SS frequency-ERP response curves downward and to the right (P<.001) for sites beneath and apical to the patches; ERP shortening a t basal sites remained unchanged. Such sympathetic attenuation occurre d with shocks >10 J but not with shocks less than or equal to 10 J, wa s noted 15 minutes after the shock, and showed incomplete return to co ntrol values at 3 hours. Neither low- nor high-energy shocks affected norepinephrine dose-ERP response curves, indicating normal myocardial responsiveness. Low- and high-energy shocks did not attenuate bilatera l cervical vagal stimulation-induced ERP prolongation. High-energy sho cks delivered over patches sutured to the outside of the pericardium s howed no effects on sympathetic response, suggesting a protective effe ct of the pericardium against shock-induced sympathetic attenuation. C onclusions. DC shocks >10 J delivered directly to the epicardium atten uated efferent sympathetic neural function. Such changes may affect el ectrophysiological, as well as hemodynamic, responses to sympathetic n eural stimulation after cardioversion-defibrillation.