Defibrillating shocks delivered to the heart impair efferent sympathetic responsiveness.

Defibrillating shocks delivered to the heart impair efferent sympathetic responsiveness.
复制标题

传递到心脏的除颤电击会损害传出交感神经的反应性。

DOI:
10.1161/01.cir.88.6.2661
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发表时间:
1993
期刊:
影响因子:
37.8
通讯作者:
Zipes,DP
Zipes,DP
中科院分区:
医学1区
文献类型:
--
作者:
Ito,M;Pride,HP;Zipes,DP

文献摘要

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功能研究表明,交感神经传出位于心内膜下浅层,迷走神经传出位于心内膜下。直接施加于心脏的电击可能会影响这些自主神经的功能。方法与结果在麻醉开胸犬心包内缝合可植入贴片,通过与窦性心律R波同步的慢(<或= 1 J)、中(6 ~ 16 J)或高(30 ~ 35 J)能量截断单相指数电击。观察休克前后双侧锁骨下刺激(SS)对心室有效不应期(ERP)缩短的影响。高能冲击使斑块下方和顶端的SS频率- erp响应曲线向右下移(P < 0.001);基部ERP缩短保持不变。这种交感神经衰减发生在bbb10 J的电击中,而不发生在<或= 10 J的电击中,在电击后15分钟被注意到,并在3小时时显示不完全恢复到对照值。低能和高能电击均不影响去甲肾上腺素剂量- erp反应曲线,表明心肌反应正常。低能和高能电击均未减弱双侧颈迷走神经刺激引起的ERP延长。通过缝合在心包外部的贴片传递的高能电击对交感神经反应没有影响,这表明心包对休克引起的交感神经衰减具有保护作用。结论直接作用于心外膜的sdc电击bbb10j可减弱交感神经的传出功能。这种变化可能影响复心除颤后交感神经刺激的电生理和血流动力学反应。
BACKGROUNDFunctional studies indicate that sympathetic efferents are located in the superficial subepicardium and vagal efferents are located in the subendocardium. It is possible that electrical shocks applied directly to the heart might affect the function of these autonomic nerves.METHODS AND RESULTSLow- (< or = 1 J), medium- (6 to 16 J), or high- (30 to 35 J) energy truncated monophasic exponential shocks, synchronized to the R wave during sinus rhythm, were delivered over implantable patches sutured inside the pericardium in anesthetized open-chest dogs. Shortening of ventricular effective refractory period (ERP), produced by bilateral ansae subclaviae stimulation (SS), was measured before and after shock delivery. High-energy shocks shifted the SS frequency-ERP response curves downward and to the right (P < .001) for sites beneath and apical to the patches; ERP shortening at basal sites remained unchanged. Such sympathetic attenuation occurred with shocks > 10 J but not with shocks < or = 10 J, was noted 15 minutes after the shock, and showed incomplete return to control 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 bilateral cervical vagal stimulation-induced ERP prolongation. High-energy shocks delivered over patches sutured to the outside of the pericardium showed no effects on sympathetic response, suggesting a protective effect of the pericardium against shock-induced sympathetic attenuation.CONCLUSIONSDC shocks > 10 J delivered directly to the epicardium attenuated efferent sympathetic neural function. Such changes may affect electrophysiological, as well as hemodynamic, responses to sympathetic neural stimulation after cardioversion-defibrillation.