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在急性缺血期间刺激脊髓可通过减弱心肌的局部兴奋性降低室性心律失常

 罂粟花anesthGH 2021-07-21

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Spinal cord stimulation reduces ventricular arrhythmias during acute ischemia by attenuation of regional myocardial excitability

背景与目的

心肌缺血引起自主神经系统失调,并可诱发心律失常。我们假设脊髓刺激(SCS)的神经调节可减弱缺血诱发的传入信号增强所致的局部心脏交感神经激活,在急性缺血期间可提高心肌功能,并降低室性心律失常。

方  法

约克郡猪(n= 20)随机分配到SCS组或对照组。四极SCS引线经皮放置在硬膜外腔(T1-T4)中,56针电极网放置在心脏上用于高分辨率电生理记录,包括:激活恢复间隔(ARI),激活时间,复极时间和复极化分散。在基线,SCS /对照,急性缺血(冠状动脉结扎300秒)期间以及整个再灌注过程中,测量并记录电生理和血液动力学。

结  果

SCS减弱缺血心肌的交感神经激活引起的激活恢复间隔(ARI)和复极化时间的缩短,降低复极分散,降低快速性室性心律失常,改善心肌功能。在基线没有心肌应激的状态下或者在非缺血的心肌中,心室电生理学并没有变化。

结  论

在急性心室缺血猪模型中,SCS减弱了局部心肌交感神经激活,降低了室性心律失常,改善了心肌功能。 SCS降低缺血心肌交感神经的激活,但是对正常心肌并没影响,这为SCS的抗心律失常和心肌保护作用提供客观认识。

原始文献摘要

Howard-Quijano K,Takamiya T,Dale EA,Kipke J, Kubo Y,Grogan T,Afyouni A,Shivkumar K,Mahajan A.Spinal cord stimulation reduces ventricular arrhythmias during acute ischemia by attenuation of regional myocardial excitability.Am J Physiol Heart Circ Physiol. 2017 Jun 2:ajpheart.00129.2017. doi:10.1152/ajpheart.00129.2017.

Background: Myocardial ischemia creates autonomic nervous system imbalance and can trigger cardiac arrhythmias. We hypothesize that neuromodulation by spinal cord stimulation (SCS) willattenuate local cardiac sympathoexcitation from ischemia-induced increases in afferent signaling,reduce ventricular arrhythmias, and improve myocardial function during acute ischemia. 

Methods: Yorkshire pigs (n=20) were randomized to SCS (50 Hz at 200μsec duration, current 90% motor threshold) or Sham for 30 min prior to ischemia. A 4 pole SCS lead was placed percutaneously in the epidural space (T1-T4) and a 56-electrode mesh placed over the heart for high resolution electrophysiological recordings including; activation recovery intervals (ARIs),activation time, repolarization time, and dispersion of repolarization. Electrophysiological and hemodynamic measures were recorded at; baseline, after SCS/sham, during acute ischemia (300 sec coronary artery ligation), and throughout reperfusion.

Results: SCS reduced sympathoexcitation-induced ARI and repolarization time shortening in ischemic myocardium, attenuated increases in dispersion of repolarization, reduced ventricular

 tachyarrhythmias (non-sustained ventricular tachycardia – Sham: 24 (3) versus SCS: 1 (1) p<0.001), and improved myocardial function (dP/dt baseline to ischemia - Sham: 1814±213 to 1596±282 versus SCS:1442±299 to 1380±299 p<0.01) - with no change in ventricular electrophysiology during baseline conditions without myocardial stress, nor in the non-ischemic myocardium.

Conclusions: In a porcine model of acute ventricular ischemia, SCS reduced regional myocardial sympathoexcitation, decreased ventricular arrhythmias, and improved myocardial function. SCS decreased sympathetic nerve activation locally in ischemic myocardium with no 48 effect observed in normal myocardium, thus providing mechanistic insight into the anti49 arrhythmic and myocardial protective effects of SCS.

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