Huang Jie, Qian Jin, Yao Wei, Wang Neng, Zhang Zhenjian, Cao Chuanbin, Song Bo, Zhang Zhuo
Department of Cardiology, Suizhou Hospital, Hubei University of Medicine, Suizhou City, Hubei Province, PR China.
Exp Physiol. 2015 Mar;100(3):239-48. doi: 10.1113/expphysiol.2014.082842. Epub 2014 Dec 9.
What is the central question of this study? Previous studies have shown that hypersympathetic nerve activity results in ventricular electrophysiological changes and facilitates the occurrence of ventricular arrhythmias. Vagus nerve stimulation has shown therapeutic potential for myocardial infarction-induced ventricular arrhythmias. However, the actions of vagus nerve stimulation on hypersympathetic nerve activity-induced ventricular electrophysiological changes are still unknown. What is the main finding and its importance? We show that vagus nerve stimulation is able to reverse hypersympathetic nerve activity-induced ventricular electrophysiological changes and suppress the occurrence of ventricular fibrillation. These findings further suggest that vagus nerve stimulation may be an effective treatment option for ventricular arrhythmias, especially in patients with myocardial infarction or heart failure. Vagus nerve stimulation (VNS) has shown therapeutic potential for myocardial infarction-induced ventricular arrhythmias. This study aimed to investigate the effects of VNS on ventricular electrophysiological changes induced by hypersympathetic nerve activity. Seventeen open-chest dogs were subjected to left stellate ganglion stimulation (LSGS) for 4 h to simulate hypersympathetic tone. All animals were randomly assigned to the VNS group (n = 9) or the control group (n = 8). In the VNS group, VNS was performed at the voltage causing a 10% decrease in heart rate for hours 3-4 during 4 h of LSGS. During the first 2 h of LSGS, the ventricular effective refractory period (ERP) and action potential duration (APD) were both progressively and significantly decreased; the spatial dispersion of ERP, maximal slope of the restitution curve and pacing cycle length of APD alternans were all increased. With LSGS + VNS during the next 2 h, there was a significant return of all the altered electrophysiological parameters towards baseline levels. In the eight control dogs that received 4 h of LSGS without VNS, all the parameters changed progressively, but without any reversals. The ventricular fibrillation threshold was higher in the VNS group than in the control group (17.3 ± 3.4 versus 11.3 ± 3.8 V, P < 0.05). The present study demonstrated that VNS was able to reverse LSGS-induced ventricular electrophysiological changes and suppress the occurrence of ventricular fibrillation.
本研究的核心问题是什么？以往研究表明，交感神经活动亢进会导致心室电生理变化，并促进室性心律失常的发生。迷走神经刺激已显示出对心肌梗死所致室性心律失常的治疗潜力。然而，迷走神经刺激对交感神经活动亢进引起的心室电生理变化的作用仍不清楚。主要发现及其重要性是什么？我们发现迷走神经刺激能够逆转交感神经活动亢进引起的心室电生理变化，并抑制心室颤动的发生。这些发现进一步表明，迷走神经刺激可能是治疗室性心律失常的有效选择，尤其是对心肌梗死或心力衰竭患者。迷走神经刺激（VNS）已显示出对心肌梗死所致室性心律失常的治疗潜力。本研究旨在探讨VNS对交感神经活动亢进引起的心室电生理变化的影响。17只开胸犬接受左星状神经节刺激（LSGS）4小时以模拟交感神经张力亢进。所有动物随机分为VNS组（n = 9）或对照组（n = 8）。在VNS组中，在LSGS的4小时期间的第3 - 4小时，以导致心率降低10%的电压进行VNS。在LSGS的前2小时，心室有效不应期（ERP）和动作电位时程（APD）均逐渐且显著降低；ERP的空间离散度、恢复曲线的最大斜率和APD交替的起搏周期长度均增加。在接下来的2小时进行LSGS + VNS时，所有改变的电生理参数均显著恢复到基线水平。在8只接受4小时LSGS但未进行VNS的对照犬中，所有参数均逐渐变化，但无任何逆转。VNS组的心室颤动阈值高于对照组（17.3±3.4对11.3±3.8V，P<0.05）。本研究表明，VNS能够逆转LSGS引起的心室电生理变化，并抑制心室颤动的发生。
