Low-Level Vagus Nerve Stimulation Attenuates Myocardial Ischemic Reperfusion Injury by Antioxidative Stress and Antiapoptosis Reactions in Canines
Low-Level Vagus Nerve Stimulation Attenuates Myocardial Ischemic Reperfusion Injury by Antioxidative Stress and Antiapoptosis Reactions in Canines
复制标题
低水平迷走神经刺激通过抗氧化应激和抗凋亡反应减轻犬类心肌缺血再灌注损伤
DOI：
10.1111/jce.12850
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发表时间：
2016-02-01
影响因子：
2.7
通讯作者：
Zhou, Shenghua
中科院分区：
文献类型：
--
作者：
Chen, Mingxian;Zhou, Xiaoya;Zhou, Shenghua
迷走神经刺激与心肌缺血再灌注损伤背景：低水平迷走神经刺激(LL-VNS)对急性缺血/再灌注(I/R)损伤有保护作用。目的：验证LL-VNS对犬急性I/R损伤的保护作用是通过抗氧化应激和抗细胞凋亡反应实现的。方法：30只麻醉杂种犬随机分为3组：I/R组(12只，结扎左冠状动脉前降支1小时再灌流1小时)、LL-VNS组(9只，I/R+LL-VNS)和假手术组(9只)。电压阈值被设置为减缓窦性心率所需电压的80%。用伊文思蓝和氯化三苯基四氮唑测定脑梗塞面积。结果：与I/R组相比，LL-VNS显著降低了室性心律失常的发生率，增加了迷走神经张力，减少了心肌梗死面积。这种改善与减少心肌中性粒细胞的渗透、抑制氧化应激和抑制心肌细胞的凋亡有关。结论：LL-VNS对心肌I/R损伤具有保护作用。其潜在的机制包括抑制氧化应激和细胞凋亡。
Vagus Nerve Stimulation and Myocardial Ischemia-Reperfusion InjuryBackground: Low-level vagus nerve stimulation (LL-VNS) has been demonstrated to protect myocardium against acute ischemia/reperfusion (I/R) injury. However, the underlying mechanism of this protective effect remains unknown.Objective: This study aimed to test the hypothesis that LL-VNS exerts cardioprotective effect on acute I/R injury in canines via antioxidative stress and antiapoptosis reactions.Method: Thirty anesthetized mongrel dogs were randomly divided into three groups: I/R group (N = 12, the left anterior descending coronary artery was occluded for 1 hour following by 1 hour reperfusion), LL-VNS group (N = 9, I/R plus LL-VNS), and sham group (N = 9, sham surgery without LL-VNS). The voltage threshold was set at 80% of the voltage required to slow the sinus rate. Infarct size was assessed with Evans Blue and triphenyltetrazolium chloride. Activity assays, TUNEL staining, and western blotting were performed to determine markers of oxidative stress and apoptosis.Results: LL-VNS significantly decreased the incidence of ventricular arrhythmias, increased vagal tone, as confirmed by heart rate viability, and reduced infarct size compared with the I/R group. This improvement was associated with a reduction in myocardial neutrophil infiltration, the inhibition of oxidative stress, and the suppression in cardiomyocyte apoptosis. In contrast, the lack of LL-VNS in the I/R group induced the opposite effect compared with the sham group.Conclusion: LL-VNS exerts protective effects on myocardial I/R injury. Its potential mechanisms involve the suppression of oxidative stress and cellular apoptosis.