Chen Mingxian, Zhou Xiaoya, Yu Lilei, Liu Qiming, Sheng Xia, Wang Zhuo, Wang Songyun, Jiang Hong, Zhou Shenghua
Department of Cardiology, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Department of Cardiology, Renmin Hospital, Wuhan University, Wuhan, Hubei, China.
J Cardiovasc Electrophysiol. 2016 Feb;27(2):224-31. doi: 10.1111/jce.12850. Epub 2015 Nov 6.
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.
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.
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.
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.
LL-VNS exerts protective effects on myocardial I/R injury. Its potential mechanisms involve the suppression of oxidative stress and cellular apoptosis.
低水平迷走神经刺激（LL-VNS）已被证明可保护心肌免受急性缺血/再灌注（I/R）损伤。然而，这种保护作用的潜在机制仍不清楚。
本研究旨在验证LL-VNS通过抗氧化应激和抗凋亡反应对犬急性I/R损伤发挥心脏保护作用的假说。
将30只麻醉的杂种犬随机分为三组：I/R组（N = 12，左冠状动脉前降支闭塞1小时后再灌注1小时）、LL-VNS组（N = 9，I/R加LL-VNS）和假手术组（N = 9，假手术，无LL-VNS）。电压阈值设定为减慢窦性心率所需电压的80%。用伊文思蓝和氯化三苯基四氮唑评估梗死面积。进行活性测定、TUNEL染色和蛋白质印迹法以确定氧化应激和凋亡的标志物。
与I/R组相比，LL-VNS显著降低室性心律失常的发生率，增加迷走神经张力（通过心率变异性证实），并减小梗死面积。这种改善与心肌中性粒细胞浸润减少、氧化应激抑制和心肌细胞凋亡抑制有关。相比之下，I/R组缺乏LL-VNS与假手术组相比产生相反的效果。
LL-VNS对心肌I/R损伤具有保护作用。其潜在机制包括抑制氧化应激和细胞凋亡。
