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低频迷走神经刺激可减轻大鼠急性心肌梗死后SK2的表达及心律失常的发生率。

LL-VNS attenuates SK2 expression and incidence of arrhythmias following acute myocardial infarction in rats.

作者信息

Chen Mingxian, Zhu Tongjian, Wu Zhihong, Hu Lin, Wu Zhijian, Liu Qiming, Zhou Shenghua

机构信息

The Second Xiangya Hospital, Central South University, Changsha, China.

Xiangyang Central Hospital, Xiangyang, Hubei, China.

出版信息

Front Cardiovasc Med. 2023 Jan 11;9:1034888. doi: 10.3389/fcvm.2022.1034888. eCollection 2022.

Abstract

OBJECTIVES

Our previous study has demonstrated that low-level vagus nerve stimulation (LL-VNS) protects the heart against ventricular arrhythmias (VAs) induced by acute myocardial infarction (AMI). However, the potential mechanisms by which it influences ventricular electrophysiology remain unknown.

MATERIALS AND METHODS

Forty-five rats were divided into three groups: a Control group (sham AMI followed by sham LL-VNS, = 15), an AMI group (AMI followed by sham LL-VSN for 60 mins, = 15), and an AMI + LL-VNS group (AMI followed by LL-VSN for 60 mins, = 15). Heart rate variability (HRV), ventricular effective refractory period (ERP), ventricular fibrillation threshold (VFT), and left stellate ganglion (LSG) activity were measured at baseline and during AMI. Finally, myocardial tissues were collected for tissue analysis.

RESULTS

AMI directly induced hyperactivity in the LSG and reduced vagal tone as indexed by HRV. AMI also decreased VFT, and shortened ERP but increased ERP dispersion. AMI resulted in an increase in expression of ventricular small-conductance Ca-activated K (SK2). However, LL-VNS significantly mitigated or eliminated the effects of AMI.

CONCLUSION

LL-VNS altered the electrophysiological properties of the ventricles through inhibition of cardiac sympathetic nervous activity and reduction in SK2 expression.

摘要

目的

我们之前的研究表明,低水平迷走神经刺激(LL-VNS)可保护心脏免受急性心肌梗死(AMI)诱发的室性心律失常(VA)影响。然而,其影响心室电生理的潜在机制仍不清楚。

材料与方法

45只大鼠分为三组:对照组(假急性心肌梗死,随后假低水平迷走神经刺激,n = 15)、急性心肌梗死组(急性心肌梗死,随后假低水平迷走神经刺激60分钟,n = 15)和急性心肌梗死 + 低水平迷走神经刺激组(急性心肌梗死,随后低水平迷走神经刺激60分钟,n = 15)。在基线期和急性心肌梗死期间测量心率变异性(HRV)、心室有效不应期(ERP)、室颤阈值(VFT)和左星状神经节(LSG)活性。最后,收集心肌组织进行组织分析。

结果

急性心肌梗死直接导致星状神经节活动亢进,并降低以心率变异性为指标的迷走神经张力。急性心肌梗死还降低了室颤阈值,缩短了有效不应期,但增加了有效不应期离散度。急性心肌梗死导致心室小电导钙激活钾通道(SK2)表达增加。然而,低水平迷走神经刺激显著减轻或消除了急性心肌梗死的影响。

结论

低水平迷走神经刺激通过抑制心脏交感神经活动和降低SK2表达改变了心室的电生理特性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc53/9874093/adf1999d1ea7/fcvm-09-1034888-g001.jpg

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