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无创耳甲刺激通过调节心脏副交感神经活性改善缺血后心脏重构。

Non-invasive tragus stimulation improves cardiac post-ischemic remodeling by regulating cardiac parasympathetic activity.

机构信息

Department of Cardiology, The Second Xiangya Hospital of Central South University, Changsha, China.

Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.

出版信息

ESC Heart Fail. 2022 Dec;9(6):4129-4138. doi: 10.1002/ehf2.14146. Epub 2022 Sep 9.

DOI:10.1002/ehf2.14146
PMID:36085552
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9773748/
Abstract

AIMS

Our previous study proved that low-level tragus nerve stimulation (LL-TS) could improve left ventricular remodelling by cardiac down-stream mechanisms. However, the cardiac up-stream mechanisms remain unknown.

METHODS AND RESULTS

Twenty-eight adult beagle dogs were randomly divided into an MI group (myocardial infarction was induced by permanent ligation of the left coronary artery, n = 10), an LL-TS group (MI plus intermittent LL-TS treatment, n = 10), and a control group (sham ligation with the same stimulation as the LL-TS group, n = 8). Auricular tragus nerve was bilaterally delivered to the tragus via ear-clips connected to a custom-made stimulator. The voltage slowing sinus rate was used as the threshold to set the LL-TS 80% below this level. At the end of 4 weeks post-MI, LL-TS could significantly increase atrial ganglion plex (GP) activity, decreased left stellate ganglion (LSG) activity, reduced LV dilation, and improved ventricular functions. Chronic intermittent LL-TS treatment significantly attenuated left ventricular remodelling via the up-regulation of α7nAChR expression and the down-regulation of MMP-9 level in post-MI LV tissue. The elevated protein and mRNA of MMP-9 levels in remote areas were significantly ameliorated by LL-TS treatment.

CONCLUSIONS

Chronic LL-TS increased GP neural activity and improved ventricular remodelling possibly via α7nAChR/MMP-9 axis.

摘要

目的

我们之前的研究证明,低位耳轮神经刺激(LL-TS)可以通过心脏下游机制改善左心室重构。然而,心脏上游机制尚不清楚。

方法和结果

28 只成年比格犬随机分为 MI 组(通过永久性结扎左冠状动脉诱导心肌梗死,n=10)、LL-TS 组(MI 加间歇性 LL-TS 治疗,n=10)和对照组(假结扎,给予与 LL-TS 组相同的刺激,n=8)。双侧通过耳夹将耳轮神经传递到耳轮,耳夹连接到定制的刺激器。电压减慢窦率用作阈值,将 LL-TS 设置为低于该水平的 80%。在 MI 后 4 周结束时,LL-TS 可显著增加心房神经节丛(GP)活性,降低左星状神经节(LSG)活性,减少 LV 扩张,并改善心室功能。慢性间歇性 LL-TS 治疗通过上调 MMP-9 水平和下调左室组织中 MMP-9 水平显著减轻左室重构。LL-TS 治疗可显著改善远程区域 MMP-9 水平的升高的蛋白和 mRNA。

结论

慢性 LL-TS 通过α7nAChR/MMP-9 轴增加 GP 神经活性并改善心室重构。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c04/9773748/eaea1920421f/EHF2-9-4129-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c04/9773748/8cdcd1e3dbe5/EHF2-9-4129-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c04/9773748/e01a23984ac9/EHF2-9-4129-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c04/9773748/de8e3f8f00fd/EHF2-9-4129-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c04/9773748/0511b750bbb6/EHF2-9-4129-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c04/9773748/d5a273f6690c/EHF2-9-4129-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c04/9773748/eaea1920421f/EHF2-9-4129-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c04/9773748/8cdcd1e3dbe5/EHF2-9-4129-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c04/9773748/e01a23984ac9/EHF2-9-4129-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c04/9773748/de8e3f8f00fd/EHF2-9-4129-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c04/9773748/0511b750bbb6/EHF2-9-4129-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c04/9773748/d5a273f6690c/EHF2-9-4129-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c04/9773748/eaea1920421f/EHF2-9-4129-g004.jpg

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