中国神经再生研究(英文版) ›› 2018, Vol. 13 ›› Issue (9): 1609-1618.doi: 10.4103/1673-5374.237124

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

海马-孤束核-迷走神经:电针保护心肌缺血损伤的途径之一

  

  • 收稿日期:2018-06-12 出版日期:2018-09-15 发布日期:2018-09-15
  • 基金资助:

    中国国家自然科学基金项目(81273858),安徽大学研究创新平台团队建立项目(2015TD033)

Electroacupuncture modulates the activity of the hippocampus-nucleus tractus solitarius-vagus nerve pathway to reduce myocardial ischemic injury

Shuai Cui1, 2, Kun Wang1, Sheng-Bing Wu3, Guo-Qi Zhu3, Jian Cao4, Yi-Ping Zhou1, Mei-Qi Zhou1, 3   

  1. 1 Research Institute of Acupuncture and Meridian, Anhui University of Chinese Medicine, Hefei, Anhui Province, China
    2 Clinical Medical College of Acupuncture, Moxibustion and Rehabilitation, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong Province, China
    3 Key Laboratory of Xin’ An Medicine, Ministry of Education, Anhui University of Chinese Medicine, Hefei, Anhui Province, China
    4 Department of Science and Technology, Anhui University of Chinese Medicine, Hefei, Anhui Province, China
  • Received:2018-06-12 Online:2018-09-15 Published:2018-09-15
  • Contact: Mei-Qi Zhou, Ph.D.,meiqizhou@163.com
  • Supported by:

    This study was supported by the National Natural Science Foundation of China, No. 81273858; a grant from the Anhui University Research and Innovation Platform Team Construction Project in China, No. 2015TD033.

摘要:

海马通过内分泌系统、神经递质以及下丘脑和脑干核如室旁核、孤束核等参与自主神经系统的调节。而迷走神经-孤束核被认为是参与心血管反射调节的重要途径。既往研究显示心肌缺血可引起自主神经系统的改变,影响交感神经和迷走神经的动态平衡。但尚不清楚在电针治疗中海马如何与下游神经核联系,并调节自主神经系统以改善心肌缺血。实验以结扎冠状动脉左前降支的方法建立急性心肌缺血大鼠模型,在急性心肌缺血前3d损毁大脑海马CA1区孤束核,在急性心肌缺血3d后进行一次电针刺激神门和通里,连续波,2 Hz,1 mA,30 min。聚类分析结果发现正常大鼠和急性心肌缺血大鼠孤束核中只存在l种放电类型的神经元,而经电针刺激的急性心肌缺血大鼠存在3种,经海马CA1区的核损毁和电针刺激的急性心肌缺血大鼠存在6种。相关分析结果显示,上述大鼠的迷走神经放电频率与心率均呈负相关(P < 0.05, r = -0.424),而与平均动脉压和心率压力乘积呈正相关(平均动脉压:P < 0.05, r = 0.409 87;心率压力乘积:P < 0.05, r = 0.425 2);孤束核放电总次数与迷走神经呈正相关(P < 0.01, r = 0.702 1),但与血流动力学指标无相关性(心率:P > 0.05, r = - 0.032 63;平均动脉压:P > 0.05, r = - 0.089 93;心率压力乘积:P > 0.05, r = - 0.032 63)。其中电针刺激的急性心肌缺血大鼠的部分神经元与迷走神经放电、心率、平均动脉压和心率压力乘积呈负相关(迷走神经放电:P < 0.05, r = - 0.87749;心率:P < 0.01, r = - 0.919 02;平均动脉压:P < 0.05, r = - 0.856 91;心率压力乘积: P < 0.01, r = - 0.919 02),经海马CA1区的核损毁和电针刺激的急性心肌缺血大鼠的部分神经元与迷走神经放电、心率、平均动脉压和心率压力乘积呈正相关(迷走神经放电:P < 0.01, r = 0.8905,P < 0.01, r = 0.9725,P < 0.01, r = 0.905 4;心率:P < 0.01, r = 0.934 7,P < 0.01, r = 0.908 9,P < 0.05, r = 0.824 7;平均动脉压:P < 0.05, r = 0.8474,P < 0.01, r = 0.9691,P < 0.01, r = 0.902 7;心率压力乘积: P < 0.05, r = 0.8637,P < 0.01, r = 0.940 7,P < 0.01, r = 0.902 7)。说明海马-孤束核-迷走神经通路参与电针在心脏经脉中的作用,孤束核的一些中间神经元可能是调节心肌缺血的关键神经元。

orcid:0000-0002-1728-4252(Mei-Qi Zhou)

关键词: 急性心肌缺血, 海马, 孤束核, 迷走神经放电, 电针, 神门, 通里, 自主神经, 神经再生

Abstract:

The hippocampus is involved in the regulation of the autonomic nervous system, together with the hypothalamus and brainstem nuclei, such as the paraventricular nucleus and nucleus tractus solitarius. The vagus nerve-nucleus tractus solitarius pathway has an important role in cardiovascular reflex regulation. Myocardial ischemia has been shown to cause changes in the autonomic nervous system, affecting the dynamic equilibrium of the sympathetic and vagal nerves. However, it remains poorly understood how the hippocampus communicates with brainstem nuclei to regulate the autonomic nervous system and alleviate myocardial ischemic tissue damage. A rat model of acute myocardial ischemia (AMI) was made by ligating the left anterior descending branch of the coronary artery. Three days before ischemia, the hippocampal CA1 region was damaged. Then, 3 days after ischemia, electroacupuncture (EA) at Shenmen (HT7)-Tongli (HT5) was performed (continuous wave, 1 mA, 2 Hz, duration of 30 minutes). Cluster analysis of firing patterns showed that one type of neuron was found in rats in the sham and AMI groups. Three types of neurons were observed in the AMI + EA group. Six types of neurons were found in the AMI + EA + Lesion group. Correlation analysis showed that the frequency of vagus nerve discharge in each group was negatively correlated with heart rate (HR) (P < 0.05, r = .0.424), and positively correlated with mean arterial pressure (MAP) (P < 0.05, r = 0.40987) and the rate-pressure product (RPP) (P < 0.05, r = 0.4252). The total frequency of the nucleus tractus solitarius discharge in each group was positively correlated with vagus nerve discharge (P < 0.01, r = 0.7021), but not with hemodynamic index (HR: P > 0.05, r = .0.03263; MAP: P > 0.05, r = .0.08993; RPP: P > 0.05, r = .0.03263). Some neurons (Neuron C) were negatively correlated with vagus nerve discharge, HR, MAP and RPP in the AMI + EA group (vagus nerve discharge: P < 0.05, r = .0.87749; HR: P < 0.01, r = .0.91902; MAP: P < 0.05, r = .0.85691; RPP: P < 0.01, r = .0.91902). Some neurons (Neurons C, D and E) were positively correlated with vagus nerve discharge, HR, MAP and RPP in the AMI + EA + Lesion group (vagus nerve discharge: P < 0.01, r = 0.8905, P < 0.01, r = 0.9725, P < 0.01, r = 0.9054; HR: P < 0.01, r = 0.9347, P < 0.01, r = 0.9089, P < 0.05, r = 0.8247; MAP: P < 0.05, r = 0.8474, P < 0.01, r = 0.9691, P < 0.01, r = 0.9027; RPP: P < 0.05, r = 0.8637, P < 0.01, r = 0.9407, P < 0.01, r = 0.9027). These findings show that the hippocampus-nucleus tractus solitarius-vagus nerve pathway is involved in the cardioprotective effect of EA at the heart meridian. Some interneurons in the nucleus tractus solitarius may play a particularly important role in the cardiomodulatory process.

Key words: nerve regeneration, acute myocardial ischemia, hippocampus, nucleus tractus solitarius, vagus nerve discharge, electroacupuncture, Shenmen (HT7), Tongli (HT5), autonomic nerve, neural regeneration