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下丘脑室旁核电针调节神经源性低血压和心动过缓

Neurogenic Hypotension and Bradycardia Modulated by Electroacupuncture in Hypothalamic Paraventricular Nucleus.

作者信息

Tjen-A-Looi Stephanie C, Fu Liang-Wu, Guo Zhi-Ling, Gong Yiwei D, Nguyen Anh Thi Ngoc, Nguyen Ai-Thuan P, Malik Shaista

机构信息

College of Health Sciences, Susan Samueli Integrative Health Institute, University of California, Irvine, Irvine, CA, United States.

出版信息

Front Neurosci. 2022 Jul 22;16:934752. doi: 10.3389/fnins.2022.934752. eCollection 2022.

DOI:10.3389/fnins.2022.934752
PMID:35958987
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9361000/
Abstract

Electroacupuncture (EA) stimulates somatic median afferents underlying P5-6 acupoints and modulates parasympathoexcitatory reflex responses through central processing in the brainstem. Although decreases in blood pressure and heart rate by the neural-mediated Bezold-Jarisch reflex responses are modulated by EA through opioid actions in the nucleus tractus solitarius and nucleus ambiguus, the role of the hypothalamus is unclear. The hypothalamic paraventricular nucleus (PVN) is activated by sympathetic afferents and regulates sympathetic outflow and sympathoexcitatory cardiovascular responses. In addition, the PVN is activated by vagal afferents, but little is known about its regulation of cardiopulmonary inhibitory hemodynamic responses. We hypothesized that the PVN participates in the Bezold-Jarisch reflex responses and EA inhibits these cardiopulmonary responses through the PVN opioid system. Rats were anesthetized and ventilated, and their heart rate and blood pressures were monitored. Application of phenylbiguanide every 10 min close to the right atrium induced consistent depressor and bradycardia reflex responses. Unilateral microinjection of the depolarization blockade agent kainic acid or glutamate receptor antagonist kynurenic acid in the PVN reduced these reflex responses. In at least 70% of the rats, 30 min of bilateral EA at P5-6 acupoints reduced the depressor and bradycardia responses for at least 60 min. Blockade of the CCK-1 receptors converted the non-responders into EA-responders. Unilateral PVN-microinjection with naloxone reversed the EA inhibition. Vagal-evoked activity of the PVN cardiovascular neurons was reduced by 30 min EA (P5-6) through opioid receptor activation. These data indicate that PVN processes inhibitory cardiopulmonary reflexes and participates in EA-modulation of the neural-mediated vasodepression and bradycardia.

摘要

电针刺激位于P5 - 6穴位下方的躯体正中传入神经,并通过脑干的中枢处理调节副交感神经兴奋反射反应。虽然神经介导的贝佐尔德 - 雅里什反射反应引起的血压和心率下降可通过孤束核和疑核中的阿片类作用被电针调节,但下丘脑的作用尚不清楚。下丘脑室旁核(PVN)被交感神经传入激活,并调节交感神经输出和交感神经兴奋的心血管反应。此外,PVN也被迷走神经传入激活,但其对心肺抑制性血流动力学反应的调节知之甚少。我们假设PVN参与贝佐尔德 - 雅里什反射反应,并且电针通过PVN阿片系统抑制这些心肺反应。将大鼠麻醉并进行通气,监测其心率和血压。每隔10分钟在右心房附近应用苯乙双胍可诱导持续的降压和心动过缓反射反应。在PVN中单侧微量注射去极化阻断剂 kainic 酸或谷氨酸受体拮抗剂犬尿氨酸可降低这些反射反应。在至少70%的大鼠中,在P5 - 6穴位进行30分钟的双侧电针可使降压和心动过缓反应至少降低60分钟。CCK - 1受体的阻断将无反应者转变为电针反应者。单侧PVN微量注射纳洛酮可逆转电针的抑制作用。通过阿片受体激活,30分钟的电针(P5 - 6)可降低迷走神经诱发的PVN心血管神经元活动。这些数据表明PVN处理抑制性心肺反射,并参与电针介导的神经源性血管减压和心动过缓调节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844b/9361000/c8cda2ca0f86/fnins-16-934752-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844b/9361000/dbf1aa45f482/fnins-16-934752-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844b/9361000/89ebe9ed146e/fnins-16-934752-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844b/9361000/a314684c32fe/fnins-16-934752-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844b/9361000/e1ce079a605e/fnins-16-934752-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844b/9361000/80176eed2284/fnins-16-934752-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844b/9361000/f2571204b181/fnins-16-934752-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844b/9361000/7f5acd38e605/fnins-16-934752-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844b/9361000/c8cda2ca0f86/fnins-16-934752-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844b/9361000/dbf1aa45f482/fnins-16-934752-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844b/9361000/89ebe9ed146e/fnins-16-934752-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844b/9361000/a314684c32fe/fnins-16-934752-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844b/9361000/3ed825388880/fnins-16-934752-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844b/9361000/e1ce079a605e/fnins-16-934752-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844b/9361000/80176eed2284/fnins-16-934752-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844b/9361000/f2571204b181/fnins-16-934752-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844b/9361000/7f5acd38e605/fnins-16-934752-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844b/9361000/c8cda2ca0f86/fnins-16-934752-g009.jpg

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