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

Neurogenic Hypotension and Bradycardia Modulated by Electroacupuncture in Hypothalamic Paraventricular Nucleus.
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DOI:
10.3389/fnins.2022.934752
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发表时间:
2022
影响因子:
4.3
通讯作者:
Malik, Shaista
Malik, Shaista
中科院分区:
医学2区
文献类型:
--
作者:
Tjen-A-Looi, Stephanie C.;Fu, Liang-Wu;Guo, Zhi-Ling;Gong, Yiwei D.;Anh Thi Ngoc Nguyen;Nguyen, Ai-Thuan P.;Malik, Shaista

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电针 (EA) 刺激 P5-6 穴位下的躯体正中传入神经,并通过脑干的中央处理调节副交感兴奋反射反应。尽管神经介导的 Bezold-Jarisch 反射反应导致的血压和心率降低是由 EA 通过孤束核和模糊核中的阿片类药物作用来调节的,但下丘脑的作用尚不清楚。下丘脑室旁核(PVN)由交感传入神经激活,调节交感神经流出和交感兴奋性心血管反应。此外,PVN 被迷走神经传入激活,但对其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 Bezold-Jarisch 反射反应,而 EA 通过 PVN 阿片类药物系统抑制这些心肺反应。对大鼠进行麻醉和通气,并监测其心率和血压。每 10 分钟在右心房附近应用苯双胍,诱导一致的降压和心动过缓反射反应。在PVN中单侧显微注射去极化阻断剂红藻氨酸或谷氨酸受体拮抗剂犬尿酸可减少这些反射反应。在至少 70% 的大鼠中,P5-6 穴位双侧 EA 30 分钟可减少抑郁和心动过缓反应至少 60 分钟。 CCK-1 受体的阻断将无反应者转化为 EA 反应者。单侧 PVN 显微注射纳洛酮可逆转 EA 抑制。 30 分钟 EA (P5-6) 通过阿片受体激活,迷走神经诱发的 PVN 心血管神经元活动减少。这些数据表明 PVN 处理抑制性心肺反射并参与神经介导的血管抑制和心动过缓的 EA 调节。
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.
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