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首页> 外文期刊>American Journal of Physiology >Midbrain vlPAG inhibits rVLM cardiovascular sympathoexcitatory responses during electroacupuncture.
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Midbrain vlPAG inhibits rVLM cardiovascular sympathoexcitatory responses during electroacupuncture.

机译：中脑vlPAG在电针过程中抑制rVLM心血管交感兴奋反应。

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摘要

The periaqueductal gray (PAG) is an important integrative region in the regulation of autonomic outflow and cardiovascular function and may serve as a regulatory center as part of a long-loop pathway during somatic afferent stimulation with acupuncture. Because the ventrolateral PAG (vlPAG) provides input to the rostral ventrolateral medulla (rVLM), an important area for electroacupuncture (EA) regulation of sympathetic outflow, we hypothesized that the vlPAG plays a role in the EA-related modulation of rVLM premotor sympathetic neurons activated during visceral afferent stimulation and autonomic excitatory reflexes. Cats were anesthetized and ventilated, and heart rate and mean blood pressure were monitored. Stimulation of the splanchnic nerve by a pledget of filter paper soaked in bradykinin (BK, 10 mug/ml) every 10 min on the gallbladder induced consistent cardiovascular reflex responses. Bilateral stimulation with EA at acupoints over the pericardial meridian (P5-6) situated over the median nerve reduced the increases in blood pressure from 34 +/- 3 to 18 +/- 5 mmHg for a period of time that lasted for 60 min or more. Unilateral inactivation of neuronal activity in the vlPAG with 50-75 nl of kainic acid (KA, 1 mM) restored the blood pressure responses from 18 +/- 3 to 36 +/- 5 mmHg during BK-induced gallbladder stimulation, an effect that lasted for 30 min. In the absence of EA, unilateral microinjection of the excitatory amino acid dl-homocysteic acid (DLH, 4 nM) in the vlPAG mimicked the effect of EA and reduced the reflex blood pressure responses from 35 +/- 6 to 14 +/- 5 mmHg. Responses of 21 cardiovascular sympathoexcitatory rVLM neurons, including 12 that were identified as premotor neurons, paralleled the cardiovascular responses. Thus splanchnic nerve-evoked neuronal discharge of 32 +/- 4 spikes/30 stimuli in six neurons was reduced to 10 +/- 2 spikes/30 stimuli by EA, which was restored rapidly to 28 +/- 4 spikes/30 stimuli by unilateral injection of 50 nl KA into the vlPAG. Conversely, 50 nlof DLH in the vlPAG reduced the number of action potentials of 5 rVLM neurons from 30 +/- 4 to 18 +/- 4 spikes/30 stimuli. We conclude that the inhibitory influence of EA involves vlPAG stimulation, which, in turn, inhibits rVLM neurons in the EA-related attenuation of the cardiovascular excitatory response during visceral afferent stimulation.
机译：导水管周围灰色区（PAG）在调节自主神经流出和心血管功能中是重要的整合区域，在针刺体细胞传入刺激过程中可能作为长循环途径的一部分，作为调节中心。由于腹侧PAG（vlPAG）为有眉针腹侧延髓（rVLM）提供输入，该区域是电针（EA）调节交感神经流出的重要区域，因此我们假设vlPAG在EA相关的rVLM运动前交感神经元的调制中发挥作用在内脏传入刺激和自主神经兴奋性反射过程中被激活。对猫进行麻醉和通气，并监测心率和平均血压。每隔10分钟在胆囊中浸入缓激肽（BK，10杯/毫升）中的少量滤纸刺激内脏神经，从而引起持续的心血管反射反应。 EA在位于正中神经上方的心包子午线（P5-6）穴位上进行双侧刺激，在持续60分钟或60分钟的时间内，血压的升高从34 +/- 3 mmHg降低到18 +/- 5 mmHg。更多。用50-75 nl的海藻酸（KA，1 mM）使vlPAG中的神经元活性单方面失活，将BK诱导的胆囊刺激过程中的血压响应从18 +/- 3 mmHg恢复到36 +/- 5 mmHg。持续了30分钟。在没有EA的情况下，vlPAG中单侧显微注射兴奋性氨基酸dl-同型半胱氨酸（DLH，4 nM）可以模仿EA的作用并将反射性血压反应从35 +/- 6降低至14 +/- 5毫米汞柱21种心血管交感兴奋rVLM神经元的反应（包括12种被确定为运动前神经元）与心血管反应平行。因此，通过EA将内脏神经诱发的神经元放电在6个神经元中产生32 +/- 4尖峰/ 30刺激，通过EA减少到10 +/- 2尖峰/ 30刺激，通过EA迅速恢复到28 +/- 4尖峰/ 30刺激。向vlPAG中单侧注射50 nl KA。相反，vlPAG中的50 nlof DLH将5个rVLM神经元的动作电位数从30 +/- 4减少到18 +/- 4尖峰/ 30刺激。我们得出的结论是，EA的抑制作用涉及vlPAG刺激，进而在内脏传入刺激期间抑制EA相关的心血管兴奋性反应减弱中的rVLM神经元。

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