Tjen-A-Looi Stephanie C, Li Peng, Longhurst John C
Department of Medicine, Susan Samueli Center for Integrative Medicine, UCI School of Medicine, University of California-Irvine, CA 92697-4075, USA.
Am J Physiol Heart Circ Physiol. 2006 Jun;290(6):H2543-53. doi: 10.1152/ajpheart.01329.2005. Epub 2006 Jan 20.
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 nl of 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.
中脑导水管周围灰质（PAG）是自主神经输出和心血管功能调节中的一个重要整合区域，在针刺体觉传入刺激过程中，它可能作为长环通路的一部分，充当调节中心。由于腹外侧PAG（vlPAG）向延髓头端腹外侧区（rVLM）提供输入，而rVLM是电针（EA）调节交感神经输出的一个重要区域，因此我们推测vlPAG在内脏传入刺激和自主神经兴奋性反射过程中，对EA相关的rVLM运动前交感神经元的调制发挥作用。对猫进行麻醉并实施通气，同时监测心率和平均血压。每隔10分钟用浸有缓激肽（BK，10微克/毫升）的滤纸棉片刺激胆囊的内脏神经，可诱发持续的心血管反射反应。在心包经（位于正中神经上的P5 - 6）穴位处进行双侧EA刺激，可使血压升高幅度从34±3毫米汞柱降至18±5毫米汞柱，并持续60分钟或更长时间。用50 - 75纳升的 kainic 酸（KA，1毫摩尔）单侧灭活vlPAG中的神经元活动，可使BK诱导的胆囊刺激期间的血压反应从18±3毫米汞柱恢复至36±5毫米汞柱，且该效应持续30分钟。在无EA刺激时，在vlPAG中单侧微量注射兴奋性氨基酸dl - 高胱氨酸（DLH，4纳摩尔）可模拟EA的作用，使反射性血压反应从35±6毫米汞柱降至14±5毫米汞柱。21个心血管交感兴奋性rVLM神经元（包括12个被鉴定为运动前神经元）的反应与心血管反应平行。因此，在内脏神经诱发的6个神经元放电中，EA可使放电频率从32±4个脉冲/30次刺激降至10±2个脉冲/30次刺激，而通过向vlPAG单侧注射50纳升KA可迅速将其恢复至28±4个脉冲/30次刺激。相反，在vlPAG中注射50纳升DLH可使5个rVLM神经元的动作电位数量从30±4个脉冲/30次刺激降至18±4个脉冲/30次刺激。我们得出结论，EA的抑制作用涉及vlPAG的刺激，进而在内脏传入刺激期间EA相关的心血管兴奋反应减弱过程中抑制rVLM神经元。
