杨兆坤¹，王晓宇¹，何　伟¹，石　宏¹，宿杨帅¹，胡　玲¹，景向红¹

（1 中国中医科学院针灸研究所, 北京 100700）

摘要：研究目的：同步观察电针足三里、中脘穴对胃酸伤害性刺激大鼠胃运动，孤束核内脏感觉神经元及迷走神经背核内脏运动神经元的影响，比较电针不同穴位调节胃运动效应的差异及机制。研究方法： 36只SD大鼠随机分为胃酸伤害性刺激组,电针足三里穴干预组和电针中脘穴干预组。使用0.5M/L盐酸灌胃（1ml/100g体重）造成大鼠的胃酸伤害性刺激。通过在胃窦部肌肉层放置双极导联，以及在脑干放置阵列电极，同步记录胃酸伤害性刺激对大鼠胃电活动，及孤束核、迷走神经背核神经元胞外放电的影响，观察电针刺激足三里、中脘穴前后的变化。研究结果：胃酸伤害性刺激（0.5M/L盐酸灌胃）导致胃电慢波(GSW)的积分和孤束核、迷走神经背核胃酸伤害性刺激相关神经元胞外放电频率的变化。其中胃电慢波的积分和孤束核胃酸伤害性刺激兴奋神经元的放电频率在灌胃后90秒至45分钟之间明显增加（P＜0.01），迷走神经背核胃酸伤害性刺激抑制神经元的放电频率在灌胃后4分钟至1个小时之间明显减少（P＜0.01）。电针足三里、中脘穴的干预在灌胃后10分钟至40分钟之间进行。电针足三里、中脘穴均可抑制胃酸伤害性刺激引起的胃电慢波积分增加（P＜0.05），电针这两个穴位所产生的抑制作用无显著差别（P＞0.05）。电针足三里、中脘穴均可抑制孤束核胃酸伤害性刺激兴奋神经元的放电频率（P＜0.05），电针足三里穴的抑制效应较电针中脘穴更加明显（P＜0.05）。电针足三里、中脘穴对迷走神经背核中胃酸伤害性刺激抑制神经元的放电频率无明显影响（P＞0.05）。结论：电针足三里穴和中脘穴均可抑制胃酸伤害性刺激下胃运动的亢进，这个抑制效应与电针抑制胃酸伤害性刺激的内脏感觉传入密切相关。电针足三里穴与中脘穴效应的差别可能在于：电针异神经节段的”足三里穴”主要通过孤束核发挥效应，电针同神经节段的中脘穴主要通过脊髓背角的感觉神经元发挥效应。

关键词：电针，穴位，胃酸伤害性刺激，内脏感觉，内脏运动

Effect of electroacupuncture at ST36 and CV12 on visceral sensory and motor in gastric acid challenge rat

YANG Zhaokun1, WANG Xiaoyu1, HE Wei1, SHI Hong1, SU Yangshuai1, HU Ling1, JINGXianghong1

(1 Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Sciences, Beijing ,100700)

Abstract: Objective: The aim of this study was to synchronous observe the regulative effect of  electroacupuncture (EA) at ST36 and CV12 on gastrointestinal motility and the firing rate of gastric related neurons in the NTS and DMV after intragastric administration of acid. Methods: 36 rats were randomly divided into three groups: intragastric acid administration group, EA ST36 group and EA CV12 group. Neuronal spikes in the rat brainstem after intragastric administration of HCl(0.5 mol/L) was recorded by electrode, which was acutely implanted to span the the nucleus of solitary tract (NTS) and dorsal motor nucleus of vagus (DMV). EGG was continuously monitored and recorded synchronously by the bipolar electrode, which was in the muscle layer of gastric Antrum. Results: Intragastric administration of 0.5M/L HCL led to a rapid increase in integral of gastric slow wave (GSW) and firing rates of excitatory neurons in the NTS, which was significant at 90 seconds and remained elevated for 45mins（P＜0.01）. Acid administration led to a slow decline in firing rates of inhibitory neurons in the DMV that was significant at 4 mins and continued to decline for 1 hour（P＜0.01）. In the time-window from 8 mins to 30 mins after intragastric acid administration, EA at ST36 and CV12 elicited inhibitory effects on severe gastric motility. There was no difference between EA at ST36 and CV12（P＞0.05）. EA at ST36 and CV12 elicited inhibitory effects on excitatory neurons in NTS with intragastric acid administration, and the inhibition rate induced by EA ST36 significantly increased in comparison with EA CV12（P＜0.05）. EA at ST36 and CV12 did not cause significant changes in firing rates of inhibitory neurons in DMV（P＞0.05）. Conclusion: In conclusion, EA at ST36 and CV12 regulated gastric nociceptive visceral afferent in NTS, rather than visceral motor efferent in DMV in gastric acid challenge. The difference between the two points possibly connected with different never afferent. EA at ST36 directly contacted with NTS through the vagus visceral afferent, and EA at CV12 through sympathetic splanchnic afferent contacted with spinal dorsal horn.

Key words: Electroacupuncture, Acupoint, Gastric Acid Challenge，Visceral Sensory, Visceral Motor