电针足三里激活胆碱能抗炎通路抗大鼠失血性休克的研究

Study on electroacupuncture at Zusanli points(足三里穴) against hemorrhagic shock of rats through activating cholinergic antiinflammatory pathway

目的：观察电针足三里穴对失血性休克大鼠平均动脉压（MAP）、动脉血乳酸及生存指标的影响，探讨其对失血性休克的保护作用及其可能机制。方法：100只雄性SD大鼠按随机数字表法分为假休克组、休克组、非经非穴组、足三里组、迷走神经切断组、迷切后电针组、M受体拈抗组、N受体拮抗组、N受体α-7亚单位拈抗组和胆碱酯酶抑制组10组，每组10只。采用股动脉间断放血法复制失血性休克模型，于模型制备成功即刻（Omin），以2～4V和3Hz的强度持续电针刺激双侧足三里穴30min。刺激开始前颈总动脉置管连续监测MAP,0min和43min时分别取股动脉血检测乳酸值。另取40只大鼠随机分为假休克组、休克组、非经非穴组和足三里组（处理与以上前4组相同）4组，观察生存状况，除此以外不作其他干预，记录生存时间及存活率。结果：休克组MAP持续较低。43min时的乳酸值较0min明显上升，平均生存时间和各时间点的存活率也显著降低（P均〈0．01）；而非经非穴组上述情况与休克组相比无明显改变（P均〉0．05）；但电针足三里穴后MAP迅速显著升高，43min时的乳酸值较0min显著下降，平均生存时间和各时间点的存活率均显著提高（P均〈0．01）。电针足三里前离断迷走神经，上述作用则完全消失。电针足三里前静脉注射阿托品，仍可产生与足三里组类似的保护效应，但电针足三里前静脉注射六烃季胺或α-BGT，均可完全抵消上述保护效应。结论：电针足三里穴具有潜在的抗失血性休克作用，并且是通过激活胆碱能抗炎通路而实现的。

Objective： To investigate the therapeutic effect and mechanism of electroacupuncture （EA） at Zusanli points （足三里穴） on the changes of mean arterial pressure （MAP）, arterial lactate levels and survival indexes in rats with hemorrhagic shock （HS）. Methods： One hundred SD rats were randomly divided into ten groups （n= 10） ： sham shock group, HS group, non - acupoint group, Zusanli point group, bilateral cervical vagotomy group, vagotomy and EA group, muscarinic antagonist group, nicotinic antagonist group, α-bungarotoxin （α- BGT） group and tetrahydroaminoacridine （THA） group. Zusanli points were electroacupunctured with constant voltage （2 - 4V, 3 Hz） for 30 minutes immediately after the shock model was established. Before the stimulation the carotid artery was intubated for continuously mornitoring MAP. The levels of serum lactate in the femoral artery were detected at 0 and 43 minutes. Another 40 rats were randomly divided into sham shock group, HS group, non -acupoint group and Zusanli point group. Survival time and survival rate were observed in the four groups. Results： MAP was lower continuously, and the survival time and survival rate were lower in HS group, the levels of lactate was higher at 43 minutes compared with that of 0 minute （all P〈0. 01）. The differences of MAP, lactate level, survival time and survival rate were not significant in non -acupoint group compared to those of the HS group （all P〉.0. 05）. After EA at Zusanli point, MAP, survival time and survival rate gradually increased but lactate obviously decreased at 43 minutes compare with that at 0 minute （all P〈0. 05）. And muscarinic antagonist group still had such effects （P〈0. 01）, but nicotinic antagonist group and tx -BGT group had no such effects （P〉0.05）. Atropine injected intravenously before EA at Zusanli point could produce the protective effects as same as that of Zusanli group, but after injecting hexamethonium bromide or α- BGT, the protective effects disappeared. Conclusion： The results suggest that EA Zusanli points produce a protective effect on HS of rats by the way of activating cholinergic anti-inflammatory pathway.