电针大鼠足三里调节下食管括约肌压力神经通路的探讨

An Approach to Regulation of Electro-acupuncture at Zusanli Acupoint on LESP in Rats

目的通过观察胆碱能M受体阻断剂阿托品和一氧化氮合成酶抑制剂N-硝基-L-精氨酸甲酯(L-NAME)对电针足三里调节大鼠下食管括约肌压力(LESP)的影响,探讨电针调节LESP的神经通路。方法将48只Wistar大鼠随机分成对照组、电针组、阿托品组、阿托品+电针组、L-NAME组和L-NAME+电针组,应用三通道微细注水式测压管和荷兰UPS-2020型食管测压系统测定大鼠LESP。结果电针足三里可使LESP明显升高。阿托品可部分减弱电针足三里增加LESP的作用,电针可以使胆碱能神经阻断大鼠降低的LESP恢复至正常水平。L-NAME能够增加LESP,电针可以使LESP进一步增加。结论电针足三里作用的传出途径可能是迷走神经中的胆碱能神经纤维,但也有其它途径。

Objective To observe the effect of atropine and N-nitro-L-arginine methyl ester （L-NAME） on the pressure of lower esophageal sphincter （LESP） regulated by electro-acupuncturing （EA） at Zusanli acupoint （He-Sea, st 36） of stomach meridian and explore the neural mechanism of E.A. Methods Forty-eight rats were divided into six groups： control group, EA group, atropine group, atropine＋EA group, L-NAME group and L-NAME ＋ EA group. LESP was observed and recorded by using three-channel perfusion manometric measurement system. Results LESP increased significantly under or after EA at Zusanli acupoint. Cholinergic M receptor blocker partly abolished the influence of EA on,LESP, but EA could restore the decreased pressure of cholinergic M receptor blocked rats. Nitric oxide synthase （NOS） inhibitor increased LESP, and EA could make it higher. Conclusions The main efferent pathway of regulating effect of EA at Zusanli acupoint on LESP is via the chlinergic nerve of vagus, and other mechanism possibly exits.