Iwa Masahiro, Nakade Yukiomi, Pappas Theodore N, Takahashi Toku
Department of Surgery, Duke University and Durham Veterans Affairs Medical Center, Durham, North Carolina 27705, USA.
Dig Dis Sci. 2006 Aug;51(8):1493-500. doi: 10.1007/s10620-006-9083-7. Epub 2006 Jul 26.
Acupuncture has been used for treating functional gastrointestinal (GI) disorders. Animal studies have demonstrated that acupuncture antagonized various stress-induced responses. We investigated the effects of electroacupuncture (EA) at ST-36 (Zusanli; lower limb) on stress-induced alteration of GI motor activities. Solid gastric emptying was significantly delayed by restraint stress (29.6+/-2.4%; n=7) compared to that of controls (60.0+/-2.5%; n=8). Delayed gastric emptying was significantly improved by EA at ST-36 (47.2+/-1.8%). Intracisternal (IC) injection of corticotropin releasing factor (CRF; 1 microg) delayed gastric emptying to 25.4+/-3.1%, which was also improved by EA at ST-36, to 53.0+/-7.1% (n=8). The stimulatory effect of EA on stress-induced delayed gastric emptying was abolished by atropine (17.6+/-1.9%) but not by guanethidine (42.2+/-2.3%). Colonic transit was significantly accelerated by restraint stress (GC=7.2+/-0.3; n=8) compared to that of controls (GC=5.2+/-0.2; n=8). Accelerated colonic transit was significantly reduced by EA at ST-36 (GC=4.9+/-0.3). IC injection of CRF accelerated colonic transit (GC=6.9+/-0.2), which was also normalized by EA at ST-36 (GC=4.7+/-0.2). The inhibitory effect of EA on stress-induced acceleration of colonic transit was not affected by guanethidine (GC=4.6+/-0.3). In conclusion, EA at ST-36 showed dual effects: stimulation of stress-induced delayed gastric emptying and inhibition of stress-induced acceleration of colonic transit. The stimulatory effect of EA on stress-induced delayed gastric emptying is mediated via cholinergic pathways. The inhibitory effect of EA on stress-induced acceleration of colonic transit is independent of the sympathetic pathway.
针刺已被用于治疗功能性胃肠疾病。动物研究表明,针刺可对抗各种应激诱导的反应。我们研究了电针刺激足三里穴(位于下肢)对应激诱导的胃肠运动活动改变的影响。与对照组(60.0±2.5%;n = 8)相比,束缚应激显著延迟了固体胃排空(29.6±2.4%;n = 7)。电针刺激足三里穴显著改善了延迟的胃排空(47.2±1.8%)。脑池内注射促肾上腺皮质激素释放因子(CRF;1微克)使胃排空延迟至25.4±3.1%,电针刺激足三里穴也将其改善至53.0±7.1%(n = 8)。阿托品(17.6±1.9%)可消除电针刺激对应激诱导的延迟胃排空的促进作用,而胍乙啶(42.2±2.3%)则不能。与对照组(GC = 5.2±0.2;n = 8)相比,束缚应激显著加速了结肠转运(GC = 7.2±0.3;n = 8)。电针刺激足三里穴显著降低了加速的结肠转运(GC = 4.9±0.3)。脑池内注射CRF加速了结肠转运(GC = 6.9±0.2),电针刺激足三里穴也使其恢复正常(GC = 4.7±0.2)。电针刺激对应激诱导的结肠转运加速的抑制作用不受胍乙啶影响(GC = 4.6±0.3)。总之,电针刺激足三里穴显示出双重作用:刺激应激诱导的延迟胃排空和抑制应激诱导的结肠转运加速。电针刺激对应激诱导的延迟胃排空的促进作用是通过胆碱能途径介导的。电针刺激对应激诱导的结肠转运加速的抑制作用与交感神经途径无关。