西沙必利治疗胃电节律失常机制的实验研究

目的　探讨西沙必利治疗胃电节律失常的机制。方法　建立大鼠胃电节律失常模型 ,给予西沙必利治疗 ,并设正常大鼠作为对照 ,检测胃窦肌间神经丛内胆碱能神经、氮能神经及cAMP、cGMP含量变化情况。结果　西沙必利使模型大鼠胃电节律失常明显减少 ,慢波频率变异系数 (2 3 2 0± 1 89%vs36 0 1± 8 6 6 % )、异常节律指数 (6 4 3±3 6 0 %vs 18 0 1±11 0 8% )显著下降 (P <0 0 1) ;胃窦肌间神经丛内胆碱能神经增多 (2 2 95± 8 37%vs15 2 1± 5 6 0 % )、氮能神经减少 (9 5 1±3 16 %vs15 0 2± 4 4 6 % ) (P <0 0 1) ,平滑肌组织中cAMP(2 4 5 0 5 5±6 8 6 6 1FM/mgvs5 10 4 93± 2 6 9 6 79FM/mg)、cGMP(13 791± 2 15 8FM/mgvs 17 5 78± 4 5 82FM/mg)含量降低 (P<0 0 5 )。结论　西沙必利治疗胃电节律失常是通过增加胃窦肌间神经丛胆碱能神经含量、减少氮能神经含量 ,进而使胃窦平滑肌组织中cAMP、cGMP含量减少实现的。

Mechanism of cisapride in the treatment of gastric eletro-dysrhythmia

Objective To study the mechanism of cisapride in the treatment of gastricelectric dysrhythmia. Methods Cisarpride was gavage fed to rats in which gastricelectric dysrhythmia hed been reproduced. The cholinergic and nitriergic nerves in myenteric plexus of gastric antrum were examined with histochemical staining methods and whole mount preparation technique. The levels of cAMP and cGMP in the antral smooth muscle were measured by radioimmunoassay. Results Gastricelectric dysrhythmia in the model group was ameliorated after the treatment with cisapride(P<0.01). The number of cholinergic nerves was significantly increased, while the nitriergic nerves were reduced after the treatment with cisapride(P<0.01). The levels of cAMP and cGMP were much lower in cisapride group than those in the control group(P<0.05). Conclusion Cisapride ameliorates gastric electro-dysrythmia by increasing the amount of cholinergic nerves, decreasing nitriergic nerves, and reducing the levels of cAMP and cGMP.