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目的:探讨胃肠舒促进胃肠动力的作用机制。方法:将50只Wister大鼠随机分为正常对照组、模型对照组、胃肠舒小剂量组、胃肠舒大剂量组、西沙必利组。除正常对照组外,其余四组均制备胃肠动力障碍动物模型。各组用等容积的受试药液灌胃,连续7天,将各组动物麻醉后选取胃肠标本。免疫组化法观察神经递质Ach的表达变化,图像分析仪测定其肌间神经丛光密度值。结果:胃肠舒组及西沙必利组均能明显升高胃肠组织中AchE含量,与模型组比较有显著差异(P<0.01),胃肠舒大剂量组升高胃窦中AchE含量较西沙必利组显著(P<0.01)。结论:通过增加胃肠道Ach分泌,Ach作用于平滑肌M受体,开放质膜上L型Ca2+通道,使Ca2+内流而加强胃肠平滑肌收缩。
Objective: To explore the mechanism of gastrointestinal motility promoting gastrointestinal motility. Methods: Fifty Wistar rats were randomly divided into normal control group, model control group, Weishushu low dose group, Weiweishu high dose group, and Cisapride group. In addition to the normal control group, the other four groups were prepared animal models of gastrointestinal motility disorders. Each group was intragastrically administered with an equal volume of the test liquid for 7 consecutive days. The gastrointestinal specimens were selected after anesthetizing the animals in each group. The expression of neurotransmitter Ach was observed by immunohistochemistry and the optical density of myenteric nerve plexus was measured by image analyzer. RESULTS: Gastrointestinal and cisapride groups all significantly increased AchE content in gastrointestinal tissues, which was significantly different from that in the model group (P<0.01). Gastrointestinal high-dose group had higher AchE content in gastric antrum. Cisapride group was significantly (P<0.01). CONCLUSION: By increasing Ach secretion in the gastrointestinal tract, Ach acts on the smooth muscle M receptor and opens the L-type Ca2+ channel on the plasma membrane, causing Ca2+ influx and enhancing gastrointestinal smooth muscle contraction.