慢性胰腺炎大鼠胃运动功能的变化及机制研究

目的：探讨慢性胰腺炎（CP）大鼠胃运动功能的变化及可能机制。方挂：健康Wistar大鼠30只，随机分为对照组、假手术组、实验组，每组10只。实验组应用油酸经胰胆管灌注的方法制作慢性胰腺炎模型，造模时间为6周。分别检测各组粪脂肪滴计数，粪弹力蛋白酶I（FE—1）及胰腺病理检查验证实验；检测血清胆囊收缩素（CCK）水平；观测胃窦环行平滑肌肌条收缩能力、环行平滑肌细胞收缩反应的变化；测定胃肌层诱导型一氧化氮合酶（iNOS）mRNA的表达量和平滑肌细胞培养基中一氧化氮（N0）含量的变化。结果：与假手术组比较，实验组大鼠粪脂肪滴个数明显增加、粪FE-1水平明显降低，胰腺呈典型慢性胰腺炎改变。胃窦环行平滑肌条收缩能力、环行平滑肌细胞收缩反应明显下降（P〈0．05），血清CCK水平，iNOSmRNA的表达量，细胞培养基中NO含量均明显升高（P〈0．05）。结论：慢性胰腺炎大鼠胰腺外分泌功能不全可导致CCK分泌增加，而CCK通过上调胃窦肌层iNOSmRNA的表达并产生过量的NO，抑制胃窦环行平滑肌的收缩能力可能是慢性胰腺炎胃运动功能障碍的机制之一。

Changes of gastric motility and mechanism in rats with chronic pancreatitis

Objective： To explore the changes of gastric motility and the possible mechanism in the rats with chronic pancreatitis （CP）. Methods： Thirty Wistar rats were divided into control, sham and model group randomly （n=10）. Model of CP were induced by injecting oleic acid into the pancreatic duct. No operation was performed in control group while laparotomy was performed in sham. Six weeks after the operation, spot fecal fat, fecal elastase-1（FE-1） and pathologic examination of pancreas were used to verify the models. Serum cholecystokinin （CCK） was detected, contractility of gastric circular muscle stripe and the contractile response of dispersed gastric circular smooth muscle cells stimulated by aceylcholine （Ach） were measured. RT-PCR was used to detect the expression of inducible nitric oxide synthase （iNOS） mRNA in gastric muscularis, the level of nitric oxide （NO） in cell cultures was quantified. Results： The counts of fecal fat in model group increased, level of FE-1 decreased obviously than in sham and there were typical pathologic changes of CP in model group, gastric circular smooth muscle stripes contractility and contractile response of dispersed circular smooth muscle cells stimulated by Ach were declined obviously than those in the sham （P〈0.05） while the levels of serum CCK, iNOS mRNA expression and NO production were significantly elevated （P〈0.05）. Conclusion： Elevated CCK secretion caused by insufficiency of pancreatic exocrine secretion up-regulates the expression of iNOS mRNA and increases the output of NO within the gastric muscularis. It may be one of the mechanisms of gastric motility dysfunction in CP that NO inhibites the contractility of gastric circular smooth muscle.