摘要
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。方法选择健康Wistar大鼠30只,随机分为对照组、假手术组和模型组,每组10只。模型组应用油酸经胰胆管灌注的方法制作CP模型,假手术组大鼠开腹后仅翻动十二指肠并触摸胰腺数次,对照组大鼠不进行任何手术。造模时间为6周。然后分别检测3组大鼠粪脂肪滴计数、粪弹力蛋白酶1(FE-1)、胰腺病理以及血清胆囊收缩素(CCK)的水平;同时观测胃窦环行平滑肌肌条及细胞收缩变化;反转录-聚合酶链式反应法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(NO)含量的变化。结果与假手术组比较,模型组大鼠粪脂肪滴个数显著增加,粪FE-1水平显著降低,胰腺呈典型CP改变。模型组大鼠胃窦环行平滑肌条收缩能力和细胞收缩反应较假手术组和对照组显著下降,血清CCK水平、胃肌层iNOSmRNA表达量及平滑肌细胞培养基中NO水平均较假手术组和对照组显著升高,差异有统计学意义(P<0.05)。结论CP大鼠胰腺外分泌功能不全可导致CCK分泌增加,引起胃窦肌层iNOSmRNA的表达上调并产生过量的NO,从而抑制胃窦环行平滑肌的收缩能力,这可能是CP胃运动功能障碍的机制之一。
Objective To explore the changes of gastric motility and the possible mechanism in the rats with chronic pancreatitis.Methods Thirty Wistar rats were divided into control,sham and model group randomly（n=10）.Rats in model group were used to induce chronic pancreatitis by injecting oleic acid into the pancreatic duct.No operation was performed in control group while laparotomy was performed in sham group.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.Reverse transcription-polymerase chain reaction was adopted to detect the expression of inducible nitric oxide synthase（iNOS）mRNA within 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 sham and there were typical pathologic changes of chronic pancreatitis 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 the sham（P0.05）while the levels of serum CCK,iNOS mRNA expression and NO production were significantly elevated（P0.05）.Conclusions Elevated CCK secretion caused by insufficiency of pancreatic exocrine secretion up-regulated the expression of iNOS mRNA and increased the output of NO within the gastric muscularis.It might be one of the mechanisms of gastric motility dysfunction in chronic pancreatitis that NO inhibited the contractility of gastric circular smooth muscle.
出处
《医学综述》
2010年第5期770-772,共3页
Medical Recapitulate
