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目的通过观察Cajal间质细胞介导的糖尿病大鼠和普通大鼠胃离体平滑肌条的收缩功能,体外高糖状态对大鼠胃离体平滑肌条收缩功能的影响,以及糖尿病大鼠胃壁Cajal间质细胞含量及形态学的改变,探讨Cajal间质细胞在糖尿病胃轻瘫发病机制中的作用。方法 (1)动物分组处理:将20只雄性Wistar大鼠随机分为正常对照组、1型糖尿病组。后组以腹腔注射STZ建立1型糖尿病动物模型。(2)胃离体平滑肌条收缩功能的测定:用瞿颂义方法,取胃体上1/3和胃窦环行肌肌条,与张力换能器相连,并输入生理记录仪,记录糖尿病组和对照组胃肌条的机械收缩运动。(3)给予体外不同浓度高糖,观察胃离体平滑肌条收缩状态的变化。(4)用免疫组化的方法,比较糖尿病组和对照组胃壁Cajal间质细胞含量及形态学的改变。结果与正常组比较,糖尿病组液体胃排空率较正常对照组显著延迟(正常组74.38±3.62%,糖尿病组52.00±5.40%)(P<0.01);糖尿病大鼠胃平滑肌条体外收缩振幅和频率较正常对照组减少(P<0.05);体外高血糖状态并没有直接影响到胃平滑肌条的收缩;免疫组化结果显示糖尿病组Cajal间质细胞在胃体及胃窦的分布稀疏,数量减少,胃体与胃窦的减少比较没有明显差异。结论本研究结果显示,Cajal间质细胞的病变可能是糖尿病胃轻瘫的重要发病机制,而体外高糖状态不作为直接导致为平滑肌收缩功能异常的独立危险因素。
Objective To observe the effects of interstitial cells-mediated contractile function of smooth muscle strips of gastric smooth muscle strips of diabetic rats and normal rats on the contractile function of gastric smooth muscle strips in vitro and the changes of Cajal The content and morphological changes of Cajal cells, and explore the role of Cajal interstitial cells in the pathogenesis of diabetic gastroparesis. Methods (1) Animal grouping: 20 male Wistar rats were randomly divided into normal control group and type 1 diabetic group. The latter group was given intraperitoneal injection of STZ to establish type 1 diabetic animal model. (2) Determination of contractile function of isolated gastric smooth muscle strips: Using the method of Qu Songyi, take the upper third of the gastric body and the antral muscle strips of the gastric antrum connected with the tension transducer and input the physiological recorder to record the diabetic group and the control Mechanical muscle contraction of gastric muscle strips. (3) To give different concentrations of high glucose in vitro to observe the change of contractile state of gastric smooth muscle strips. (4) Immunohistochemical method was used to compare the content of Cajal interstitial cells and morphological changes of gastric wall in diabetic group and control group. Results Compared with the normal group, the gastric emptying rate of diabetic group was significantly delayed than that of the normal control group (74.38 ± 3.62% in the normal group and 52.00 ± 5.40% in the diabetic group) (P <0.01); the amplitude of gastric smooth muscle strips contracted in vitro and (P <0.05). The in vitro hyperglycemia did not directly affect the contractions of gastric smooth muscle strips. Immunohistochemistry showed that the distribution of Cajal interstitial cells in gastric and gastric antrum was sparse and the number decreased There was no significant difference in the reduction of gastric body and gastric antrum. Conclusion The results of this study show that the pathological changes of Cajal interstitial cells may be an important pathogenesis of diabetic gastroparesis. However, the in vitro high glucose status is not an independent risk factor for the contractile function of smooth muscle.