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背景:有关脑-胃肠综合征的研究国内外多从临床应激性消化道出血角度来探讨,缺乏相关实验理论依据。目的:观察脑出血血肿高峰阶段,胃肠局部生长抑素通过旁分泌机制,对胃黏膜组织中胃泌素的调节作用,阐明脑出血时脑-胃肠综合征的发生与胃肠局部脑肠肽平衡失调的内在联系。设计:随机对照的实验研究。地点和对象:实验地点:解放军第三军医大学大坪医院动物实验中心,动物采用Wistar大鼠40只。干预:建立大鼠脑出血动物模型,应用原位杂交技术分析胃肠局部表达生长抑素mRNA的阳性细胞变化,同期测定胃黏膜组织中胃泌素的含量,并与表达生长抑素mRNA阳性细胞计数值进行相关分析。主要观察指标:生长抑素mRNA的表达及胃泌素的活性测定。结果:脑出血的高峰期,胃肠局部生长抑素mRNA表达明显增强。与此同时,相同部位组织中胃泌素的含量明显升高,两者之间呈现显著的正相关(r=0.36;P<0.05)。结论:脑出血血肿形成的高峰期,通过上调生长抑素mRNA的表达和抑制胃泌素的产生,预防脑胃肠综合征的发生。
BACKGROUND: Studies on brain-gastrointestinal syndrome are mostly studied at home and abroad from the angle of clinical stress gastrointestinal bleeding, lacking the relevant experimental theory basis. Objective: To observe the peak stage of intracerebral hemorrhage hematoma, gastrointestinal somatostatin through the paracrine mechanism of gastric mucosal tissue gastrin regulation, elucidation of cerebral hemorrhage brain - gastrointestinal syndrome and gastrointestinal local brain The intrinsic link between peptide imbalances. Design: Randomized controlled experimental study. Location and Subjects: Experimental Location: Animal Experiment Center, Daping Hospital, Third Military Medical University of PLA, 40 Wistar rats were used in the experiment. Intervention: The animal model of intracerebral hemorrhage in rats was established. The in situ hybridization was used to analyze the changes of somatostatin mRNA expression in the stomach and intestine. Gastrin levels in gastric mucosa were measured at the same time. The expressions of somatostatin mRNA positive cells Counting values for correlation analysis. MAIN OUTCOME MEASURES: Expression of somatostatin mRNA and determination of gastrin activity. Results: At the peak of cerebral hemorrhage, the expression of somatostatin mRNA in gastrointestinal tract increased significantly. At the same time, the content of gastrin in the same tissue was significantly increased, showing a significant positive correlation (r = 0.36; P <0.05). Conclusion: The peak of cerebral hematoma formation can prevent the occurrence of gastrointestinal syndrome by up-regulating the expression of somatostatin mRNA and inhibiting the production of gastrin.