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目的:探讨大鼠慢性支气管炎对结肠组织的影响。方法:采用改良烟熏法进行大鼠慢性支气管炎的造模,在不同时间段通过比较粪便干湿重、粪便含水率、胃残留率、小肠推进率,并对大鼠肺肠组织切片,测量肺肠组织中降钙素基因相关肽(CGRP)表达含量。结果:病理上,造模后模型组大鼠肺组织出现慢性炎症改变,结肠组织出现炎症改变。与空白组比较,模型组大鼠造模开始后第20天胃残留率明显增加,小肠推进率明显下降,肺肠CGRP表达明显增加(P<0.01);在第50天,模型组大鼠粪便干重明显增加,粪便含水率明显降低,胃残留率明显增加,小肠推进率明显下降,肺肠CGRP表达明显增加(P<0.01);在第70天,模型组大鼠粪便湿重明显减轻,干重明显增加,粪便含水率明显降低,胃残留率明显增加,小肠推进率明显下降,肺肠CGRP表达明显增加(P<0.01)。结论:大鼠慢性支气管炎会引起肠组织病变,CGRP参与肺病及肠传变过程,是肺病及肠病理传变的介质之一。
Objective: To investigate the effect of chronic bronchitis on colon in rats. Methods: The rat model of chronic bronchitis was established by modified smoking method. The wet and dry weight of feces, the stool moisture content, the residual rate of small intestine and the rate of intestinal propulsion were compared at different time points. Expression of calcitonin gene-related peptide (CGRP) in lung tissue. Results: Pathologically, the lung tissue of rats in the model group showed chronic inflammatory changes and inflammatory changes in the colon tissues. Compared with the blank group, the gastric residual rate increased significantly, the small intestine propulsion rate decreased obviously, and the expression of CGRP in lung tissue increased significantly (P <0.01). On the 50th day, the feces of rats in the model group (P <0.01). On the 70th day, the wet weight of the feces of the model group was significantly reduced, the dry weight was significantly increased, the stool moisture content was significantly decreased, the gastric residual rate was significantly increased, the small intestine propulsion rate was significantly decreased, lung CGRP expression was significantly increased The dry weight was significantly increased, the stool water content was significantly reduced, the gastric residual rate was significantly increased, the small intestine propulsion rate was significantly decreased, lung CGRP expression was significantly increased (P <0.01). Conclusion: Chronic bronchitis in rats can cause intestinal tissue lesions. CGRP is involved in lung diseases and intestinal metachronous changes. It is one of the mediators of pulmonary pathology and intestinal pathological changes.