论文部分内容阅读
目的:探索结肠慢传输型便秘的发病机制。方法:采用免疫组织化学方法研究33例慢传输型便秘的病人(STC组)和25例非便秘性结肠(对照组)升、横、降及乙状结肠肌间神经丛内神经丝蛋白和S-100蛋白的表达,并利用图像分析系统作定量分析。结果:STC组结肠HE染色显示肌间神经丛未见明显异常。免疫组织化学染色示,对照组各段肠壁肌间神经丛内神经丝蛋白和S-100蛋白的含量较恒定(P>0.05),STC组结肠各段与对照比较,神经丝蛋白的含量无明显减少(P>0.05),但出现堆积聚集现象,平均光密度明显高于对照组(P<0.01);S-100蛋白的含量及平均光密度明显高于对照组(P<0.01),且随着病程的延长而增加,二者呈直线相关(P<0.02)。结论:STC结肠肌间神经丛的病理改变是全结肠性改变,神经丝蛋白的堆积聚集和神经间质的增生是造成结肠动力减弱的主要原因。
Objective: To explore the pathogenesis of slow transit constipation. Methods: Immunohistochemical method was used to study the changes of neurofilament and S-100 in the ascending, descending, descending, and sigmoid colon myenteric plexus of 33 cases of slow transit constipation (STC group) and 25 cases of non-constipation colon (control group) Protein expression, and the use of image analysis system for quantitative analysis. Results: HE staining of colon in STC group showed no obvious abnormality in myenteric plexus. Immunohistochemical staining showed that the contents of neurofilament protein and S-100 protein in the intestinal wall myenteric plexus were constant in each group (P> 0.05). Compared with the control group, the content of neurofilament protein in STC group was no (P <0.01). The content of S-100 protein and average optical density were significantly higher than those of the control group (P <0.01), and the average optical density was significantly higher than that of the control group As the duration of the disease increased, there was a linear correlation between them (P <0.02). Conclusion: The pathological changes of colon myenteric plexus of STC are all-enteral changes. The accumulation of neurofilament protein and the proliferation of neuronal interstitium are the main causes of the decrease of colonic motility.