摘要
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。
ve: To explore the pathogenesis of slow transit constipation. Methods: Thirty three female patients with STC underwent subtotalcolectomy. By using quantitative immunohis-tochemistry with computer-assisted image analysis system, resected specimens of colonic wall from 33 patients with STC and 25 nonobstructed cancer controls were studied with polyclonal an-tineurofilament antibody and monoclonal anti-S-100 protein antibody. Results: Hematoxylin and eosin staining revealed no significant histologic abnormality throughout the colonic myenteric plexus in all subjects apart from four cases with atrophic smooth muscle in the STC group. There was no significance about the content of NF inmyenteric plexus between the two groups, but ob-served microscopically, the positive granulae of NF appeared accumulated locally and stained densely. However, the mean optical density (OPTDM) of NF was higher significantly, compared with the controls (P<0.01) . The content and OPTDM of S-100 protein in colonic myenteric plexus was increased in the STC patients( P <0. 01). The courses of patients with STC had close relation with the content and with the integral of optical density (OPTDI) of S-100 protein in myenteric plexus (P<0. 02) , but not with the content of NF. Conclusions: The pathological changes of colonic myenteric nuroplexus in the patients with STC involve tolal colon. Accumulation of neurofilaments and hyerplasia of neuroglia are main causes of slow transit.
出处
《大肠肛门病外科杂志》
1999年第3期1-4,共4页
Journal of Coloproctological Surgery