本文關(guān)鍵詞： Cajal 細(xì)胞 KIT 受體 BrdU 再生 干細(xì)胞因子 神經(jīng) 平滑肌細(xì)胞　出處：《第三軍醫(yī)大學(xué)》2005年碩士論文　論文類型：學(xué)位論文

【摘要】：Cajal 細(xì)胞(Interstitial cells of Cajal, ICCs) 作為一種特殊的間質(zhì)細(xì)胞,以細(xì)胞網(wǎng)絡(luò)的形式分布于整個胃腸道。近二十余年,國內(nèi)外學(xué)者通過對胃腸壁內(nèi)ICCs 的形態(tài)特征、超微結(jié)構(gòu)、起源及生理功能等的一系列研究表明:ICCs 具有產(chǎn)生自發(fā)性電慢波、參與神經(jīng)信息傳遞等功能,在調(diào)節(jié)胃腸道平滑肌運動中發(fā)揮重要作用。 動物實驗發(fā)現(xiàn):胃腸壁內(nèi)ICCs 減少、細(xì)胞網(wǎng)絡(luò)缺如的大鼠和小鼠,胃腸運動自主節(jié)律性消失,呈擴(kuò)張性腸麻痹狀態(tài),胃和腸的內(nèi)容物反流,提示ICCs 減少及其細(xì)胞網(wǎng)絡(luò)完整性的破壞可能與上述現(xiàn)象的發(fā)生有關(guān)。臨床可見胃腸道手術(shù)后患者常常出現(xiàn)一過性腸麻痹和胃腸蠕動運動功能消失等假性腸梗阻癥狀,推測可能與ICCs 細(xì)胞網(wǎng)絡(luò)斷裂和手術(shù)部位ICCs 的表型(phenotype)發(fā)生急性變化(不能被其特異性標(biāo)志物所染色),喪失正常功能有關(guān)。近年臨床研究亦發(fā)現(xiàn)ICCs 與一些胃腸運動功能障礙性疾病:例如賁門失弛緩癥、慢傳輸型便秘、假性腸梗阻、先天性巨結(jié)腸等密切相關(guān)。盡管上述疾病的發(fā)生機(jī)制尚不清楚,但均有一個共同的特點:病變部位胃腸壁內(nèi)ICCs數(shù)量呈不同程度減少,甚至缺如,ICCs 彼此間及其與平滑肌之間不能形成完整的細(xì)胞網(wǎng)絡(luò)。但因?qū)ι鲜黾膊〉陌l(fā)病機(jī)理及ICCs 減少、細(xì)胞網(wǎng)絡(luò)完整性被破壞的原因等尚不清楚,一直是臨床治療的難題。 設(shè)想如果能夠闡明成年動物消化管壁內(nèi)ICCs 損傷丟失后,是否通過再生、細(xì)胞突起生長延長、重新形成細(xì)胞網(wǎng)絡(luò)的調(diào)控機(jī)制,勢必可為臨床相關(guān)疾病的治療及腹部外科術(shù)后胃腸運動功能的恢復(fù)提供有益的思路。因此,本實驗利用外科手術(shù)的方法,模擬術(shù)后胃腸運動功能障礙,制作小腸壁內(nèi)ICCs 受損及細(xì)胞網(wǎng)絡(luò)完整性被破壞的動物模型,結(jié)合免疫組化染色、雙重標(biāo)記技術(shù)、透射電鏡觀察等方法,動態(tài)分析小腸半橫斷吻合術(shù)后ICCs 的變化。該模型不僅能夠使我們了解小腸術(shù)后ICCs 的變化,同時也有助于闡明成年動物腸壁內(nèi)ICCs 是否具有分裂增殖能力、隨著時間的經(jīng)過ICCs 的突起能否通過生長延長重新形成細(xì)胞網(wǎng)絡(luò),及其平滑肌細(xì)胞和神經(jīng)對此過程的影響等問題,為治療胃腸運動功能障礙性疾病開辟新的思路和方法。 主要結(jié)果如下: 根據(jù)吻合斷端的特點,將其分為3 區(qū)域:Ⅰ區(qū)位于腸壁橫斷末端,平滑肌層因回縮而稍增厚,該區(qū)突出于腸腔;Ⅱ區(qū)是緊靠Ⅰ區(qū)正常側(cè)的平滑肌層,是吻合部位,由于縫線張力的牽拉作用使該區(qū)腸壁肌層變薄;Ⅲ區(qū)是Ⅰ區(qū)和Ⅱ區(qū)漿膜面與吻合中線間的區(qū)域。
[Abstract]:As a special mesenchymal cell, Cajal cells are distributed in the whole gastrointestinal tract in the form of cellular network. In the past 20 years, the morphological features and ultrastructure of ICCs in the wall of stomach and intestine were analyzed by domestic and foreign scholars. A series of studies on the origin and physiological function of ICCs have shown that ICCs have the functions of producing spontaneous slow waves and participating in the transmission of neural information. They play an important role in regulating the movement of gastrointestinal smooth muscle. Animal experiments showed that in rats and mice with decreased ICCs in gastrointestinal wall and absent cellular network, the autonomic rhythm of gastrointestinal motility disappeared, showing dilated intestinal paralysis, and reflux of the contents of stomach and intestine. The results suggest that the decrease of ICCs and the destruction of cellular network integrity may be related to the occurrence of these phenomena. The clinical symptoms of pseudo-intestinal obstruction such as transient intestinal paralysis and disappearance of gastrointestinal peristaltic motor function are often found in patients with gastrointestinal tract operation. It is speculated that the acute changes of ICCs cell network breakage and phenotype of ICCs at the site of operation (which can not be stained by its specific markers) may be related to the loss of normal function. In recent years, clinical studies have also found that ICCs and some gastrointestinal motility have been involved. Disorders such as achalasia, Slow transit constipation, pseudo-intestinal obstruction and Hirschsprung's disease are closely related. Although the pathogenesis of these diseases is not clear, they all have a common characteristic: the number of ICCs in gastrointestinal wall decreases in varying degrees. Even without ICCs and smooth muscle cells can not form a complete network, but the pathogenesis of the disease and the reduction of ICCs, the reasons for the destruction of the integrity of the cell network are still unclear, which has been a difficult problem in clinical treatment. Imagine that if we can clarify the regulatory mechanisms of ICCs damage loss in the digestive walls of adult animals, whether it is possible to regenerate, prolong the growth of the cell processes and reform the cellular network. It will provide useful ideas for the treatment of clinical related diseases and the recovery of gastrointestinal motility after abdominal surgery. The animal model of damaged ICCs and damaged cellular network integrity in the small intestine wall was made by immunohistochemical staining, double labeling technique, transmission electron microscopy and other methods. Dynamic analysis of the changes of ICCs after semi-transverse anastomosis of small intestine. This model can not only help us understand the changes of ICCs after intestinal surgery, but also help us to clarify whether the ICCs in the intestinal wall of adult animals has the ability to divide and proliferate. Over time, whether the processes of ICCs can reform the cellular network through growth prolongation, and the effects of smooth muscle cells and nerves on this process, will open up new ideas and methods for the treatment of gastrointestinal motility disorders. The main results are as follows:. According to the characteristics of anastomotic end, it is divided into three regions: zone I is located at the end of the transverse section of the intestinal wall, the smooth muscle layer is slightly thickened by the retraction of the smooth muscle layer, and the region protrudes out in the intestinal cavity, and area 鈪，

本文編號：1530860