中文摘要：

目的：观察多器官功能障碍综合征（MODS）大鼠小肠深肌层Cajal间质细胞（ICC-DMP）的凋亡现象，以及表型标志酪氨酸激酶受体（c-kit）、线粒体凋亡信号通路Bcl-2和Bax表达的变化，揭示MODS状态下胃肠运动功能障碍的机制。方法健康成年Wistar大鼠40只，按随机数字表法分为对照组（20只）和MODS组（20只）。经腹腔注射8×10^8 cfu/mL大肠杆菌混悬液1 mL制备细菌性腹膜炎致MODS大鼠模型；对照组给予等量生理盐水。制模24 h后，取大鼠上段小肠肌层制作全厚标本，分别应用透射电镜扫描、免疫荧光双标染色、激光扫描共聚焦显微镜，观察两组大鼠小肠ICC-DMP的超微结构、网络结构及c-kit和Bax/Bcl-2的表达。结果大体标本观察显示：对照组大鼠胃肠蠕动正常；MODS组大鼠麻痹性胃肠梗阻症状明显。透射电镜下观察显示：ICC-DMP中间丝结构清晰，无肿胀线粒体，染色质分布均匀，核周聚集少量异染色质；MODS组ICC-DMP中间丝模糊，线粒体肿胀明显，细胞核内有大量染色体聚集。共聚焦显微镜下观察显示：对照组ICC-DMP网络结构清晰，c-kit和Bcl-2表达强烈且区域重合，而Bax表达较弱并呈散点样分布；MODS组ICC-DMP数量较对照组显著减少（个/HP：15.80±2.30比25.70±3.97，t＝6.819，P＝0.000），网络完整性损伤明显；c-kit和Bcl-2的表达较对照组明显降低〔c-kit（荧光强度）：129.56±36.90比307.23±40.07，t＝10.314， P＝0.000；Bcl-2（荧光强度）：103.23±25.19比378.92±43.79，t＝17.259，P＝0.000〕，而Bax表达较对照组明显增加（荧光强度：270.94±36.98比92.57±20.92，t＝-13.277，P＝0.000）。结论 MODS致胃肠动力障碍的机制可能与ICC-DMP超微结构损伤、c-kit表型改变和线粒体凋亡途径的激活密切相关。

英文摘要：

Objective To observe the apoptosis of interstitial cells of Cajal in deep muscular layer （ ICC-DMP ） of small intestine in rats with multiple organ dysfunction syndrome （ MODS ） as a result of bacterial peritonitis, and the expression of c-kit （ an ICC phenotype marker ） and Bax/Bcl-2, in order to investigate the mechanism of gastrointestinal motility dysfunction in MODS. Methods According to the random number table, 40 Wistar rats were randomly divided into two groups：control group （ n=20 ） and MODS group （ n=20 ）. The MODS model in rats was reproduced by intraperitoneal injection of 8×10^8 cfu/mL Escherichia coli suspension 1 mL, and the control group was given the same amount of normal saline. After 24 hours, the upper small intestine was harvested for examination. Ultrastructure of ICC-DMP was observed using electron microscope. The network structure of ICC-DMP and the expression of c-kit and Bax/Bcl-2 were observed and determined with immunofluorescence and laser scanning confocal microscope. Results Macroscopic observation revealed that the gastrointestinal motility of rats was normal in the control group. Compared with the control group, gastro intestine was significantly expanded with parulytic ileus in MODS group. It was shown by transmission electron microscopy that intermediate filament structure of ICC-DMP was clear without swelling of mitochondria; chromatin distributed uniformly with small amounts of heterochromatin aggregated in perinuclear. Compared with the control group, intermediate filament structure of ICC-DMP was fuzzy, and mitochondria were swollen obviously in MODS group;chromatin was assembled in nucleus centre. It was shown by laser scanning confocal microscope that the network structure of ICC-DMP was clear, the expression of c-kit and Bcl-2 was strongly and overlapping;the expression of Bax was weak and scatter distributed. Compared with control group, ICC-DMP quantity in MODS group was significantly reduced （ cells/HP： 15.80±2.30 vs. 25.70±3.97, t = 6.819,