腹腔感染对肠吻合口愈合影响机制的研究  

Healing mechanism of intestinal anastomosis in intra-abdominal sepsis rats

作　　者：鲍扬[1] 李幼生[1] 马捷[2] 孙桂勤[2] 黎介寿[1] 

机构地区：[1]南京军区南京总医院解放军普通外科研究所,江苏南京210002 [2]南京军区南京总医院病理科,江苏南京210002

出　　处：《医学研究生学报》2007年第8期809-811,共3页Journal of Medical Postgraduates

基　　金：全军"十五"重点项目资助(批准号:01Z013);江苏省自然科学基金创新人才基金资助项目(批准号:BK2005432)

摘　　要：目的:探讨腹腔感染对肠吻合口愈合的影响机制。方法:雄性Wistar大鼠分为两组:正常对照组行肠切除肠吻合,感染组在腹腔感染后行肠切除肠吻合。检测吻合口纤维连接蛋白(FN)、α-平滑肌肌动蛋白(α-SMA)和血管内皮细胞生长因子(VEGF)的表达及细胞凋亡和常规病理学检查。结果:正常对照组术后FN、α-SMA、VEGF表达均显著高于感染组,术后吻合口细胞凋亡明显低于感染组。结论:感染后组织细胞的修复与清除出现失调,组织修复的起始过程延迟,成纤维细胞和上皮细胞的迁移减缓,毛细血管再生缓慢、肉芽组织形成减少,作为限制肉芽组织过度生长的细胞凋亡却过早出现,很大程度上影响了早期和中期的组织愈合。Objective：To investigate the mechanism of intestinal anastomosis in a rat model of intra-abdominal sepsis. Methods：Male Wistar rats were randomized into 2 groups. Control rats underwent intestinal anastomosis. Sepsis group underwent intestinal anastomosis after intestinal fistula operation, fibronectin （FN）, α-smooth muscle actin （α-SMA）, vascular endorthelial growth factor（VEGF） and apoptosis in anastomoses were measured. Results：FN, α-SMA, VEGF in control group were higher than sepsis group and apoptosis were lower than the other. Conclusion：It is indicated that the repair of tissue was out of balance after infection, and the organization repair was retarded. The collagenoblast and the epithelial cell migration were slowed down, and the blood capillary regeneration was slowly. Not only the granulati

关 键 词：腹腔感染 创伤愈合机制 Α-SMA 

分 类 号：R574[医药卫生—消化系统]