Verhofstad M H, Lange W P, van der Laak J A, Verhofstad A A, Hendriks T
Department of Surgery, University Hospital Nijmegen, The Netherlands.
Dis Colon Rectum. 2001 Mar;44(3):423-31. doi: 10.1007/BF02234744.
The mechanisms that cause diabetes to impair the development of anastomotic strength in the intestine are poorly understood. We investigated whether short-term uncontrolled diabetes causes alterations in microscopic aspects of anastomoses from the ileum and colon.
Eighteen Wistar rats were rendered diabetic one week before operation by intravenous streptozotocin injection (50 mg/kg), resulting in nonfasting blood glucose levels of approximately 20 mmol/l. Another 18 age-matched rats were used as controls with a normal blood glucose range of 5 to 7 mmol/l. All rats underwent resection and anastomosis of both the ileum and colon. Animals were killed at one, three, or seven days after operation. Cellular and architectural parameters of anastomotic healing were scored in hematoxylin and eosin-stained sections. Anastomotic collagen content was analyzed by image analysis in picrosirius red-stained sections.
Anastomotic necrosis, edema, and epithelial recovery were not affected by diabetes. In diabetic rats, the number of polymorphonuclear cells and macrophages was significantly (P = 0.025 and 0.0002, respectively) increased in ileal anastomoses one and three days after operation. In colonic anastomoses, the number of polymorphonuclear cells was increased at one (P = 0.001) and seven (P = 0.014) days after operation. Repair of the submucosal-muscular layer in colonic anastomoses from diabetic rats was impaired seven days after surgery (P = 0.0071), but in ileal anastomoses no difference was found. In the anastomotic area, collagen deposition at postoperative Days 1, 3, and 7 remained unaffected by diabetes.
Experimental diabetes leads to alterations in cellular components involved in the early phase of repair of intestinal anastomoses but not to a reduced accumulation of wound collagen.
糖尿病损害肠道吻合口强度的发生机制尚不清楚。我们研究了短期未控制的糖尿病是否会导致回肠和结肠吻合口微观层面的改变。
18只Wistar大鼠在手术前一周通过静脉注射链脲佐菌素（50mg/kg）制成糖尿病模型，非空腹血糖水平约为20mmol/L。另外18只年龄匹配的大鼠作为对照，血糖正常范围为5至7mmol/L。所有大鼠均接受回肠和结肠的切除及吻合术。术后1天、3天或7天处死动物。在苏木精-伊红染色切片中对吻合口愈合的细胞和结构参数进行评分。在天狼星红染色切片中通过图像分析来分析吻合口胶原含量。
吻合口坏死、水肿和上皮修复不受糖尿病影响。在糖尿病大鼠中，术后1天和3天回肠吻合口中多形核细胞和巨噬细胞的数量显著增加（分别为P = 0.025和0.0002）。在结肠吻合口中，术后1天（P = 0.001）和7天（P = 0.014）多形核细胞数量增加。糖尿病大鼠结肠吻合口黏膜下层-肌层在术后7天的修复受损（P = 0.0071），但在回肠吻合口中未发现差异。在吻合口区，术后第1天、3天和7天的胶原沉积不受糖尿病影响。
实验性糖尿病导致肠道吻合口早期修复过程中细胞成分发生改变，但不会导致伤口胶原积累减少。
