Microscopic analysis of anastomotic healing in the intestine of normal anddiabetic rats

PURPOSE: The mechanisms that cause diabetes to impair the development of an astomotic 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. METHODS: Eighteen Wistar r ats were rendered diabetic one week bt fore operation by intravenous strept ozotocin injection (50 mg/kg), resulting in nonfasting blood glucose levels of approximately 20 mmol/l. Another 18 age-matched rats were used as contr ols 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 pa rameters of anastomotic healing were scored in hematoxylin and eosin-staine d sections. Anastomotic collagen content was analyzed by image analysis in picrosirius red-stained sections. RESULTS: Anastomotic necrosis, edema, and epithelial recovery were not affected by diabetes. In diabetic rats, the n umber of polymorphonuclear cells and macrophages was significantly (P = 0.0 25 and 0.0002, respectively) increased in ileal anastomoses one and three d ays after operation. In colonic anastomoses, the number of polymorphonuclea r cells was increased at one (P = 0.001) and seven (P = 0.014) days after o peration. Repair of the submucosal-muscular layer in colonic anastomoses fr om diabetic rats was impaired seven days after surgery (P = 0.0071), but in ileal anastomoses no difference was found. In the anastomotic area, collag en deposition at postoperative Days 1, 3, and 7 remained unaffected by diab etes. CONCLUSION: Experimental diabetes leads to alterations in cellular co mponents involved in the early phase of repair of intestinal anastomoses bu t not to a reduced accumulation of wound collagen.