Dexamethasone down-regulates endothelial expression of intercellular adhesion molecule and impairs the healing of bowel anastomoses.

Abstract

To find out the role of endothelial expression of intercellular adhesion molecule-1 (ICAM-1) in the healing of intestinal anastomoses in rats, and to establish the effects of peroperative treatment with corticosteroids. Experimental animal study. University hospital, Turkey. 78 Male Wistar rats. Rats were divided into four groups: Group I, colonic anastomosis only (=18); Group II, colonic anastomosis plus caecal ligation and puncture (=18); Group III, colonic anastomosis plus dexamethasone (=18); and Group IV, colonic anastomosis, plus caecal ligation and puncture, plus dexamethasone (=18). Six animals served as the sham group. The animals underwent bowel transsection and primary anastomosis Infection was produced by caecal ligation and puncture Preoperatively, dexamethasone was given intramuscularly in a dose of 2 mg/kg/day. After 1, 3 and 5 days, anastomotic healing and endothelial expression of ICAM-1 were measured microscopically. Anastomotic healing was significantly impaired in dexamethasone-treated animals, and endothelial expression of ICAM-1 was reduced. Endothelial expression of ICAM-1 was no higher in the infected group than in controls. Maximum expression of ICAM-1 on endothelial cells was seen on the first day in each group, and declined on the following days, although the sebsequent reduction in expression was not significant. Dexamethasone down-regulated expression of ICAM-1, which is important in migration of leucocytes from the circulation to the wound site, and significantly impaired the healing of intestinal anastomoses in rats.