BACKGROUND: The gastrointestinal tract is highly responsive to the tropic effect of growth hormone (GH). GH stimulates the healing of colonic anastomoses either directly or through insulin-like growth factor I (IGF-I) since specific GH receptor as well as IGF-I receptor have been demonstrated in colon. AIM: To determine whether exogenous treatment with IGF-I could stimulate the healing of left colonic anastomoses in rats. METHODS: After colonic anastomotic operations adult rats were randomised to treatment with either IGF-I (500 mu g per day) or vehicle (controls). Anastomotic breaking strength and collagen deposition were determined at day after surgery. RESULTS: IGF-I treatment increased the anastomotic collagen content by 23% compared with controls. This resulted in a lower extensibility of the anastomosis (P < 0.05), whereas the anastomotic breaking strength did not differ between groups. The treatment resulted in a 3 fold increase in serum IGF-I of IGF-I treated rats, compared to controls. The postoperative body weight increased by 5% in the IGF-I rats from day 0 to day 3, while the control group had a weight loss of 2% in the same period (P < 0.001). CONCLUSION: Treatment of colon-operated rats with IGF-I increased the postoperative body weight and stimulates the collagen deposition of left colonic anastomoses, whereas the anastomotic strength may be unaffected by IGF-I treatment.
BACKGROUND: The gastrointestinal tract is highly responsive to the tropic effect of growth hormone (GH). GH stimulates the healing of colonic anastomoses either directly or through insulin-like growth factor I (IGF-I) since specific GH receptor as well as IGF-I receptor have been demonstrated in colon. AIM: To determine whether exogenous treatment with IGF-I could stimulate the healing of left colonic anastomoses in rats. METHODS: After colonic anastomotic operations adult rats were randomised to treatment with either IGF-I (500 mu g per day) or vehicle (controls). Anastomotic breaking strength and collagen deposition were determined at day after surgery. RESULTS:IGF-I treatment increased the anastomotic collagen content by 23% compared with controls. This resulted in a lower extensibility of the anastomosis (P < 0.05), whereas the anastomotic breaking strength did not differ between groups. The treatment resulted in a 3 fold increase in serum IGF-I of IGF-I treated rats, compared to controls. The postoperative body weight increased by 5% in the IGF-Irats from day 0 to day 3, while the control group had a weight loss of 2% in the same period (P < 0.001). CONCLUSION: Treatment of colon-operated rats with IGF-I increased the postoperative body weight and stimulates the collagen deposition of left colonic anastomoses, whereas the anastomotic strength may be unaffected by IGF-I treatment.
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