The Beneficial Effect of Enhanced Macrophage Function on the Healing of Bowel Anastomoses
Inadequate healing and subsequent leakage of bowel anastomoses are serious postoperative complications in abdominal surgery. Previous studies have demonstrated the macrophage to be a key cell in the physiology of wound healing. The current study was undertaken to evaluate the effects of enhanced macrophage function on the healing of bowel anastomoses. Sprague-Dawley rats (250 gm) underwent laparotomy and jejunojejunostomy following IV treatment with glucan (100 mg per kg), a potent macrophage stimulant, or 5 per cent dextrose 24 hours before surgery and again on the day of surgery. Animals were killed and the anastomoses underwent wound tensiometry on Day 3 using a computer-assisted constant velocity tensiometer. The glucan treated animals had a significantly greater anastomotic breaking strength (88.5 gm ± 10.7 versus 45.45 gm ± 5.1) (P < 0.01). Formalin fixation increased the breaking strength of the untreated anastomosis but not of the treated anastomosis (92.9 gm ± 11.77 versus 92.3 ± 12.44). Analysis of macrophage supernatant for the growth factors epidermal growth factor (EGF), platelet derived growth factor (PDGF), and transforming growth factor-β (TGF-β) was accomplished by immunoblot assay. Results indicated no difference in the presence of EGF in the stimulated and unstimulated macrophage supernatants. PDGF and TGF-β were decreased in the stimulated macrophage supernatants. We conclude that 1) Enhanced macrophage function had a beneficial effect on the early tensile strength of bowel anastomoses. 2) Effects of the activated macrophage on bowel anastomoses may not be related to secretion of conventional growth factors. 3) Immunopharmacologic agents that enhance macrophage function may be an important adjunct to surgical therapy requiring bowel anastomosis.
Compton, Ray; Williams, David; and Browder, William. 1996. The Beneficial Effect of Enhanced Macrophage Function on the Healing of Bowel Anastomoses. American Surgeon. Vol.62(1). 14-18. https://pubmed.ncbi.nlm.nih.gov/8540639/ PMID: 8540639 ISSN: 0003-1348