Mitogenesis in wound-healing cells in diabetic rats

The healing of perforated mesenterial window is delayed in insulin-deficient rats after 4 weeks of streptozoticin-induced diabetes. In the present study we investigated the mitogenic capacity of the two predominating cell types in the healing mesenterial window in such rats. The labelling index (LI) in fibroblasts and mesothelial cells, normally constituting approximately 96% of all tissue-bound cells, was estimated in early and later phases of healing within (a) a 1 mm-wide zone surrounding the perforation and (b) centrally in wounds after healing by closure. The mitotic index (MI) of these cells was estimated at various distances from the perforation. Adjacent unperforated control mesenteric windows served as internal controls. Proliferation increased on days 1 and 2 post-perforation, whereafter it gradually diminished, fibroblasts showing a higher LI than mesothelial cells days 3-7 after closure. On day 1 post-perforation the relative increase of LI was greatest in diabetic mesenteries. During the period just preceding healing by closure. LI of both fibroblasts and mesothelial cells was, however, significantly reduced in diabetic animals. The impaired mitogenesis in these wound-healing cells in diabetic rats may thus be of pathogenic significance in the delayed healing in such animals.