Norrby K, Franzén L
Acta Pathol Microbiol Immunol Scand A. 1984 Nov;92(6):411-6. doi: 10.1111/j.1699-0463.1984.tb04422.x.
The effects of inflicting trauma on the mesentery of diabetic and control rats by perforation with a scalpel were studied with regard to time-course of healing and rate of healing by closure. In this tissue, which is virtually free from blood vessels and nerves, healing precedes vascularization of the wound area. Insulin-deficient rats with streptozotocin diabetes of 4 weeks' duration were used. Non-specific histamine release and cell proliferation (expressed as specific DNA activity) lasting 30 h took place after opening the abdomen and handling the mesentery. Wounding caused further histamine release and cell proliferation. These variables were the same in diabetic and control rats. The time-course of healing was significantly delayed in diabetes, whereas the rate of healing (number of wound closures per day) during the phase of rapid healing was not. Because the rate of healing was normal in diabetic rats the impairment of healing in diabetes can be ascribed to pre-healing reparative events unrelated not only to vascular and neural factors but apparently also to the amount of histamine released and to the cell proliferation elicited by wounding. The delayed healing thus seems to be related to some cellular or metabolic feature of diabetes as yet unknown.
通过用手术刀穿孔对糖尿病大鼠和对照大鼠的肠系膜造成创伤，研究了愈合的时间进程和闭合愈合率。在这个几乎没有血管和神经的组织中，伤口愈合先于伤口区域的血管化。使用了患有持续4周链脲佐菌素糖尿病的胰岛素缺乏大鼠。打开腹腔并处理肠系膜后，会发生持续30小时的非特异性组胺释放和细胞增殖（以特定DNA活性表示）。创伤导致进一步的组胺释放和细胞增殖。这些变量在糖尿病大鼠和对照大鼠中是相同的。糖尿病患者的愈合时间进程明显延迟，而在快速愈合阶段的愈合率（每天伤口闭合的数量）则没有延迟。由于糖尿病大鼠的愈合率正常，糖尿病患者愈合受损可归因于愈合前的修复事件，这些事件不仅与血管和神经因素无关，而且显然也与释放的组胺量和创伤引起的细胞增殖无关。因此，延迟愈合似乎与糖尿病某些尚未知晓的细胞或代谢特征有关。
