Franzén L E, Roberg K
Department of Pathology II, University Hospital, Linköping, Sweden.
J Surg Res. 1995 Apr;58(4):407-14. doi: 10.1006/jsre.1995.1063.
Streptozotocin-induced diabetes mellitus is known to impair connective tissue repair in the perforated rat mesentery. The aim of the present investigation was to study quantitatively by morphometrical techniques the influence of diabetes on some aspects of the cellular ultrastructure related to connective tissue contraction in such healing. The cellular volume density increased significantly with time, presumably as a consequence of disappearance of interstitial edema. No difference was found in the amount of healing tissue formed between controls and diabetics. The surface volume density of the plasma membrane was significantly higher in control animals on Days 1-10, indicating an increased number of cellular protrusions and spikes which relate to the motility of the cells. The volume density of contractile filaments did not differ between controls and diabetics. The results suggest a reduced surface density of plasma membrane in diabetic cells, a finding which is compatible with reduced wound contraction in diabetes.
已知链脲佐菌素诱导的糖尿病会损害大鼠穿孔肠系膜中结缔组织的修复。本研究的目的是通过形态计量学技术定量研究糖尿病对这种愈合过程中与结缔组织收缩相关的细胞超微结构某些方面的影响。细胞体积密度随时间显著增加，推测是间质水肿消失的结果。对照组和糖尿病组之间形成的愈合组织量没有差异。在第1 - 10天，对照动物的质膜表面体积密度显著更高，表明与细胞运动性相关的细胞突起和刺的数量增加。对照组和糖尿病组之间收缩丝的体积密度没有差异。结果表明糖尿病细胞中质膜的表面密度降低，这一发现与糖尿病中伤口收缩减少相一致。
