Harada I
Department of Orthopaedic Surgery, National Defense Medical College, Saitama, Japan.
Nihon Seikeigeka Gakkai Zasshi. 1992 Jul;66(7):763-70.
Glucocorticoids administration presumably affects the vascular system and causes avascular necrosis of the femoral head. However, the mechanism by which this occurs is still unknown. In order to clarify the action of glucocorticoids on the vascular system, we investigated the effects of dexamethasone on an angiogenesis model in vitro. The angiogenesis model was obtained by co-culturing vessel fragments and myofibroblastic cells from rat epididymal fat pads. In this model, myofibroblastic cells induce capillary formation by producing an endothelial cell growth factor and collagen. Dexamethasone at physiological doses inhibited significantly capillary growth by suppressing the collagen synthesis by myofibroblastic cells. However, dexamethasone had no effect on endothelial cells. These results indicate that glucocorticoids are related to the pathogenesis of avascular necrosis of the femoral head by inhibiting the repair of the vascular system in vivo.
糖皮质激素的使用可能会影响血管系统并导致股骨头缺血性坏死。然而，其发生机制仍不清楚。为了阐明糖皮质激素对血管系统的作用，我们研究了地塞米松对体外血管生成模型的影响。血管生成模型是通过将大鼠附睾脂肪垫的血管片段和肌成纤维细胞共培养获得的。在该模型中，肌成纤维细胞通过产生内皮细胞生长因子和胶原蛋白诱导毛细血管形成。生理剂量的地塞米松通过抑制肌成纤维细胞的胶原蛋白合成，显著抑制了毛细血管的生长。然而，地塞米松对内皮细胞没有影响。这些结果表明，糖皮质激素通过抑制体内血管系统的修复与股骨头缺血性坏死的发病机制有关。
