激素性股骨头缺血坏死发病机制的实验研究

An experimental study of pathogenesis of steroid-induced avascular necrosis of femoral head

目的 探讨股骨头缺血坏死的发病机制 ,以冀正确指导临床。方法 2 4只日本大耳白兔随机分为模型组和对照组。给模型组动物大剂量肌注醋酸泼尼松龙 (8mg/kg) 8周 ,造成股骨头缺血坏死模型。造模开始后第 4周、8周、12周两组动物各取 2只进行光镜和扫描电镜观察 ,并在两组动物中各取 4只测定晨空腹血中一氧化氮、组织型纤溶酶原激活物、纤溶酶原激活物抑制物的含量。结果 与对照组相比 ,模型组股骨头骨质疏松 ,光镜下空骨陷窝数增多 ,脂肪细胞数增多 ,扫描电镜下骨小梁断裂塌陷 ,骨基质表面胶原纤维松解、断裂。模型组动物与对照组相比血浆中一氧化氮、组织型纤溶酶原激活物含量下降 (P <0 0 1) ,纤溶酶原激活物抑制物的含量升高 (P <0 0 1)。结论 激素性股骨头缺血坏死可能与一氧化氮含量及纤溶系统的活性下降有关。

Objective To explore the pathogenesis of avascular necrosis of femoral head (ANFH) in order to search for an effective method for clinical treatment Methods 24 rabbits were divided into two groups of the experimental models and controls.ANFH models were produced by intramuscular injection of large dosage of steroid to rabbits in 8 weeks period.From the 4th,8th,12th week after production of models,2 rabbits of model group and 2 rabbits of control group were sacrificed to observe the structure of femoral head.The contents of nitric oxide (NO),tissue-type plasminogen activator(t-PA),plasminogen activator inhibitor (PAI) in plasma of the 4 rabbits of the tow groups were determined at the same time.Results Compared with control group,the rabbits of model group exhibited many changes such as osteoporosis of femoral head,the presence of more bone lacuna and fat cell,the rarely seen and broken thinner trabeculae.Compared with control group,the contents of NO and t-PA in plasma of the model rabbits decreased obviously,but the contents of the PAI increased obviously.Conclusion The steroid-induced ANFH might be related to the lower level of NO and the descent of fibrinolytic activity.