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目的 研究内皮素 (ET 1)、一氧化氮 (NO)在激素性股骨头缺血坏死中的作用 ,进一步探讨激素性股骨头缺血坏死的发病机制。方法 给家兔注射大剂量的醋酸氢化可的松 (每周 12mg/kg)后4、8、12周 ,用放射免疫法测定血浆、股动脉组织ET 1的含量变化 ;用硝酸还原酶法测定其NO含量的变化。观察股骨头组织病理学改变并行X线检查。结果 用药后不同时间的血浆和股动脉组织ET 1含量不断升高 (P <0 0 1) ,而其NO的含量持续下降 (P <0 0 1)。光镜下 4～ 8周的股骨头标本见脂肪细胞增多、肥大 ,生骨细胞、成骨细胞减少 ,微血管栓塞 ,管壁增厚 ,骨小梁变细、萎缩 ,骨细胞核边聚、固缩、溶解 ,骨细胞坏死 ,空骨陷窝增多。随着时间的延续上述改变加重。结论 ①激素性股骨头缺血坏死动物模型的血浆和血管组织中ET 1含量增多 ,而其NO含量减少 ,这种改变在激素性股骨头缺血坏死中可能起着重要作用。②大剂量激素短期内就可诱发股骨头缺血坏死。
Objective To investigate the role of endothelin (ET 1) and nitric oxide (NO) in the pathogenesis of steroid-induced avascular necrosis of femoral head and to explore the pathogenesis of steroid-induced avascular necrosis of femoral head. Methods Rabbits were injected with high dose of hydrocortisone acetate (12mg / kg weekly) 4, 8 and 12 weeks after the injection. Radioimmunoassay was used to determine the content of ET 1 in plasma and femoral artery. Nitric acid reductase Its NO content changes. Observation of femoral head histopathological changes and X-ray examination. Results The levels of ET 1 in plasma and femoral artery tissue were increased at different time points after treatment (P <0.01), while the content of NO decreased continuously (P <0.01). Light microscope 4 to 8 weeks of the femoral head specimens see fat cells, hypertrophy, osteoblasts, osteoblasts, microvascular embolism, wall thickening, trabecular thinning, atrophy, bone cell nucleus edge aggregation, shrinkage , Dissolved, osteocytic necrosis, empty bone lacuna increased. As time goes by, the above change is aggravated. Conclusion ① The content of ET 1 in plasma and vascular tissue of the animal model of steroid-induced avascular necrosis of the femoral head increases, while the content of NO decreases. This change may play an important role in steroid-induced avascular necrosis of femoral head. ② high-dose hormone can induce short-term osteonecrosis of the femoral head.