激素性股骨头坏死与凝溶紊乱的实验研究  被引量:5

Hypofibrinolysis and Hyperthrombosis in Dexamethasone-induced Osteonecrosis of the Femoral Head in Rabbits

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作  者:尹良军[1] 王爱民[1] 杜全印[1] 孙红振[1] 邓少丽[1] 

机构地区:[1]第三军医大学附属大坪医院,重庆400042

出  处:《中国矫形外科杂志》2001年第3期261-264,共4页Orthopedic Journal of China

摘  要:目的 :观察激素性股骨头坏死家兔模型的血液凝溶功能变化 ,探讨激素性股骨头坏死的发病机理。方法 :健康雄性成年家兔 36只 ,随机分为对照组 (注射生理盐水 ) ,实验组 (冲击注射地塞米松 )。检测血脂、血浆组织纤溶酶原激活物 (tPA)、纤溶酶原激活物抑制物 (PAI)、血栓素A2 (TXA2 )、前列环素 (PGI)的阶段性变化。观察实验 35、70d双侧股骨头的病理变化。结果 :实验组 15d甘油三脂、总胆固醇、TXA2 /PGI比值均显著高于对照组。实验 30、6 0d ,实验组tPA/PAI比值显著低于对照组。实验组 35、70d双侧股骨头软骨下区骨陷窝空虚率均较对照组显著增高。结论 :地塞米松冲击应用可引起家兔血液高凝、低纤溶。血液凝溶功能紊乱可能参与兔激素性股骨头坏死的发病。Objective: To investigate the change of thrombotic and fibrinolytic systems in dexamethasone(DEX) induced osteonecrosis of the femoral head(ONFH) in rabbits, and study the pathogenesis of the DEX induced ONFH. Methods: 36 male adult rabbits were divided into group A(injected with saline) and group B(injected with massive dose of DEX). Serum lipids, plasma tissue plasminogen activator(tPA) and plasminogen activator inhibitor (PAI) activities, plasma thromboxane (TX) A 2 and prostacyclin(PGI) concentrations were measured in different stages.Pathology of the femoral heads were observed in 35 and 70 days. Results: Serum lipids, the ratio of TXA 2/PGI in plasma increased in group Bin 15 days as compared with group A. The ratio of tPA/PAI in plasma decreased in group B in 30 and 60 days. Empty bone lacunae were higher in group B than in group A in 35 and 70 days. Conclusion: Massive dose of DEX can induce hypofibrinolysis and hyperthrombosis in rabbits, which might be involved in the pathogenesis of the DEX induced ONFH in rabbits.

关 键 词:股骨头缺血坏死 地塞米松 低纤溶血质 高凝血质 

分 类 号:R363[医药卫生—病理学]

 

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