激素性股骨头缺血坏死发病机制的实验研究
摘要点击次数: 2351   全文下载次数: 1522   投稿时间:2002-04-17    
作者Author单位AddressE-Mail
李毅 LI Yi 西安交通大学第二临床医院骨科,陕西西安710004 Second Hospital of Xi’an Jiaotong University GhanXi xi'an 710004  
同志超 TONG Zhichao 西安交通大学第二临床医院骨科,陕西西安710004 Second Hospital of Xi’an Jiaotong University GhanXi xi'an 710004  
陈君长 CHEN Junchang 西安交通大学第二临床医院骨科,陕西西安710004 Second Hospital of Xi’an Jiaotong University GhanXi xi'an 710004  
王坤正 西安交通大学第二临床医院骨科,陕西西安710004 Second Hospital of Xi’an Jiaotong University GhanXi xi'an 710004  
期刊信息:《中国骨伤》2003年,第16卷,第1期,第20-22页
DOI:doi:10.3969/j.issn.1003-0034.yyyy.nn.zzz
基金项目:陕西省中医管理局科研课题(编号:99017)
中文摘要:

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:24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<0.01),纤溶酶原激活物抑制物的含量升高(P<0.01).

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。
【关键词】股骨头坏死  病理过程  一氧化氮  纤溶酶原激活物,组织型  纤溶酶原激活物抑制物
 
An experimental study of pathogenesis of steroid-induced avascular necrosis of femoral head
ABSTRACT  

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.
KEY WORDS  Femur head necrosis  Pathologic processes  Nitric oxide  Plasminogen activator,tissue-type(t-PA)  Plasminogen activator inhibitor (PAI)
 
引用本文,请按以下格式著录参考文献:
中文格式:李毅,同志超,陈君长,王坤正.激素性股骨头缺血坏死发病机制的实验研究[J].中国骨伤,2003,16(1):20~22
英文格式:LI Yi,TONG Zhichao,CHEN Junchang.An experimental study of pathogenesis of steroid-induced avascular necrosis of femoral head[J].zhongguo gu shang / China J Orthop Trauma ,2003,16(1):20~22
阅读全文  下载  查看/发表评论  下载PDF阅读器
关闭




版权所有:《中国骨伤》杂志社京ICP备12048066号-2  版权声明
地址:北京市东直门内南小街甲16号,100700
电话:010-64089487 传真:010-64089792 Email:zggszz@sina.com

京公网安备 11010102004237号