摘要
目的 :研究肢体制动对失神经支配骨骼肌超微结构及酶组织化学影响。方法 :用SD大鼠 ,建立左下肢失神经支配腓肠肌及右下肢制动加失神经支配腓肠肌的实验模型 ,观察肌细胞直径、截面积 ,超微结构及Na+、K+ ATP酶和Ca2 + ATP酶活性变化。结果 :制动侧肌细胞直径及截面积较对照侧下降速度明显加快 ;肢体制动加速了肌细胞的线粒体 ,肌质网退变 ;Na+、K+ ATP酶活性制动侧较对照侧下降速度快 18.2 4% ;而Ca2 + ATP酶活性在术后 2周无明显差异 ,术后 4周制动侧较对照侧下降速度快 13 .99%。结论 :肢体制动加速了失神经支配骨骼肌萎缩的发生与发展。因此 ,临床上神经损伤合并有肌腱、骨折等复合损伤情况下 ,肢体制动范围及时间尽可能予以减少。
Objective: To study limb immobilization influencing on the histology, ultrastructure,Na +, K +-ATPase and Ca 2+ -ATPase activities on denervated muscle atrophy. Methods: SD rats were used and the model of denervated muscle in the left lower limb was made by cutting off the tibial nerve, and limb immobilization in the right lower limb was established by inserted into tibial and femoral marrow cavity with Kirschner pin. The diameter and cross section of muscle cell,ultrastructure, Na + ?K +-ATPase and Ca 2+ -ATPase activities were observed. Results: The muscle cell diameter and cross section were reduced more significantly in the immobilized limb side .The degeneration of mitochondria and sarcoplasmic reticulum was accelerated after limb fixation. The reduction rates of Na + ?K +-ATPase and Ca 2+ -ATPase activity in immobilized limb were faster 18.24 per cent and 13.99 per cent respectively than that of the control side. Conclusions: The limb immobilization could accelerate the development and severity of muscle atrophy. The time and range of limb fixation should be reduced as soon as possible on basis of meeting the need of the necessary treatment when nerve injury accompanied by tendon injury or bone fracture.
出处
《中国矫形外科杂志》
CAS
CSCD
2003年第7期465-467,共3页
Orthopedic Journal of China
基金
上海市医学领先学科基金资助 (项目编号 :95-Ⅲ-001)
