研究缺血对失神经支配骨骼肌萎缩的影响

目的　研究缺血对失神经支配骨骼肌萎缩的影响。方法　选用 SD大鼠 2 4只 ,建立右下肢缺血加腓肠肌失神经支配的动物模型 (实验组 ) ,左侧为对照组。术后 2、4周取双侧腓肠肌 ,另取 6只正常大鼠腓肠肌作正常对照 ,观察组织学、肌电图及酶组织化学的变化。结果　术后 2、4周 ,实验组肌细胞直径比正常对照组减少 5 1.1%和 6 3.6 % (t =2 .94,P <0 .0 5 ) ,截面积减少 5 3.6 %和 6 2 .0 % (t =2 .88,P <0 .0 5 )。实验组肌细胞线粒体呈空泡状、数量减少 ;肌质网明显扩张退变。肌肉出现纤颤电位 ,和对照组比 ,其波幅无明显差异 (t=2 .11,P<0 .0 5 )。术后 2周实验组的 Na,K- ATP酶活性比正常对照组增高 74.6 % ,术后 4周则下降至对照组的 88.0 % (t=7.6 4,2 .2 4,P<0 .0 1、<0 .0 5 )。术后2周 Ca- ATP酶活性比正常对照组下降 2 8.32 % ,术后 4周下降至 35 .8% (t=2 .98、2 .2 1,P<0 .0 5 )。结论　缺血可加速失神经支配肌肉萎缩的发生与发展

Influence of ischemia on denervation skeletal muscle atrophy

Objective To observe the influence of ischemia on denervation muscle atrophy. Methods 24 SD rats were used to establish the gastrocnemius muscle denervation model in both hind limbs and muscle ischemia model in the right hind limb. Denervation resulted from resection of the sciatic nerve. Ligation of the femoral artery caused ischemia. Muscle cell histology, ultrastructure, fibrillation potential amplitude, Na,K ATPase and Ca ATPase activity were examined 2 and 4 weeks postoperatively. Results Degeneration of mitochondria and sarcoplasmic reticulum were speeded up on the ischemic side. Diameter and cross sectional area of the muscle fibers on the ischemic side reduced more rapidly than that of the control side. There was no difference of the fibrillation potential amplitude on both sides. Na,K ATPase activity on the ischemic side increased 74.6 % in 2 weeks, and reduced to 88.0 % in 4 weeks.The activity of Ca ATPase on the ischemic side reduced to 28.32 % and 35.8 % after 2 and 4 weeks respectively. Conclusions Ischemia aggravates muscle atrophy. If possible, the blood vessel should be repaired in case nerve injury is accompanied by artery injury in the extremities.