职业性肌肉骨骼疾患发病机制的探讨——被动牵拉对大鼠离体骨骼肌线粒体钙、丙二醛及肌酸激酶的影响

A Study on the Mechanism of Occupational Musculoskeletal Disorder—the Changes of Rat Isolated Soleus Mitochodrial[Ca 2+ ],Malondialdehyde and Creatine Kinase with Passive Stretch

通过大鼠比目鱼肌体外实验，探讨牵拉负荷导致的肌肉损伤与肌细胞内酶的流出，骨骼肌细胞线粒体钙浓度（ＭＣＣ）以及细胞脂质过氧化反应之间的关系。４ｈ培养和牵拉后发现，牵拉负荷使肌肉ＭＣＣ显著性增高（Ｐ＜０．０１），且比对照组高６７．９％。脂质过氧化反应终产物丙二醛（ＭＤＡ）和肌酸激酶（ＣＫ）的释放无显著性变化（与对照组比较，Ｐ＞０．０５）。结果提示，骨骼肌细胞ＭＣＣ的增接与肌肉损伤有密切关系，并且可能是肌肉损伤的始发因素，介导一系列肌肉损伤机制的发生；脂质过氧化反应也可能发生在ＭＣＣ变化之后；

In order to study the relationship of muscle injury,the release of intracellular enzyme,muscle mitochondrial [Ca 2+ ](MCC)and lipid peroxidation through the stretch of rat soleus in vitro.After the culture and stretch of 4h ours,MCC of the experimental group increased significantly compared with control( P <0.05),the concentration of malondialdehyde(MDA) and the efflux of creatine kinase(CK) had not significant change( P >0.05).Result showd that increases in MCC are closely connected with muscle injury,and may be the initial factor of muscle injury;lipid peroxidation may occur after the change of MCC;and the release of CK seems has not directed connect with muscle injury.