|Budget Amount *help
¥2,800,000 (Direct Cost : ¥2,800,000)
Fiscal Year 2000 : ¥500,000 (Direct Cost : ¥500,000)
Fiscal Year 1999 : ¥500,000 (Direct Cost : ¥500,000)
Fiscal Year 1998 : ¥800,000 (Direct Cost : ¥800,000)
Fiscal Year 1997 : ¥1,000,000 (Direct Cost : ¥1,000,000)
The purpose of our study was to determine whether hindlimb suspension induce necrosis in the atrophied muscles and whether oxidative stress play any role in the process. Light and electron microscopic observation of hindlimb muscles of Wistar rats (8 weeks of age, male), which were unloaded for two weeks, and control rats were performed. The fiber diameters of the rectus femoris, vastus medialis, vastus lateralis, intermedius, gastrocnemius, soleus muscles of the suspended rats were smaller than those of the controls, especially type 1 fiber in the soleus muscle and type 2B fiber in the vastus lateralis and medialis muscles. Necrotic fibers were found in deep portions of the vastus lateralis, vastus medialis, lateral and medial heads of gastrocnemius, and soleus muscles of the suspended rats, and the following were the rate of necrotic fibers (number/10 rats) : 1.4, 1.3, 1.7, 1.4, 0.3, and 1.9, respectively. Reticular structures stained with monoclonal antibodies of desmin and plectin were irregular after hindlimb suspension, and irregularity of myofibrillar arragement and Z-bands was also found by electron microscopy. A few necrotic fibers in the deep portion of the hindlimb muscles had a positive reaction to the monoclonal antibody to superoxide dismutase. Alfa-tocopherol content of the soleus muscle was approximately 40% as much as that of the rectus femoris muscle. In conclusion, hindlimb suspension induces muscle fiber necrosis in the deep portion of the muscles, which were rich in oxidative fibers, and disuse muscle atrophy is not only decrease in muscle fiber diameter, but also complicated dynamic process of the muscle. Although oxidative stress may concern the process of necrosis after hindlimb suspension, α-tocopherol content did not reveal all mechanism of muscle fiber necrosis.