Transcutaneous carbon dioxide application inhibits muscle atrophy after fracture in rats.

Abstract

BACKGROUND: Muscle atrophy causes difficulty in resuming daily activities after a fracture. Because transcutaneous carbon dioxide (CO) application has previously upregulated oxygen pressure in the local tissue, thereby demonstrating its potential in preventing muscle atrophy, here we investigated effects of COapplication on muscle atrophy after femoral shaft fracture. METHODS: Thirty fracture model rats were produced and randomly divided into a no treatment (control group) and treatment (COgroup) groups. After treatment, the soleus muscle was dissected at post-fracture days 0, 14, and 21. Evaluations were performed by measuring muscle weight and performing histological examination and gene expression analysis. RESULTS: Muscle weight was significantly higher in the COgroup than in the control group. Histological analysis revealed that the muscle fiber cross-sectional area was reduced in both groups. Nevertheless, the extent of atrophy was lesser in the COgroup. Muscle fibers in the control group tended to change into fast muscle fibers. Vascular staining revealed that more capillary vessels surrounded the muscle fibers in the COgroup than in the control group. Messenger RNA (mRNA) analysis revealed that the COgroup had a significantly enhanced expression of genes that were related to muscle synthesis. CONCLUSION: Transcutaneous COapplication may be a novel therapeutic strategy for preventing skeletal muscle atrophy after fracture.