title: Pathology study of rabbit calf muscles after repeated compression.
abstract: : To elucidate the pathogenesis of chronic compartment syndrome, we examined pathological changes in the soleus (red) and extensor digitorum longus (EDL; white) muscles in Japanese white rabbits after repeated compression with a pneumatic tourniquet. Repeated tourniquet compression via cuff inflation was carried out on the rabbits, calves daily, for 2 h, then stopped for 30 min, and then applied for another 2 h. The contralateral hindlimb, which was not compressed, served as a control. Animals were allocated to 15 groups, with pressures of 40, 80, and 120 mmHg for periods of 1 day, 3 days, 1 week, 2 weeks, and 4 weeks. Skeletal muscle specimens in each group were studied by histopathological and histochemical (ATPase) methods. After compression for 1 day, regardless of pressure, and compression for 3 days in the 40-mmHg pressure group, edematous changes in regions with mild inflammation and increases in fiber diameter were observed in the muscles. After compression for 3 days in the 80- and 120-mmHg pressure groups, and after 1, 2, or 4 weeks in the 40-mmHg pressure group, a few necrotic fibers and scattered fibers with some mononuclear cell infiltrates indicative of early-stage necrosis were detected. In the groups with 80 or 120 mmHg pressure for 1, 2, or 4 weeks, muscle fibers exhibited marked degenerative changes, which were more pronounced in the 120-mmHg group than in the 80-mmHg group. The pathological changes were more pronounced in the soleus than in the EDL muscles, indicating that these two muscles differed in sensitivity to repeated compression. Additionally, average muscle wet weight and average fiber diameter for both types of muscle were increased in the 1-day and 3-day compression groups and decreased in the 1-week, 2-week, and 4-week compression groups. These findings clearly differ from those of previously reported single-compression experiments. Our findings indicate that repeated compression may cause serious muscle degeneration, particularly in red muscles.
authors.affiliation: Department of Orthopaedic Surgery, Asahikawa Medical College, Nishikagura 4-5, 3-11, Asahikawa, Hokkaido 078-8510, Japan.
authors.forename: Y H
authors.initials: YH
authors.lastname: Bai
authors.forename: M
authors.initials: M
authors.lastname: Takemitsu
authors.forename: Y
authors.initials: Y
authors.lastname: Atsuta
authors.forename: Y
authors.initials: Y
authors.lastname: Takemitsu
mesh_terms: D000251:Adenosine Triphosphatases / Q000032:analysis; D000818:Animals; D002908:Chronic Disease; D003161:Compartment Syndromes / Q000209:etiology* / Q000473:pathology; D004487:Edema / Q000473:pathology; D005260:Female; D006614:Hindlimb / Q000473:pathology; D006651:Histocytochemistry; D007963:Leukocytes, Mononuclear / Q000473:pathology; D018656:Muscle Fibers, Fast-Twitch / Q000473:pathology; D018657:Muscle Fibers, Slow-Twitch / Q000473:pathology; D018482:Muscle, Skeletal / Q000473:pathology*; D009220:Myositis / Q000473:pathology; D009336:Necrosis; D009929:Organ Size; D011312:Pressure; D011817:Rabbits; D014111:Tourniquets
chemical_list: D000251:Adenosine Triphosphatases