ABSTRACT
Objective To investigate the regenerating effect of muscle satellite cells autografted onto mus-cles injured by chronic compartment syndrome (CCS). Methods Twenty-four adult rabbits were randomly divided into an experimental group (model-transplantation), a non-graft group (model) and a control group (transplanta-tion). The CCS model was established in the experimental and non-graft groups. Transplantation was done in the ex-perimental and control groups. Satellite cells from the experimental and control group rabbits were isolated and then proliferated in vitro. The specific protein was identified by immnochemistry before engrafting. Then the 4',6-diamidi-no-2-phenylindole-tagged satellite cells were transplanted back to the original soleus muscles. After transplantation,the proliferation and differentiation of the satellite cells in vivo was observed and morphological changes at the site of the injury were compared by HE staining. Results At the 28th day after grafting, the satellite cells from the com-pressed soleus muscles in the experimental group had increased significantly, whereas those in the control group had remained the same. In both the graft group and the non-graft group, HE staining showed a large cluster of myofibers and interstitial fibers necrosed in the compressed muscle, while the skeletal muscle fibers and interstitial fibers were in-tact in the control group. At the 28th day after engrafting, the engrafted muscle showed much repair; but the non-en-grafted muscle demonstrated dominant fibrosis. The morphology of the skeletal muscle in the control group was normal.Conclusions Autografting of muscle satellite cells after a small amount of expansion in vitro could improve their regen-eration efficiency for repairing a large cluster of damaged myofibers caused by chronic compartment syndrome.
ABSTRACT
Objective To discuss pathogenesis of low back pain induced by chronic compartment syndrome. Method Thirty patients who had definite chronic lumboscaral compartment syndrome without other lumbal diseases were choosed respectively to test muscle force of lumbar and abdomen,intra-sacrospinal muscle pressure,blood routine,ESR,CK,CK-MM,LDH and LDHs.All patients received decompressive operation.Skeletal muscle specimens taken from sacrospinal muscle in each operation were possessed for histological and ultrastructuml observation. Result All of enzyme tests were normal.The author could observe the dissolved degeneration of part of sacrospinal muscle fibers,muscle fiber hypertrophy,and a small quantity of inflammatory cell infiltration with a light microscope.Focal solution of muscle fiber,the aggregation of mitochondria around the nucleus,the increase of lipid droplet and lysosome in cyte,and the proliferation and differentiation of muscle satellite cell could be observed with an electron microscope. Conclusion Pathogenesis of chronic lumboscaral compartment syndrome may be as followed.Intra-compartmental pressures increase,causing metabolism disturbance of the tissues under fascia compartment,damaging skeletal muscle chronically,then inflammatory factors are released,which stimulates posterior branch of spinal nerves,and finally induces low back pain.
ABSTRACT
Objective To study the methods of clinic al diagnosis and treatment of chronic lumbar pain induced by chronic compartment s yndrome. Methods Thirty-nine patients with chronic lumbar pain induced by chronic compartment syndrome were recruited. Their diagno sis was confirmed by physical examination and measurement of of lumbar muscle in tra-compartment pressure. Micro-invasive opening decompression of the lumbar c ompartment was performed for treating these patients. Therapeutic exercises of t he lumbar and abdomen muscles were administered 2-days after operation. Results After treatment, the symptoms were significantly r elieved, distance of walk in creased as compared with those before operation. Th e ranges of trunk flexion and extension were increased. A comparison with the pr etreatment showed that the lumbar muscle intra-compartment pressures at rest du ring movement and 6 min after movement were decreased(6.6?0.7 vs 11.1?0.7),(16 0.3?11.15 vs 188.1?12.08)and(6.9?0.8 vs 14.1?1.2)mmHg, respectively ( P