| AbstractObjective: To study the immunohistochemistry change of excitatory amino acids(EAAs) and neuronal nitric oxide synthase(nNOS) and their roles in chronic spinal cord compression.Material and methods: 36 healthy rabbits were randomly divided into three groups. Group A: normal group(n=10);Group B: control group(n=10);Group C: compressed group(n=16). Membranous sac filled with cardiografin was applied to produce an animal model of chronic spinal cord compression. The sac was gradually enlarged resulting in chronic spinal cord compression in Group C during 12 weeks. Nissl's staining was applied to observe the histopathological change and immunohistochemistry to excitatory amino acids(EAAs; Glu,Asp) and neuronal nitric oxide synthase(nNOS) changes. Results:After 12 weeks, posterior limb muscle strength of Group C was Ⅳ± grade according to the open field walking standard(OFW),while no strength descent was observed in Group B and A. Histopathological change in compressed segments of Group C was as follows: The atrophy of neurons and decline of Nissl bodies were observed; the hyperplasia of gliacytes was also observed in gray matters. No histopathological change was observed in Group B and A.Glutamate(Glu) and Aspartate(Asp) immunoreactivity in the compressed segment of Group C was higher than in the segments of Group B,A and the adjoining and distal segments in itself. The number of nNOS positive motor neurons in the compressed segments of Group C was larger than that in Group B and A. It's immunoreactivity was also higher than that in Group B and A. The changes of EAAs,nNOS and histopathological change were observed in the spinal cord of the same level in Group C.Conclusions:1. The model proved to be an ideal chronic spinal cord compression model according to the observation, and medium grade compression was induced. 2. Compression of the membranous sac was the main factor for CSCI. 3. EAAs and nNOS both played an important role during the secondary spinal cord injury. |
PDF Full Text Request