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目的:建立马尾神经综合征的实验模型,进一步探讨马尾神经综合征形成的机制。方法:将纯种健康雄性封闭群清洁级新西兰兔80只随机分为3组:对照组、模型1加压组、模型2加压组,应用改良的EirenToh马尾神经实验压迫模型,进入椎管矢状径的1/9,2/9,1/2,造成马尾神经压迫产生神经症状,对症状、骶神经功能检测,并进行定量分析、马尾神经、神经根、骶髓做组织病理学和免疫组织化学的研究,并进行定性分析。结果:模型2较模型1同等条件下,易导致马尾神经损害;各实验组马尾神经综合征发病1/2d,其马尾神经组织均出现广泛的炎性反应,骶髓前角细胞出现凋亡;骶神经功能综合测定,A1,A2,A3(1.8±0.9,2.0±1.6,6.3±2.1),B1,B2,B3(4.3±1.9,6.4±3.0,9.6±2.7)同对照组和其他时间段比较,差异有显著性差异意义(P<0.05)。结论:压迫马尾神经导致马尾神经损害,双节段压迫比单节段压迫更易出现广泛马尾神经损害;马尾神经压迫点的病理改变向头、尾两端扩散,形成广泛病理损害;骶髓前角细胞出现凋亡,且骶神经损伤症状出现1/2d时达到高峰。
Objective: To establish an experimental model of cauda equina syndrome and to further explore the mechanism of the formation of cauda equina syndrome. Methods: Eighty pure New Zealand male rabbits were randomly divided into three groups: control group, model 1 pressure group and model 2 pressure group. The model was induced by modified EirenToh cauda equina nerve and spinal canal Diameter of 1/9, 2/9, 1/2, resulting in cauda equina nerve compression symptoms, symptoms, sacral nerve function testing, and quantitative analysis, cauda equina, nerve root, sacral histopathology and immune Histochemistry, and qualitative analysis. Results: Compared with model 1, model 2 could easily lead to cauda equina injury. In the experimental group, cauda equina appeared extensive inflammatory reaction in cauda equina neurons 1 / 2d after the onset of cauda equina syndrome and apoptotic sacral anterior horn cells appeared. Sacral nerve function, A1, A2, A3 (1.8 ± 0.9,2.0 ± 1.6,6.3 ± 2.1), B1, B2, B3 (4.3 ± 1.9,6.4 ± 3.0,9.6 ± 2.7) with the control group and other time periods The difference was significant (P <0.05). Conclusion: The cauda equina nerve resulted in cauda equina nerve injury, double segmental compression is more prone to extensive cauda equina injury than single segmental compression. The pathological changes of cauda equina compression point diffuse to the head and tail, forming extensive pathological damage; sacral anterior horn Apoptotic cells appeared, and the sacral nerve injury symptoms peaked 1 / 2d.