CAJ | 학술논문

背景:在脊髓型颈椎病脊髓损伤发生机制的研究过程中,建立稳定且同人类体内疾病演变过程相似的疾病模型对于研究脊髓型颈椎病发病机制至关重要.目的:构建慢性颈脊髓压迫模型,观察该模型病理生理变化特点,进一步明确脊髓型颈椎病受压脊髓组织的病理改变.方法:30只 SD 大鼠随机均分为对照组、轻度压迫组、重度压迫组.将不同大小吸水性压迫材料聚乙烯醇丙烯酰胺互穿网络水凝胶植入 C5-C7椎板下,制作慢性颈脊髓压迫动物模型,对照组不植入压迫材料.结果与结论:MRI 检查显示两压迫组大鼠出现不同程度的椎管狭窄和脊髓压迫,而对照组椎管宽度正常无脊髓压迫.电生理检测显示两压迫组大鼠运动诱发电位潜伏期较对照组明显延长且振幅明显降低(P <0.05).神经元免疫荧光染色显示对照组大鼠脊髓有大量形态规则的神经元,而两压迫组大鼠神经元计数明显减少且神经元胞体形态明显皱缩,脱髓鞘现象明显,3组间比较差异有显著性意义(P <0.05).压迫组大鼠脊髓压迫节段发现较多凋亡细胞,而对照组未发现.说明构建的大鼠慢性颈脊髓压迫模型符合脊髓型颈椎病的病理改变,且手术操作简便,不易感染死亡率低;神经元损伤、脱髓鞘改变和凋亡机制参与了大鼠慢性颈脊髓压迫损伤的发生发展过程.
배경:재척수형경추병척수손상발생궤제적연구과정중,건립은정차동인류체내질병연변과정상사적질병모형대우연구척수형경추병발병궤제지관중요.목적:구건만성경척수압박모형,관찰해모형병리생리변화특점,진일보명학척수형경추병수압척수조직적병리개변.방법:30지 SD 대서수궤균분위대조조、경도압박조、중도압박조.장불동대소흡수성압박재료취을희순병희선알호천망락수응효식입 C5-C7추판하,제작만성경척수압박동물모형,대조조불식입압박재료.결과여결론:MRI 검사현시량압박조대서출현불동정도적추관협착화척수압박,이대조조추관관도정상무척수압박.전생리검측현시량압박조대서운동유발전위잠복기교대조조명현연장차진폭명현강저(P <0.05).신경원면역형광염색현시대조조대서척수유대량형태규칙적신경원,이량압박조대서신경원계수명현감소차신경원포체형태명현추축,탈수초현상명현,3조간비교차이유현저성의의(P <0.05).압박조대서척수압박절단발현교다조망세포,이대조조미발현.설명구건적대서만성경척수압박모형부합척수형경추병적병리개변,차수술조작간편,불역감염사망솔저;신경원손상、탈수초개변화조망궤제삼여료대서만성경척수압박손상적발생발전과정.
BACKGROUND: Establishing a stable model of cervical spondylotic myelopathy is essential for the study of cervical spondylotic myelopathy pathogenesis. OBJECTIVE: To clarify the mechanism of cervical spondylotic myelopathy by establishing a cervical spondylotic myelopathy model and observing the pathophysical changes of this model. METHODS: A total of 30 Sprague-Dawley rats were divided into three groups: control group, mild compression group and severe compression group. Water-absorbing compression materials of different size were implanted below the C5-7 to prepare chronic cervical spinal cord compression models. Control group was implanted nothing. RESULTS AND CONCLUSION: The normal morphology in the control group and varying degrees of compression on the spinal cord and spinal canal stenosis in the two compression groups were shown in MRI. The lower amplitude and longer latency of motor evoked potential after spinal cord compression was found in the two compression groups as compared with the control group (P < 0.05). Immunofluorescence staining showed that that a great number of healthy-shaped neurons were found in the control group. But, the number of neurons in the two compression groups was significantly decreased, and the neurons shrunk and demyelination was obvious. The difference of neuron number among the three groups was statistical y significant (P < 0.05). Apoptosis in the segment of compressed spinal cord was found in the two compression groups rather than in the control group. In conclusion, rat models of chronic spinal cord compression are in line with the pathological changes of cervical spondylotic myelopathy. The surgical procedure is simple and the rate of infection and mortality is lower. Neuronal injury, demyelination and apoptosis are involved in the process of chronic spinal cord compression in rats.