摘要
目的 探讨闭合性小脑挫伤病变发生发展过程。 方法 建立闭合性小脑挫伤动物模型 ,分别于损伤后不同时间组 5min、10min、3 0min、45min、60min、2h、4h、6h、8h、12h与正常组对照 ,观察其电镜变化。 结果 损伤后不同时间组 ,小脑蒲肯野氏细胞线粒体水肿、空泡化从轻到重 ,线粒体嵴逐渐消失。神经纤维髓鞘疏松断裂 ,神经原丝及微管结构模糊 ,并随着时间推移 ,其损伤越来越重。损伤后 3 0min ,线粒体胞浆中充满了游离核糖体。损伤后 1～ 2小时小脑蒲肯野氏细胞胞浆浓缩 ,细胞核开始发生染色质边集。个别细胞核发生核溶解。至 4～ 6小时小脑蒲肯野氏细胞细胞核坏死发展到高峰 ,然后逐渐减轻。损伤后 8小时 ,小脑血管内皮细胞线粒体水肿 ,嵴消失 ,神经纤维髓鞘松解 ,胶质细胞核周间隙扩张。 结论 闭合性小脑挫伤后不同时间电镜变化 ,为早期损伤时间推断的法医学鉴定提供了病理学基础。
Objective To explore the pathogenesis of closed cerebellum concussion in SD rats. Methods Animal model of closed cerebellum concussion in SD rats were established, the samples was taken at 5 min,10 min,30 min,45 min,60 min,2 h,4 h,8 h,12 h after injury respectively, tissue changes in injury group were observed under electron microscope compared with normal. Results At earler post-injury stage such as 5 min,10 min,30 min,45 min,60 min,2 h, vacuole and edema of mitochondria as well as disappeared mitochondria crista become increasingly serious in Purkinje cells. Myelinolysis such as myelin loose and rupture in partly, and the structure obscure of neurofibrils and microtube were seen in time-depended. After injury 1～2 h, Purkinje cells of plasma began concentrated. Cellular nucleus began to happen chromatin margination. A few of cellular nucleus was karyolysis. The peak of Cellular necrosis was found at post-injury 4～6 h. After injury 8 h, mitochondria edema and crista disappearance in vascular epithelium cells was observed. In addition to, loose myelin of nerve fibers and expansion astrocyte interval were also observed. Conclusion This experiment results provides the pathological basis for forensic investigation of closed cerebellum concussion in early stage.
出处
《法律与医学杂志》
2004年第2期126-128,共3页
Journal of Law & Medicine
基金
浙省温州市科委课题 (S2 0 0 2A0 71 )
