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慢性压迫性颈脊髓损害的超微结构观察 被引量:5

Ultrastructural observation of damaged cervical cord by chronic compression
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摘要 目的:对颈脊髓慢性压迫性损伤的超微结构进行观察研究,探讨其病理生理机制。方法:短毛豚鼠12只,8只用于模型制备,4只为正常对照。建立颈脊髓慢性压迫动物模型,分别于术后4周、8周对实验动物进行运动功能及电生理评价,并分批处死动物取样切片,以日本东芝H-600型透射电镜(每次动物4只),与正常组进行对照。结果:术后4周脊髓前角运动神经元胞体肿胀,胞浆内粗面内质网排列尚规则,核糖体仅部分脱落,部分线粒体肿胀,线粒体嵴清晰。白质前索呈原发性脱髓鞘改变,髓鞘变薄排列松散,胶质细胞水肿,部分有脱髓鞘改变,轴索结构基本正常。脊髓内毛细血管腔变细,内皮细胞肿胀。术后8周脊髓前角神经元胞体缩小或固缩,核内染色质成团块状,粗面内质网排列紊乱,线粒体广泛肿胀,嵴模糊。白质侧索髓鞘排列松散,出现原发性脱髓鞘改变,前索广泛脱髓鞘改变,部分轴索出现变性、坏死等改变。脊髓内毛细血管腔闭塞,内皮细胞凋亡变性。结论:来自前方的颈脊髓慢性压迫性损害,早期主要引起脊髓前索的原发性脱髓鞘改变。随着压迫程度的加重和时间的延长,逐渐出现脊髓内血供障碍、脊髓前角运动神经元退变、前索轴突变性等不可逆性改变。 Objective: To observe spinal ultrastructures on the animal modal of the chronic cervical cord compression and explore its pathogenesy. Methods: 8 guineapigs were used to establish the models of the chronic cervical cord compression by BMP implantation, and 4 were taken as the controls. The animals were sacrificed 4 and 8 weeks postoperatively for the evaluation of motor functions and electrophysiology, while the spinal sections from the models and the controls were performed ultrastructural observation. Results: On the cervical cord sections obtained from animals at the 4 week postoperatively, the swell of motoneurons and chondrosomes, the abalation of ribosomes, the degeneration of myelin sheaths and the decreased diameter of capillary vessels can be found. After 8 weeks, motoneurons in the grey horn began to shrink, chromatin clumped, rough endoplasmic reticulum deranged, capillary vessels obliterated, endothelial cell started the apoptosis, chondrosome swelled extensively, as well the primary demyelination appeared. Conclusions: Chronic anterior cervical cord compression will induce primary demyelination of anterior tract at the early stage. Poor blood perfusion and the degeneration of motoneurons and axons gradually appeared following the development of the compression.
出处 《中国临床解剖学杂志》 CSCD 北大核心 2008年第5期536-538,共3页 Chinese Journal of Clinical Anatomy
关键词 脊髓 颈脊髓慢性压迫 超微病理 spinal cord chronic cervical cord compressiom ultrastructural change ultrastructure
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