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小鼠经腹腔内注射丙烯酰胺每日60mg/kg,每周5次,于染毒14次后出现双后肢严重瘫痪。光镜及电镜下观察到坐骨神经、肌间神经束、脊髓后索及后外侧索神经纤维呈轴索变性,以轴索内大量神经微丝聚集为其早期病理特征,比目鱼肌出现肌纤维萎缩。病变分布符合中枢-周围性远端型轴索病(Central-Peripheral Distal Axonopathy)。中毒早期即见有神经节细胞中央染色质溶解及核偏位等病理变化,脊髓前角细胞未见异常,提示感觉神经受累较早较重。中毒极期时小鼠小脑大量浦氏细胞固缩,电镜下发现浦氏细胞胞浆中滑面内质网扩张聚集,呈洋葱皮样排列,并可见血管壁旁星形细胞终足肿胀,压闭微血管腔。
Mice were injected intraperitoneally with acrylamide 60mg / kg daily for 5 times a week, and severe paralysis of both hind limbs occurred after 14 times of exposure. Under the light microscope and electron microscope, sciatic nerve, myenteric nerve bundle, posterior spinal cord and posterior lateral optic nerve fibers were observed axonal degeneration, a large number of neurofilaments gathered in the axonal pathological features of the early, soleus muscle fibers appeared atrophy. The distribution of the lesions conforms to the Central-Peripheral Distal Axonopathy. In the early stage of poisoning, there were pathological changes such as central chromatin dissolution of ganglion cells and nuclear deviation, no abnormality of anterior horn cells of the spinal cord, indicating that the sensory nerve involvement was earlier and heavier. Poisoning period when a large number of mouse cerebellum Purkinje cell shrinkage, Pu found in the cytoplasm of Puce cells in the endoplasmic reticulum expansion and aggregation, onion skin-like arrangement, and visible end of the blood vessel wall astigmatism, pressure Closed microvascular lumen.