实验性外伤性视神经萎缩动物模型的建立

An experimental model of traumatic optic nerve atrophy

目的 探索并确立实验性外伤性视神经萎缩模型的建立方法。方法 采用改良的Kr lein术式 ,在定量致伤的条件下建立实验性外伤性兔视神经萎缩模型 ,于 2 0d和 40d后分批作闪光视觉诱发电位 (F VEP)和病理形态学检查。结果 改良的Kr lein术式造模 40d后 ,造模组兔眼视觉电生理的F VEPP1波和N1波波幅极显著降低 (P <0 0 1) ,峰时极显著延长 (P <0 0 1) ;神经纤维数量极显著减少 (P <0 0 1)、髓鞘积分光密度极显著降低 (P <0 0 1)、神经胶质细胞显著增生 (P <0 0 5 )。结论 采用改良的Kr lein术式建立的实验性外伤性兔视神经萎缩模型是成功的。

Objective To establish an experimental animal model of traumatic optic atrophy(TOA). Methods With a fixed amount of wound,the rabbit model of TOA was established by reformative Krlein operation.After 20 and 40 days,all the rabbits received the examinations of flash visual evoked potential(F-VEP) and pathomorphology. Results The amplitudes of P 1and N 1 of F-VEP were significantly low(P<0.01),and the latencies of P 1 and N 1 were significantly prolonged (P<0.01).The amount of optic nerve fiber was significantly decreased (P<0.01) because of demyelination (P<0.01) and neuroglia cell hyperplasia (P<0.05) after 40 days of trauma. Conclusion Ligaturing optic nerve can induce experimental rabbit model of optic nerve atrophy.