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选取健康成年新西兰大耳白兔 30只 ,随机分为 5组 ,每组 6只 ,均一眼为高眼压模型眼 ,另一眼为自身对照眼。5组兔分别于制造模型眼后 1、3、7、15和 30天处死。应用辣根过氧化物酶 (HRP)组织化学染色方法和透射电镜技术观察急性高眼压对视神经顺行轴浆运输和超微结构的影响。结果显示实验组较对照组 HRP积分光密度的差异有极显著性 (P<0 .0 1) ;自高眼压后 1天始 ,实验组部分轴突出现肿胀、变性 ,第 15天部分轴突明显萎缩。认为急性高眼压可使视神经顺行轴浆运输发生障碍 ,轴突变性 ,髓鞘松解 ,最终导致 RGC凋亡乃至死亡。
Thirty healthy adult New Zealand white rabbits were randomly divided into 5 groups with 6 in each group. Five rabbits were sacrificed at 1, 3, 7, 15 and 30 days after model eyes were made. The effects of acute intraocular hypertension on the paraxial axoplasmic transport and ultrastructure of the optic nerve were observed by HRP histochemical staining and transmission electron microscopy. The results showed that there was a significant difference (P <0.01) in HRP integral optical density between the experimental group and the control group. In the first day after the intraocular tension, some axons of the experimental group showed swelling and degeneration, Suddenly contracted suddenly. That the acute intraocular hypertension can make optic nerve parastheniosis axial transport disorder, axonal degeneration, myelin sheath release, and ultimately lead to RGC apoptosis and even death.