摘要
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。
To observe in vitro the effects of acute ocular hypertension on the apoptosis of retinal ganglion cells,thirty white-rabbits (body weight2 5~3 0kg)were divided into five groups Six rabbits in each group were made by forcing perfusion of normal saline solution into the anterior chamber until the Iop reached 6 667Kpa and sustained for 6 hours of one eye,another eye 2Kpa The optic nerve and retina was surgically removed at five different time points(1 st day,3 rd day,7 th day,15 th day,30st day)after operation,six rabbits for each time point With the HRP orthograde tracing technique and transmitted electron microscope,the effects of acute ocular hypertension on the RGC was observed by the changes of axonal transport and ultrastructure of optic nerve Compare with control groups,HRP reactive products of experimental groups markedly decreased(P<0 01) The axons in experimental groups were degenerated after one day and some atrophied after fifteen days We concluded that acute ocular hypertension could interrupt the axonal transport and make the axons degenerate,further more,could cause the apoptosis of retinal ganglion cells [WT5”HZ]
出处
《山东医药》
CAS
北大核心
2000年第14期7-8,共2页
Shandong Medical Journal
关键词
急性高眼压
视风膜神经节细胞
兔
细胞凋亡
Ocular hypertension Retinal ganglion cells Axonal transport Ultrastructure Apoptosis Rabbits