摘要
目的 :动态观察视神经夹挫伤后视网膜、视神经形态学和视功能变化 ,揭示其病理过程的内在规律 ,为视神经保护研究提供依据。方法 :应用光镜、电镜观察正常及视神经夹挫伤 2 4、4 8、72小时 ,1、2、4周大鼠的视神经和视网膜形态学改变 ,闪光视觉诱发电位检测正常及视神经损伤后 1小时、4周大鼠的视功能状况。结果 :视神经部分损伤诱导视网膜神经节细胞 (RGCs)严重下降 ,损伤后的前 2周RGCs快速减少 ,2周以后缓慢减少 ;电镜下可见RGCs染色质明显聚集 ,胞体皱缩 ,核膜、胞膜完整 ;也可见核膜溶解 ,细胞器水肿、崩解 ;视神经纤维在损伤过程交错存在着轴突空泡样变 ,髓鞘崩解、消失 ,胶质细胞增生 ;视神经急性损伤F VEP波形较正常变得低而宽 ,损伤 4周波形消失。结论 :神经元继发性损伤是视功能进行性下降的重要原因 ,保护神经元免受继发性损伤是视神经保护的重要方面 。
Objective:To understand the featares of morphological and functional changes of optic nerve and retina after optic nerve crush.Methods:The changes of optic nerve and retina were observed using the light microscope and electron microscope,and the visual evoked potential response to flash (F VEP)was recorded in normal and optic nerve crush rats.Results:Retinal ganglion cells (RGCs) were reduced significantly due to partial lesion of optic nerve crush.An initial loss was accelerated by 2 weeks after nerve crush,thereafter declines was protracted in RGCs densities.Under electron microscopy chromatin aggregation of RGCs became conspicuous.Cell bodies were prominently furrowed.Condensed nuclei presented in the retina.Cytoplasmic atrophy was profound,and nucleus membrane was in its integrity.Other injured ganglion cells membranes might be dissolved and showed dropsy and disintegration of organelle.Under electron microscopy and light microscopy,the optic nerve fiber collapsed and their axons showed vacuolation after optic nerve crush.Glial cell showed hyperplasia.The latency extended and the amplitude was depressed 1 hour after crush.No response was observed in animals 4 weeks later.Conclusion:It shows that the excessive loss of neurons due to secondary degeneration following optic nerve crush is the most important factor for visual impairment.Therefore,it is highly crucial to protect neurons from secondary damage for improving visual function.
出处
《眼科》
CAS
2003年第6期357-360,共6页
Ophthalmology in China
基金
北京市卫生局科研基金资助 (编号 :12 8)
