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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 ,对改善视功能有极其重要的意义
OBJECTIVE: To dynamically observe the changes of retina and optic nerve morphology and visual function after optic nerve clip contusion, reveal the inherent rules of the pathological process and provide the basis for the study of optic nerve protection. Methods: The morphological changes of optic nerve and retina in normal and optic nerve contusion rats at 4, 4, 8, 72 hours, 1, 2 and 4 weeks were observed by light microscope and electron microscope. The visual acuity of flash light was detected normal and 1 hour after optic nerve injury , 4 weeks rat visual function status. Results: RGCs decreased significantly in the part of optic nerve, the number of RGCs decreased rapidly in the first two weeks after injury, and decreased slowly after 2 weeks. The chromatin of RGCs was obviously aggregated, Intact; nuclear membrane lysis can also be seen, organelle edema, disintegration; optic nerve fibers staggered axonal vacuolar degeneration in the injury process, myelin disintegration, disappearance, glial cell proliferation; optic nerve injury F VEP waveform more normal Low and wide, damage 4 weeks waveform disappears. Conclusion: Secondary neuronal injury is an important reason for the progressive decline of visual function. Protecting neurons from secondary injury is an important aspect of optic nerve protection and has an extremely important significance for improving visual function