中文摘要：

目的建立慢性视神经损伤动物模型，为进一步实验研究提供基础。方法模仿临床翼点入路，在猫视交叉视神经下植入球囊，分次注入造影剂使球囊逐渐增大，对视交叉视神经形成慢性压迫。所有动物在术前2周用DiI逆行标记视网膜神经节细胞（RGC），在受压后1、2、4和8周分别进行闪光视觉诱发电位（F-VEP）记录，在光镜、电镜下观察视网膜和视神经及对RGC进行计数。结果在光镜下视网膜在8周时出现明显的变化；视神经在2周开始出现髓鞘脱失，随时间延长病变加重，4周出现轴索变性，8周时变性更为明显。电镜下RGC在4周时出现病变，随时间延长进一步加重；视神经在2周时见轻微脱髓鞘，细胞骨架排列轻度紊乱，随时间延长脱髓鞘和轴索变性进一步加重，在8周时可见髓鞘再生。RGC计数显示8周时数量下降约37％（293／465）。F-VEP在4周组开始出现异常，8周组改变更为显著。结论所建立的慢性视神经压迫损伤模型稳定可靠，易于重复。视神经慢性受压后的病理学改变随受压时间的延长和压迫程度的增加而逐渐加重，视网膜发生继发变性，且明显晚于轴索变性。

英文摘要：

Objective To establish an animal model of chronic optic nerve injury which is suitable for experimental research. Methods Dil, a tracer, was injected through the bone windows into the brain of 48 cats so as to mark the retinal ganglion cells （RGCs）. Two weeks later the 48 cats were randomly divided into 6 equal groups. The normal group did not receive any other treatment. Other 8 cats underwent sham operation. Imitating the clinical pterional approach, a balloon was implanted into the place under the optic nerve and chiasm in the other 32 cats, then the volume of the balloons were increased by injecting contrast agent at different times to cause the optic nerve and chiasm compressed chronically for 1, 2, 4, or 6 weeks. Flashvisual evoked potential （F-VEP） was measured before operation and at the corresponding observation times in different groups. By the end of the experiment the cats were killed with the specimens of retina and optic nerve taken out to undergo light microscopy and electron microscopy to observe the pathological changes. Eight eyes were taken out from each group to calculate the number of RCGs 1, 2, 4, and 8 weeks after operation respectively. Results Microscopy showed retina showed profound morphological changes 8 weeks after compression; Demyelination of optic nerve began to occur 2 weeks after compression and progressed later. Axonal degeneration was found 4 week after compression and became more significant 8 weeks later. Under electron microscopy, pathological changes of retina was found 4 weeks and more prominent 8 weeks after compression; Slight demyelination and disorganized of cytoskeleton in the optic nerve were shown 2 weeks after compression, and became more profound later; Myelin regeneration was found 8 weeks after compression. The number of RGCs was reduced significantly by 37% （293/465）since 8 weeks after compression. F-VEP recording showed an extension of latency and depression of amplitude 4 weeks after compression, and the changes were more significant 8 weeks later