外伤性视神经损伤动物模型的建立及F-VEP评价

Establishment of animal model of traumatic optic neuropathy and its function evaluation by F-VEP

目的建立视神经损伤和视神经损伤复合晶状体损伤动物模型,了解2种模型损伤后不同时间闪光视觉诱发电位(F-VEP)的变化规律。方法应用液压冲击颅脑损伤仪(FPI)建立兔外伤性视神经损伤模型和视神经损伤复合晶状体损伤模型。于损伤前及损伤后1、2、4、7、10、14、21、28 d行F-VEP检查并进行比较,并于上述各时间点制作视网膜切片,采用免疫组织化学法检测视网膜中巨噬细胞的数量,用焦油紫染色标记存活的视网膜神经节细胞(RGCs),对存活的RGCs进行计数。结果损伤后1 d,实验组与对照组的P100波隐含值和振幅降低,与损伤前相比差异均有统计学意义(P<0.05)。损伤后实验组P100波隐含值延长的时间与对照组相比持续的时间短(P<0.05),14 d后实验组比对照组P100波隐含值恢复得更快(P<0.05)。实验组随着损伤时间的延长巨噬细胞数量明显增加(P<0.05),而RGCs存活数逐渐减少(P<0.05),至损伤后28 d有所恢复。对照组表现出相同的变化趋势。结论应用FPI可以成功建立外伤性视神经损伤动物模型。视网膜组织病理学检测结果印证了F-VEP的检查结果。

Background Visual electrophysiology is a sensitive index for the evaluation of visual function. It has an important value in the assessment of traumatic optic neuropathy. Rabbit is an ideal animal model of traumatic optic neuropathy, and it is simple for the record of flash visual evoked potential（F-VEP） in rabbits. Objective The present study is to establish the animal model of traumatic optic neuropathy with or without lens injury and observe the repairing procedure using F-VEP. Methods Models of traumatic optic neuropathy associated with lens injury were established in the right eyes and only traumatic optic neuropathy were created in the left eyes of 64 healthy SPF Chinese white rabbits using fluid percussion brain injury device （FPI）. F-VEP was recorded based on the Proposal of International Visual Electrophysiology on 1,2,4,7,10,14,21,28 days after injury of optic nerves. Experimental animals were sacrificed in above time points for the histopathological examination. Macrophages were labeled by ED-1 antibody and survival retinal ganglion cells （RGCs）were stained by Nissl method. Results At the first day after injury,the lateneies of Plo0 in both group were longer, and the amplitudes of P100 in both group were lower than before injury, showing statistically significant differences among different time points（ P 〈0. 05 ） ,but no significant difference was seen between the two groups （ P 〉 0.05 ）. The duration of latency in traumatic optic neuropathy associated with lens injury group was shorter than that in only traumatic optic neuropathy group （P 〈 0. 05）. The restore of latency in traumatic optic neuropathy associated with lens injury group was much faster than that in only traumatic optic neuropathy group（ P 〈0.05 ）. The numbers of maerophages were significantly increased and numbers of survival RGCs were considerably decreased with lapse of injury time （ P 〈 0.05 ）. The abnormalities of VEP P100 and RGCs were obviously improved in 28 days after injury in both groups. Conclusion This animal model can be established successfully by FPI. The result of retinal histopathological examination confirms F-VEP findings in this model.