摘要
目的建立大鼠前部缺血性视神经病变（rAION）模型，为缺血性视神经病变的实验研究奠定基础。方法通过光动力疗法诱导rAION。30只实验性SpragueDawley大鼠随机分为4组，空白对照组5只、激光组5只、光敏剂组5只、光动力模型组15只。右眼为实验眼，左眼为对照眼。光动力模型组从大鼠尾静脉注入血卟啉衍生物（HPD）后避光2h，使用多波长氪离子激光机对大鼠右眼视盘中上范围进行照射，激光波长647nm，能量80mw，照射时间120S，光斑直径2／3个视盘直径（DD）；激光组使用光动力模型组相同参数的激光持续照射大鼠右眼视盘120s；光敏剂组单纯从鼠尾静脉注入HPD；空白对照组未做任何处理。通过眼底、荧光素眼底血管造影（FFA）、光相干断层扫描（OCT）、视觉诱发电位（VEP）检查及组织病理学检查观察其形态和组织学变化。结果3只鼠麻醉意外死亡，共27只鼠进入结果分析。造模后光动力模型组第1～6天眼底检查发现视盘上半水肿，第16天视盘上半边界稍清晰，第23天视盘上半灰白萎缩边界清晰直至第90天；造模后30min时FFA检查即可见到大鼠视盘上部强荧光，第1天时FFA检查视盘上部早期弱荧光、中期强荧光；≥16d时视盘上部始终弱荧光；闪光VEP检查P100潜伏期延长、波幅值降低改变（P〈0．003）；第6天时OCT检查显示视盘视神经反射面高出视网膜反射面，且表面粗糙不平厚度增加，第23天时视盘视神经反射面低于视网膜反射面；组织病理学检查，第1天见视盘部分高度水肿，组织疏松，伴盘周视网膜移位；第23天见视盘及附近神经纤维层变薄，盘周神经节细胞核数明显减少。激光组、光。敏剂组和空白组在不同观察点和时段未见眼底、FFA、OCT、VEP和组织病理学上的改变。结论通过光动力方法诱导建立的拟rAION模型，经眼底、FFA、OCT、视电生理和组织病理学证实是成功的，并相似于人类的前部缺血性视神经病变。
Objective To establish an rat model of the Anterior Ischemic Optic Neuropathy （rAION）, and identify its reliability by observing the fundus, fluorescein fundus angiography （FFA）, optical coherence tomography （OCT）, visually evoked potential （VEP） and histopathology. Methods Thirty male Sprague-Dawley rats were randomly divided into group Naive with 5 rats, group Laser with 5 rats, group hematoporphyrin derivative（HPD） with 5 rats, group rAION with 15 rats. All of the right eyes were the experimental eyes and the left ones were the control, after administration of HPD in rats＇ vena caudalis. The rats in group Laser were treated with a krypton red 647nm/2/3disc spot laser for 120 seconds, the rats in group HPD were treated by administration of HPD in rats＇ vena caudalis, and the rats in group Na？ ve were not treated. Results From 1 day to 6 days after rAION induction, the ON was pale and swollen in the superior part. The ON at 90 days after induction was pale and shrunken. 30 minutes after rAION induction, hyperfluorescence appeared in the superior part of the optic disc, and the hypofluorescence in the 23rd day. In early FFA, hypofluorescence appeared at the ischemic area of the optic disc, and in midst and later stage the ischemic area revealed hyperfluorescence in the 1st day after rAION induction, the hypofluorescence in midst and later stage in the sixth day after r-AION model. The latent period of F-VEP expanded. The amplitude cut down in the 1-2 days after r-AION induction and did not changed in 35nd day. The surface of optic disc showed higher and rougher than the surface of retina in the 6th day after r-AION induction in OCT. After fixation and hematoxylin-eosin staining of 6-μm sections, in high power field the optic disc showed edema with the displacement of retina surrounding the disc 1 day after treatment. Rarefaction and degeneration in the nerve fiber of retina and reduction of the number of nuclei of ganglion cells in the 23st day after the model induction, and the thinning of nerve fiber of the optic disc and its surroundings. In contrast, there was no change in group Na？ ve, group Laser and group HPD. Conclusions The r-AION model is like the human AION in fundus, FFA, OCT, VEP and histopathology. The rAION model provides the ischemic changes of occurrence of AION, and is helpful for the fundamental study of the AION.
出处
《中华眼底病杂志》
CAS
CSCD
北大核心
2008年第2期90-94,共5页
Chinese Journal of Ocular Fundus Diseases
基金
陕西省卫生厅科研基金资助项目（04AC1）
