维替泊芬光动力疗法诱导大鼠前部缺血性视神经病变模型研究

A Rat Model of Anterior Ischemic Optic Neuropathy Induced by Verteporfin and 689 nm Laser

目的观察维替泊芬联合689 nm激光光动力疗法诱导建立大鼠前部缺血性视神经病变模型(rat model of the anterior ischemicoptic neuropathy,rAION)的眼底和荧光眼底血管造影(FFA)的变化。方法45只SD雄性大鼠随机分光动力组30只、单纯激光组5只、单纯光敏剂组5只、空白对照组5只。均以大鼠左眼为实验眼。光动力组,分为3个小组,从大鼠尾静脉注入维替泊芬1 mg/kg,在前置镜下用800 mW/cm2能量的689 nm激光分别持续照射大鼠视盘中上2/3区域83、118和236 s,每个时间段各照射10只。单纯激光组仅用689nm激光采用相同激光参数持续照射大鼠视盘118 s;单纯光敏剂组从大鼠尾静脉注入维替泊芬(剂量同上),此两组术后均避强光5 d。空白对照组不做任何处理。通过眼底镜及荧光眼底血管造影观察眼底视神经乳头损伤情况。结果光动力118 s小组造模后第1～6天眼底见视盘上半水肿,236 s小组造模后30 min左右眼底见视盘上半水肿伴视网膜出血,83 s小组眼底视盘未出现明显异常改变;荧光素眼底血管造影表现:光动力118 s小组造模后30 min可见到大鼠视盘上半部早期弱荧光,中后期视盘强荧光,造模≥14 d视盘上部始终低荧光。236 s小组有视网膜血管阻塞。光动力83 s小组、单纯光敏剂组、单纯激光组、空白对照组均未出现眼底及FFA典型改变。结论维替泊芬联合689 nm激光光动力疗法诱导的rAION与人AION相同的眼底和FFA表现。

Objective To establish a rat model of the anterior ischemic optic neuropathy（rAION）,and identify its reliability by observing the fundus,and fluorescein fundus angiography（FFA）. Methods Forty-five male Sprague-Dawley rats were randomly divided into control group with 5 rats,laser group with 5,verteporfin group with 5,low-dose PDT-verteporfen model group with 15,and high-dose PDT-verteporfen model group with 15 rats.All of the right eyes were the test eyes and the left ones were for the control.In the PDT-verteporfen groups the 1 mg/kg or 6 mg/kg drug was injected into the caudal vein of rat after 15 minutes a krypton red laser with 689 nm was used to irradiate the 2/3 disc for 83,118 and 236 seconds.In theverteporfin group the rats were treated by injection of verteporfin into caudal vein.In the control group the rats were not treated. Results In the 118 seconds subgroup from 1 to 6 days after rAION induction the optic neuropathy was pale and swollen in the superior part,at 30 days it was pale and shrunken.In the 236 seconds subgroup the optic disc was bleeding in the superior part 30 minutes after rAION induction and till the first day,bue in the 83 seconds subgroup there was not seen.The FFA showed,in the 118 seconds subgroup there was a hypofluorescence in the superior part of the optic disc at early stage（30 min after）,a hyperfluorescence at midst and late stages,but a hypofluorescence always seen after 14 days.In the 236 seconds subgroup the retinal vein occlusion was seen.In contrast,there was no change in control,laser and verteporfin groups. Conclusions The r-AION model is like as the human AION in fundus and FFA.The rAION model provides the ischemic changes of occurrence of AION,and is helpful for the fundamental study of the AION.