溴莫尼定对视网膜缺血性损伤神经保护作用的实验研究

目的：探讨溴莫尼定(brimonidine)对视网膜缺血性损伤神经的保护作用。方法：新西兰大耳白兔32只，随机分为正常对照组、生理盐水治疗组、噻吗心安(timolol)治疗组、brimonidine治疗组，每组8只。后3组为损伤治疗组，通过生理盐水前房高压灌注的方法，制成视网膜缺血动物模型，在视网膜缺血前lh其结膜囊内分剐给予生理盐水、0．5％timolol眼液或0．2％brimonidine眼液局部治疗。在灌注后7d，观察图形视网膜电图(P-ERG)b波振幅变化，并进行组织形态学观察和视网膜神经节细胞(RGC)计数分析。结果：灌注后7d，3个损伤治疗组相对b波振幅恢复率为：7％、11％和64％，RGC标准丢失率为：43％、38％和12％，brimori-die治疗组视网膜组织形态结构接近正常对照组，而生理盐水治疗组和timolol治疗组视网膜内层组织结构损伤明显。结论：Brimonidine局部治疗对缺血诱导的视网膜结构和功能的损害有明显的神经保护作用。

Study of the neuroprotective effects of brimonidine for ischemia-induced retinal injury

Objective: In this study, we examined the effect of administering brimonidine to rabbit retina after transient ischemia was induced by elevated intraocular pressure(IOP) and verified the potential neuroprotective effect of brimonidine. Methods: Thirty-two New Zealand rabbits were divided into one normal control group and three injury/treatment groups. Transient ischemia was induced in anesthetized rabbit eyes by raising intraocular pressure above systolic blood pressure for 50 minutes. 2 drops of 0.1 milliliter saline, 0.5% timolol or 0.2 % brimonidine were topically administered 1 hour before ischemia. Functional and morphological injury was evaluated. Functional assessment of ischemic damage was recorded by pattern electroretinogram (P-ERG) , and b-wave amplitudes 1 hour before and 7 days after reperfusion were compared and evaluated. The rabbits were sacrificed 7 days after reperfusion and 8 animals in each group were examined by light microscopy and by counting retinal ganglion cells (RGCS) in paraffin-embedded sections. Results: Compared with the animals treated with saline or 0.5% timolol, eyes treated with 0. 2% brimonidine suffered significantly less damage to function and morphology at 7 days after reperfusion. Among the three treatment groups, the recovery rates of P-FRG b-wave amplitude were 7% , 11 % and 64% and the loss rates of RGCS were 43%, 38% and 12% , respectively. The histomor-phology of the brimonidine-trested eyes was almost the same as for the normal control eyes, while the inner structure of the retina was clearly damaged in saline-treated or timolol-treated eyes. Conclusion: Topical treatment with 0. 2% brimonidine 1 hour before ischemia significantly reduced the damage to ocular neurology. These data indicate that brimonidine has the potential to be an optimal neuroprotective agent.