摘要
目的:探讨局部滴用倍他洛尔眼药水对实验性视网膜缺血再灌注损伤的治疗作用及其可能的作用机理。方法:采用升高眼内压的方法,制作大鼠实验性视网膜缺血再灌注损伤模型。将SD大鼠随机分为正常组、治疗组和对照组。治疗组右眼滴入0.25%倍他洛尔眼药水,对照组右眼滴入生理盐水。分别在恢复灌注1,3,7d后进行光镜、透射电镜、视网膜电图(ERG)及神经性一氧化氮合酶(nNOS)表达的检测。结果:再灌注1,3,7d后治疗组与对照组相比,病理组织损害明显减轻,ERGb波的恢复程度明显增高。正常视网膜内核层及节细胞层有少量nNOS表达,缺血后nNOS阳性神经元明显增多,治疗组nNOS阳性神经元较对照组明显减少。结论:局部滴用倍他洛尔眼药水对大鼠实验性视网膜缺血再灌注损伤有一定的保护作用,可能与倍他洛尔减少细胞内Ca2+超载,抑制自由基的作用有关。
Objective: To investigate the neuroprotective effect and mechanism of betaxolol on experimental retinal ischemia-reperfusion injury. Methods: Retinal ischemia was induced in SD rats by increasing intraocular pressure to 110 mmHg for 60 minutes.The rats were divided into the nomal group, treatment group and control group randomly.Betaxolol was applied to the treatment group and normal saline to the control group. At the 1st, 3rd and 7th day after reperfusion, rats’ histological and ultrastructural changes in retina and the electroretinography (ERG) b-wave of every group were observed. The expression of nNOS was studied by immunocytochemistry. Results: The histopathologic damages of retina in the control group were more serious compared with the treatment group. The amplitudes of ERG b-wave recovery was significantly higher in the treatment group than in the control group.The nNOS immunoreactive cells were located at the inner nuclear layer(INL)and the ganglion cell layer(GCL)of normal retina.After ischemia-reperfusion, the number of nNOS-located cells increased significantly. Fewer nNOS-positive cells were found in the betaxolol-treated group than in the control group. Conclusion: Betaxolol,by reducing calcium influx and NO production,can protect retina neurons from ischemia-reperfusion injuries.
出处
《武汉大学学报（医学版）》
CAS
2005年第3期387-390,i003,共5页
Medical Journal of Wuhan University
