尼莫地平注射液对兔急性高眼压致视网膜损伤保护作用的研究

目的探讨急性高眼压后活性氧自由基对视网膜组织的损伤情况及尼莫地平注射液(尼膜同)对高眼压致视网膜损伤的保护作用.方法观察6.67kPa(50mmHg)、维持5h的高眼压解除72h内兔视网膜丙二醛(malondialdehyde,MDA)含量、超氧化物歧化酶(superoxidedismutase,SOD)活性、还原型谷胱甘肽(glutathione,GSH)含量的变化情况及静脉注射尼莫地平注射液(尼膜同)对高眼压解除后24 h时兔视网膜组织中MDA含量、SOD活性、GSH含量的影响.结果 MDA于高眼压解除后0～24h逐渐增加,24～72h维持较高水平.SOD活性于高眼压解除4 h后增高,以后随时间延长逐渐下降.其中高眼压解除时及解除24h后SOD活性明显低于正常水平.GSH含量在高眼压解除后72h内无明显变化,且均低于正常水平.静脉注射尼莫地平能使MDA含量增高幅度下降,在一定程度上提高SOD活性和GSH含量.结论活性氧自由基参与了高眼压致视网膜损伤,静脉注射尼莫地平对提高视网膜抗氧化损伤能力有积极意义.

Protective Effects of Nimodipine on Rabbit Retinal Injuryby Acute Intraocular Hypertension

Objective To study active oxygen and free radical injury in rabbit retina during elevated intraocular pressure and the protective effect of Nimodipine on the retinal damage by the hypertension. Methods Lipid peroxidative product, malondialdehyde(MDA) , activity of superoxidedismutase(SOD) , reduced glutathione(GSH) in the retinal tissue were measured during 72h after the release of an ocular hypertension, 6. 67kPa(50mmHg) maintaining for 5h, and the effects of venous injection nimodipine on the level of MDA, GSH and the activity of SOD in the retinal tissue after the release of ocular hypertension for 24 h were observed. Results MDA increased gradually during 0~24 h after the release of ocular hypertension and maintained at a relatively high level in 24-72h. The activity of SOD increased at 4 h after the release of ocular hypertension and decreased gradually after it. GSH maintained at a relatively low level in 72 h. Venous injection of nimodipine reduced the production of MDA in the retinal tissue and enhanced SOD activity and the level of GSH. Conclusions Active oxygen and free radicals participate the rabbit retinal injury by elevated intraocular pressure. Venous injection of nimodipine plays a beneficial role in enhancing the antioxidative ability of the retina.