急性高眼压模型的建立及其诱导的脂质过氧化反应

Experimental high IOP model and hypertension - induced lipid hyperoxygen reaction

目的 探讨建立高眼压模型的方法,观察急性高眼压诱导的眼组织的脂质过氧化反应。 方法 采用α-糜蛋白酶-水门汀及2％甲基纤维素二种诱导剂于26只家兔前房注入梗阻房角的方法建立高眼压模型,持续高眼压2周后将对照眼及实验眼制备匀浆测定NO、NOS活性及MDA水平,同步测定F-ERG a、b波振幅的变化及视神经纤维层参数分析,参照病理学改变探讨高眼压的毒理作用。 结果 形态学和功能学检查表明高眼压模型建立成功,NO水平在晶状体及脉络膜组织中普遍增高,尤其显著的是视网膜内NO释放上升(P<0.05),NOS活性轻度增高。匀浆内MDA在晶状体及视网膜内显著升高(P<0.01)。该结果与青光眼视神经节细胞凋亡密切相关。结论 高眼压诱导眼内组织NO水平升高,MDA水平显著升高,证实视网膜内具有两个毒性底物(NO、MDA)将诱导形成毒性更强的凋亡剂--过氧亚硝酸阴离子。提示临床给予抗氧化剂治疗青光眼很有必要。

Objective To creat a acute high intraocular pressure (IOP) model and investigate experimental hypertension-induced lipid hyperoxygen reaction in ocular tissue in rabbits. Methods Twenty-six rabbits were randomly divided into a-Chymotrypsin group and 2% Methylcellulose group. High IOP was induced by the anterior chamber injection of above two drugs. IOP, electroretimogram(ERG) and optical nerve fiber thickness were examined, and NOS activity and MDA level in lens, retina and choroidal homogeneous plasma were measured. Results A hypertension model was successfully established in experimental rabbits. IOP was (31. 59±6.49) and (37. 59±11.41) mmHg in two groups,respectively. Loss of retinal ganglion cell was revealed from histologic examination. Biochemical parameters showed that there was a slight increase in NOS activity. NO and MDA levels were significantly increased in lens, chloroid and retina(P < 0. 05) . Change of these biochemical parameters was positive correlation with retinal ganglion cell apoptosis of glaucoma. Conclusion High IOP can induce NO and MDA, suggesting that it is necessary to treatment of glaucoma with antioxidate drug.