持续性低眼压对视功能损伤机制实验研究

Experimental study on the mechanism of the damage of visual function during the persistent ocular hypotony.

目的探讨眼外伤后或手术后持续性低眼压对视功能损伤的机制。方法健康青紫兰兔48只,随机分为6组,实验组动物双眼均接受CO2激光外路巩膜切除术,化学比色法测定视网膜匀浆中一氧化氮(NO)、丙二醛(MDA)的含量和Na+-K+-ATP酶的活性,进行统计学分析。结果各实验组动物视网膜NO、MDA含量随低眼压时间的延长而持续上升,Na+-K+-ATP酶活性持续下降,71、01、42、1天组与正常组相比差异均有统计学意义(P<0.05)。NO含量与MDA含量呈显著正相关(r=0.812,P<0.01),与Na+-K+-ATP酶活性呈显著负相关(r=-0.857,P<0.01),MDA含量与Na+-K+-ATP酶活性呈显著负相关(r=-0.835,P<0.01)。结论脂质过氧化作用及自由基反应是造成持续性低眼压时视网膜结构及功能损伤的重要原因。

Objective To explore the mechanism of the damage of visual function during the persistent ocular hpotony. Methods Forty-eight healthy black and blue rabbits were chosen and divided into 6 groups at randomly. Experimental groups were performed surgery with CO/laser sclerectomy in both eyes. Contents of nitric oxide （NO） and malonyldialohyed （MDA） and the activity of Na^＋ -K^＋ -ATPase were tested with biochemical assays. All the data were analyzed statistically. Results Biochemical assays indicated： the contents of NO and MDA increased and the activity of Na^＋ -K^＋ -ATPase decreased significantly （P 〈0.05） in 7days, 10 days, 14 days, 21 days groups. There were positive correlation between NO and MDA （ r = 0. 812, P 〈 0.01 ） and negative correlations between MDA and Na^＋-K^＋-ATPase （r = -0.835,P〈0.01）, NO and Na^＋-K^＋-ATPase （r= -0.857,P 〈 0.01）. Conclusions Free radical reactions and lipid peroxidations resulting from NO were important reasons for the injuries of retina.