急性高眼压状态大鼠虹膜睫状体一氧化氮及其合酶的变化

The changes of nitric oxide and nitric oxide synthase in rat iris and ciliary body under acute ocular hypertension

通过对急性高眼压大鼠虹膜睫状体一氧化氮及其合酶变化的分析 ,探讨一氧化氮在青光眼发病机理中可能的作用。方法 :Wister大鼠 2 4只 ,随机分为高眼压 30分钟组 ;高眼压 6 0分钟组 ;高眼压 90分钟组 ;前房加压灌主制成高眼压模型。利用镀铜镉还原法测定虹膜中 NO- 2 / NO- 3的含量从而间接反映虹膜组织中 NO的含量。利用免疫组织化学法研究睫状体内内皮结构型一氧化氮合酶 (ec NOS)的分布及其变化。结果 :正常及缺血大鼠睫状体内皮结构型一氧化氮合酶主要位于大鼠睫状体上皮细胞的胞质中。急性高眼压 30分钟 ,6 0分钟 ,90分钟 ,大鼠虹膜 NO的含量逐渐下降 (P〈0 .0 1〉) ,ec NOS阳性细胞数也逐渐减少(P〈0 .0 0 5〉) ,阳性物质表达减弱。结论 :一氧化氮参与了急性高眼压下房水引流过程 。

Obhective:To analyse the changes of nitric oxide and nitric oxide synthaze in rat iris and ciliary body under acute high ocular pressure and discuss NO possible role in glaucoma.Methods:24 wister rats are divided randomly into four groups:hypertension 30min,60min and 90min.Elevation of the ocular pressure in the anterior chamber of the rat eye caused acute ocular hypertension.The changes of iris nitric oxide content were observed indirectly by measuring NO - 2/NO - 3 content in iris.The distribution and changes of endothelium constitutive nitric oxide synthases(ecNOS)in the ciliary body were studied by immunocytochemical localization of ecNOS.Results:ecNOS positive neurons were distributed in the epithelium cell of ciliary body.During acute high IOP 30min,60min,90min,NO content decreased gradually (P〈0.001〉and ecNOS immunoreactivity weakens (P〈0.005〉after hypertension.Conclusion:NO participate the aqueous humor flow by acute elevated intraocular pressure,Nitric oxide may play an important protecting role in glaucoma.