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 ,与青光眼的发病具有密切关系 To investigate the possible role of nitric oxide in the pathogenesis of glaucoma by analyzing the changes of nitric oxide and its synthase in the iris and ciliary body of rats with ocular hypertension. Methods: Twenty-four Wister rats were randomly divided into high intraocular pressure (IOP) for 30 minutes, intraocular pressure (IOP) for 60 minutes, intraocular pressure (IOP) for 90 minutes and anterior chamber pressure (IOP) model. The content of NO-2 / NO-3 in the iris was measured by copper-cadmium reduction to indirectly reflect the content of NO in the iris. Using immunohistochemistry to study the distribution and changes of endothelial nitric oxide synthase (ecNOS) in the ciliary body. Results: The cortical nitric oxide synthase in the ciliary body of normal and ischemic rats mainly located in the cytoplasm of rat ciliary body epithelial cells. The acute intraocular pressure for 30 minutes, 60 minutes and 90 minutes, the content of NO in rats decreased gradually (P <0.01), and the number of ec NOS positive cells decreased gradually (P0.05) , The expression of positive substance weakened. Conclusion: Nitric oxide is involved in aqueous humor drainage under acute ocular hypertension and is closely related to the pathogenesis of glaucoma