青光眼患者血清及房水一氧化氮浓度的测定

目的 测定青光眼患者血清及房水一氧化氮(NO)浓度并探讨其在青光眼发病中的作用。方法 实验患者分为青光眼组和白内障组,应用硝酸还原酶法分别测定两组患者血清及房水NO浓度。结果 两组患者血清NO浓度无显著性差异,青光眼组内各类型之间血清NO浓度亦无显著性差异。原发性开角型青光眼患者房水NO浓度较对照组及其他类型青光眼显著降低,闭角型青光眼患者房水NO浓度较对照组显著升高(P<0.01)。 结论 眼压升高可引起房水NO浓度升高,过多的NO可损伤小梁网及邻近的葡萄膜及视网膜组织。开角型青光眼患者由于房角原生型一氧化氮合成酶的减少引起房水NO浓度的降低,此可能为眼压升高的原因之一。

Nitric oxide level of serum and aqueous humor in glaucoma patients

Objective To detect the nitric oxide (NO) level of serum and aqueous humor in glaucoma patients and study its possible role in the pathogenesis of glaucoma. Methods Forty-two patients (84 eyes) were divided into glaucoma group and control group. The glaucoma group included primary open-angle glaucoma (POAG) ,primary chronic angle-closure glaucoma and primary acute angle-closure glaucoma. NO levels in serum and aqueous humor were detected by NO reductase method. Results There was an insignificant difference of NO level in serum between the glaucoma group and the control group, and the difference was also seen among different types of glaucoma. The NO level of aqueous humor in POAG group was significantly lower than that of the control group and was significantly higher in the angle-closure glaucoma in comparison with the control group. Conclusion Elevation of intraocular pressure induces the increase of NO level in aqueous humor and further damages the trabecular meshwork,adjacent uvea and retina. For the POAG patients,decrease of NO synthetase in anterior chamber angle can induce decrease of NO in aqueous humor resulting in higher outflow resistance of aqueous humor.