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目的 通过对急性高眼压下大鼠视网膜一氧化氮 (nitric oxide,NO)及其合酶 (nitric oxidesynthase,NOS)变化的分析 ,探讨一氧化氮在高眼压视网膜损伤中的作用。 方法 Wistar大鼠 6 0只 ,随机分成为高眼压 30 min组 ;高眼压 6 0 min组 ;高眼压 90 min组 ;高眼压后 12 h组和高眼压后 2 4h组。前房加压灌注成高眼压模型。利用镀铜镉还原法测定视网膜中 NO- 2 / NO- 3 的含量从而间接反映视网膜组织中 NO的含量。利用免疫组织化学法研究视网膜内神经结构型一氧化氮合酶 (neuronal constitutive nitric oxidesynthase,nc NOS)的分布及其变化。 结果 正常及缺血大鼠视网膜神经结构型一氧化氮合酶 (nc NOS)主要位于大鼠视网膜内核层内侧 ,节细胞层 ,内丛状层。急性高眼压 30 min,6 0 min,90 min大鼠视网膜 NO的含量逐渐下降 (P<0 .0 1) ,nc NOS阳性细胞数也逐渐减少 (P<0 .0 5 ) ,阳性物质表达减弱 ;急性高眼压 90min后再灌注过程中 ,NO的含量比 90 min时明显升高 (P<0 .0 5 ) ,但与正常比较仍显著下降 (P<0 .0 1)。nc NOS阳性细胞数继续减少 (P<0 .0 1)。 结论 一氧化氮参与了急性高眼压下视网膜损伤过程 ;通过nc NOS催化的途径合成的 NO对缺血以及缺血再灌注的视网膜可能具有重要的作用。
OBJECTIVE: To investigate the role of nitric oxide in retinal damage in ocular hypertension by analyzing the changes of nitric oxide (NO) and nitric oxide synthase (NOS) in rat retina under acute ocular hypertension. Methods Sixty Wistar rats were randomly divided into three groups: high intraocular pressure (IOP) for 30 min, intraocular pressure (IOP) for 60 min, intraocular pressure (IOP) for 90 min, intraocular pressure (IOP) for 12 h and intraocular pressure (IOP) for 24 h. Anterior chamber pressure perfusion into high intraocular pressure model. The content of NO-2 / NO-3 in the retina was measured by copper-cadmium reduction to indirectly reflect the content of NO in the retina. The distribution and changes of neuronal constitutive nitric oxide synthase (nc NOS) in the retina were studied by immunohistochemistry. Results The nC NOS of normal and ischemic rats was mainly located in the inner retina, the ganglion cell layer and the inner plexiform layer in the rat retina. The content of nitric oxide in retina of rats with acute intraocular hypertension was decreased gradually (P <0.01) at 30 min, 60 min and 90 min, the number of nc NOS positive cells was also decreased (P <0.05), the expression of positive substance (P <0.05), while the content of NO was significantly higher than that of 90 min after reperfusion (P <0. 05), but still significantly decreased compared with the normal (P <0.01). nc NOS positive cells continued to decrease (P <0.01). Conclusions Nitric oxide is involved in the process of retinal damage under ocular hypertension. NO synthesized by nc-NOS-catalyzed pathway may play an important role in ischemia and reperfusion of the retina.