急性高眼压状态大鼠视网膜一氧化氮 及其合酶变化的研究

目的通过对急性高眼压下大鼠视网膜一氧化氮(nitric oxid e,NO)及其合酶(nitric oxide synthase，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60只，随机分成为高眼压30 min组；高眼压60 min组；高眼压90 min组；高眼压后12 h组和高眼压后24 h 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NO₂^－/NO₃^－ 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 oxide synthase,ncNOS)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(ncNOS)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30min,60min ,90min大鼠视网膜NO的含量逐渐下降(P<0.01)，ncNOS阳性 细胞数也逐渐减少(P<0.05)，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90min时明显升高(P<0.05)，但与正常比较仍显著下降(P<0.01)。ncNOS阳性细胞数继续减少(P <0.01)。结论一氧化氮参与了急性高 眼压下视网膜损伤过程；通过ncNOS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。(中华眼底病杂志,2001,17:230-233)

The changes of nitric oxide and nitric oxide synthase in rat retina under acute ocular hypertension

Objective To analyse the changes of nitric oxide and nitric oxide synthase in rat retina under acute high ocular pressure and study the effect of nitric oxide in rat retinal damage under hypertension. Methods Sixty Wistar rats were divided randomly into five groups:Ocular hypertension 30 min,60 min,90 min and 12 h,24 h after reperfusion.Elevation of the ocular pressure in the anterior chamber of the rat eye caused retina ischemic damage.The changes of retinal nitric oxide content were observed indirectly by measuring NO 2 -/NO 3 - content in retina.The distribution and changes of neuronal constitutive nitric oxide synthase (ncNOS)were studied by immunocytochemical localization of ncNOS. Results ncNOS positive neurons were distributed in the inner nuclear layer (INL),ganglion cell layer (GCL) and the inner plexiform layer of the normal and ischemic rat retina.During acute high IOP 30 min,60 min and 90 min,NO content decreased gradually and ncNOS immune activity weakens.During reperfusion,NO content increased remarkably (P<0.05)as compared with the groups of hypertension 90 min and decreased remarkably as compared with the normal rat retina.But ncNOS positive neurons continue to decrease compared with the groups of hypertension 90 min. Conclusion NO participates the rat retinal injury by acute elevated intraocular pressure,and nitric oxide synthetized by ncNOS may play an important role in protecting the retina from ischemic and post ischemic injury.