Department of Ophthalmology and Visual Science, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Brain Res. 2011 Jul 27;1403:67-77. doi: 10.1016/j.brainres.2011.06.005. Epub 2011 Jun 12.
Acute high IOP ischemia-reperfusion induces the loss of retinal ganglion cells, supporting the hypothesis that the condition of ischemia-reperfusion contributes to the induction and progression of glaucoma. This study investigated morphological changes, glial cell response, and expression of inducible nitric oxide synthase (iNOS) in the optic nerve head and retina of the rat following acute high IOP ischemia-reperfusion. A 60-min ischemic period was administered to the rat eye by raising the IOP, followed by a reperfusion period lasting 2, 5, or 7 days. Histological examination showed that acute high IOP ischemia-reperfusion injury produced optic nerve head and retina damage. In immunohistochemical staining, GFAP and OX-45 were limited to the ganglion cell layer (GCL) or inner nuclear layer (INL) of the control retina and increased to nearly all layers of the retina after acute high IOP ischemia-reperfusion. GFAP and OX-42 were detected at the control optic nerve heads and increased after acute high IOP ischemia-reperfusion. After acute high IOP ischemia-reperfusion, expression of iNOS increased, mostly at the GCL and INL of the retina and at the optic nerve head. Western blot analysis showed that expression of iNOS increased significantly, compared with the control, in the retina and optic nerve head after acute high IOP ischemia-reperfusion. Activation of glial cells and the up-regulation of iNOS may contribute to the damage of the retina and optic nerve head of the rat following acute high IOP ischemia-reperfusion.
急性高眼压缺血再灌注引起视网膜神经节细胞丢失，支持缺血再灌注状态导致青光眼发生和发展的假说。本研究通过升高眼压对大鼠眼进行 60 分钟的缺血期，然后进行 2、5 或 7 天的再灌注期，观察急性高眼压缺血再灌注后大鼠视神经头和视网膜的形态变化、神经胶质细胞反应和诱导型一氧化氮合酶（iNOS）的表达。组织学检查显示，急性高眼压缺血再灌注损伤导致视神经头和视网膜损伤。免疫组织化学染色显示，GFAP 和 OX-45 仅局限于对照组视网膜的神经节细胞层（GCL）或内核层（INL），而在急性高眼压缺血再灌注后增加到几乎所有视网膜层。GFAP 和 OX-42 在对照视神经头检测到，并在急性高眼压缺血再灌注后增加。急性高眼压缺血再灌注后，iNOS 的表达增加，主要在视网膜的 GCL 和 INL 以及视神经头。Western blot 分析显示，与对照组相比，急性高眼压缺血再灌注后视网膜和视神经头 iNOS 的表达显著增加。神经胶质细胞的激活和 iNOS 的上调可能导致大鼠急性高眼压缺血再灌注后视网膜和视神经头的损伤。
