Glial cell response and iNOS expression in the optic nerve head and retina of the rat following acute high IOP ischemia-reperfusion.

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.