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Abstract #15541 Published in IGR 1-3
Inhibition of nitric-oxide synthase 2 by aminoguanidine provides neuroprotection of retinal ganglion cells in a rat model of chronic glaucoma
Neufeld AH; Sawada A; Becker BProceedings of the National Academy of Sciences of the United States of America 1999; 96: 9944-9948
Glaucoma is an optic neuropathy with cupping of the optic disk, degeneration of retinal ganglion cells, and characteristic visual field loss. Because elevated intraocular pressure (IOP) is a major risk factor for progression of glaucoma, treatment has been based on lowering IOP. The authors have previously demonstrated inducible nitric-oxide synthase (NOS-2) in the optic nerve heads from human glaucomatous eyes and from rat eyes with chronic, moderately elevated IOP. Using this rat model of unilateral glaucoma, we treated a group of animals for six months with aminoguanidine, a relatively specific inhibitor of NOS-2, and compared them with an untreated group. At six months, untreated animals had pallor and cupping of the optic disks in the eyes with elevated IOP. Eyes of aminoguanidine-treated animals with similar elevations of IOP appeared normal. The authors quantitated retinal ganglion cell loss by retrograde labelling with Fluoro-Gold. When compared with their contralateral control eyes with normal IOP, eyes with elevated IOP in the untreated group lost 36% of their retinal ganglion cells; the eyes with similarly elevated IOP in the aminoguanidine-treated group lost less than 10% of their retinal ganglion cells. Pharmacological neuroprotection by inhibition of NOS-2 may prove useful for the treatment of patients with glaucoma.
Dr. A.H. Neufeld, Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, MO 63110; USA
Classification:
11.8 Neuroprotection (Part of: 11 Medical treatment)
