PURPOSE: To test the hypothesis that nitric oxide, synthesized by inducible nitric oxide synthase, causes degeneration of retinal ganglion cells in an animal model of glaucoma. METHODS: Rats with unilateral, chronic, moderately elevated intraocular pressure were treated orally with L-N(6)-(1-iminoethyl)lysine 5-tetrazole amide, a prodrug of an inhibitor of inducible nitric oxide synthase. The loss of retinal ganglion cells was quantitated as an indicator of glaucomatous damage. RESULTS: At the end of seven months, rat eyes with chronic, moderately elevated intraocular pressure lost approximately 20,000 retinal ganglion cells. Treatment with L-N(6)-(1-iminoethyl)lysine 5-tetrazole amide for seven months completely prevented the loss of retinal ganglion cells in eyes with chronic, moderately elevated intraocular pressure. When treatment with L-N(6)-(1-iminoethyl)lysine 5-tetrazole amide was delayed and started after three months of chronic, moderately elevated intraocular pressure, further loss of retinal ganglion cells was prevented. CONCLUSION: Pharmacological neuroprotection with a selective inhibitor of inducible nitric oxide synthase may be useful for the treatment of glaucoma.
PURPOSE: To test the hypothesis that nitric oxide, synthesized by inducible nitric oxide synthase, causes degeneration of retinal ganglion cells in an animal model of glaucoma. METHODS:Rats with unilateral, chronic, moderately elevated intraocular pressure were treated orally with L-N(6)-(1-iminoethyl)lysine 5-tetrazole amide, a prodrug of an inhibitor of inducible nitric oxide synthase. The loss of retinal ganglion cells was quantitated as an indicator of glaucomatous damage. RESULTS: At the end of seven months, rat eyes with chronic, moderately elevated intraocular pressure lost approximately 20,000 retinal ganglion cells. Treatment with L-N(6)-(1-iminoethyl)lysine 5-tetrazole amide for seven months completely prevented the loss of retinal ganglion cells in eyes with chronic, moderately elevated intraocular pressure. When treatment with L-N(6)-(1-iminoethyl)lysine 5-tetrazole amide was delayed and started after three months of chronic, moderately elevated intraocular pressure, further loss of retinal ganglion cells was prevented. CONCLUSION: Pharmacological neuroprotection with a selective inhibitor of inducible nitric oxide synthase may be useful for the treatment of glaucoma.
Authors: Haksu Kyung; Jacky M K Kwong; Vlad Bekerman; Lei Gu; Daniel Yadegari; Joseph Caprioli; Natik Piri Journal: Brain Res Date: 2015-03-24 Impact factor: 3.252
Authors: John C Morrison; Lijun Jia; William Cepurna; Ying Guo; Elaine Johnson Journal: Invest Ophthalmol Vis Sci Date: 2009-03-25 Impact factor: 4.799
Authors: Nikolaos Nissirios; Raul Chanis; Elaine Johnson; John Morrison; William O Cepurna; Lijun Jia; Thomas Mittag; John Danias Journal: Invest Ophthalmol Vis Sci Date: 2008-06 Impact factor: 4.799
Authors: Mary Ellen Pease; Donald J Zack; Cynthia Berlinicke; Kristen Bloom; Frances Cone; Yuxia Wang; Ronald L Klein; William W Hauswirth; Harry A Quigley Journal: Invest Ophthalmol Vis Sci Date: 2008-12-05 Impact factor: 4.799