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C. Park, E. Lee, J. Gwon, M. Chun; Comparison of Brain Nitric Oxide Synthase (bNOS) Expressions among the Rat Glaucoma Models: Ischemia-reperfusion, Optic Nerve Transection, and Chronic Ocular Hypertension . Invest. Ophthalmol. Vis. Sci. 2003;44(13):3344.
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Purpose: To compare the amount of bNOS expressions according to the different types of rat glaucoma models – ischemia-reperfusion, optic nerve transection, and chronic ocular hypertension. Methods: We made 35 rat ischemia-reperfusion models by increasing their intraocular pressure (IOP) up to 180 mmHg for one hour, 35 rat optic nerve transection models by cutting their optic nerve behind the eye glob, and 36 rat chronic ocular hypertension models by cauterizing their 3 episcleral veins. The retinal ganglion cells were stained with fluorgold via stereotaxic injection into their superior colicullus for detecting ganglion cell viabilities and retrograde axoplasmic flows. The western blot analysis and immunofluorescence staining for brain nitric oxide synthase (bNOS) were performed at first day, 3rd day, 1st week, 2nd week, 4th week, and 6th week, after modeling in each group. Results: Both western blot analysis and immunofluorescence staining showed that the amount of bNOS was peak at third day after ischemia-reperfusion modeling and 5th day after optic nerve transection. The amount of bNOS returned to normal level 4 weeks after modeling in both groups, but in chronic ocular hypertension model, the amount of bNOS was gradually increased until 6 weeks after episcleral vein cauterizations. Conclusions: In acute retinal ganglion cell injury models such as ischemia-reperfusion or optic nerve transection, the amount of bNOS that produce nitric oxide, one of toxic materials related with apoptosis, was elevated dramatically followed by rapid normalization within one month. However, in contrast, in chronic ocular hypertension model, that of bNOS showed gradual and continuous elevation and did not return to normal level until 6 weeks after injury. We thought that the latter model was more compatible to the nature of chronic human glaucoma.
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