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MP LaFuente, MP Villegas-Pérez, S Mayor-Torroglosa, ME Aguilera, J Miralles de Imperial, M Vidal-Sanz; Dose-dependent Neuroprotective Effects Of Brimonidine Against Ischemia-induced Retinal Ganglion Cell Death . Invest. Ophthalmol. Vis. Sci. 2002;43(13):765.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: To investigate in adult Sprague-Dawley rats the neuroprotective effects of different concentrations of topically applied Brimonidine(BMD) on retinal ganglion cell (RGC) survival, short and long periods of time after transient ligature of the ophthalmic vessels (LOV). Methods: RGCs were labeled with Fluorogold (FG) applied to both superior colliculi. Seven days later, the left ophthalmic vessels were ligated for 90 minutes. The left eyes were treated topically 1 hour before retinal ischemia with two 5µl drops of saline alone or saline containing 0.0001, 0.001, 0.01 or 0.1% BMD. Rats were analyzed 7, 14 or 21 days later, and RGC survival was estimated by counting FG-labelled cells in 12 standard areas of both ischemic and contralateral non-ischemic retinas. Results: i) Seven days after 90 minutes of transient ischemia and topical pre-treatment with saline there was loss of approximately 46% of the RGC population. At this time point, topical pre-treatment with BMD prevented ischemia-induced RGC loss in a dose-dependent manner. Administration of 0.0001% BMD had no significant neuroprotective effects. Administration of higher concentrations of BMD (0.001 or 0.01%) resulted in the survival of 76 or 90%, respectively, of the RGC population, and 0.1% BMD fully prevented RGC loss. ii) Between 7 and 21 days after ischemia, there was an additional loss of approximately 25% of the RGC population in the saline pre-treated eyes. Pre-treatment with 0.1% BMD also diminished significantly this slow RGC death. Conclusion: The neuroprotective effects of BMD, when administered topically, are dose-dependent. The 0.1% concentration achieves optimal neuroprotective effects in the first seven days after ischemia. This concentration is also effective in reducing the protracted loss of RGCs that occurs between 7 and 21 days after transient ischemia.
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