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Abstract #6876 Published in IGR 4-1
Neuroprotective effects of brimonidine against transient ischemia-induced retinal ganglion cell death: a dose response in vivo study
Lafuente MP; Villegas-Perez MP; Mayor S; Aguilera ME; Miralles de Imperial J; Vidal-Sanz MExperimental Eye Research 2002; 74: 181-189
The purpose of this study was to investigate the dose-response effects of topically administered brimonidine (BMD) on retinal ganglion cell (RGC) survival, short and long periods of time after transient retinal ischemia. In adult Sprague-Dawley rats, RGCs were retrogradely labelled with the fluorescent tracer fluorogold (FG) being applied to both superior colliculi. Seven days later, the left ophthalmic vessels were ligated for 90 minutes. One hour prior to retinal ischemia, two 5-μl drops of saline alone or saline containing 0.0001, 0.001, 0.01 or 0.1% BMD were instilled into the left eye. Rats were processed seven, 14, or 21 days later, and densities of surviving RGCs were estimated by counting FG-labelled RGCs in 12 standard regions of each retina. The following was found: (1) Seven days after 90 minutes of transient ischemia there is loss of approximately 46% of the RGC population. (2) Topical pre-treatment with BMD prevents ischemia-induced RGC death in a dose-dependent manner. Administration of 0.0001% BMD resulted in the loss of approximately 37% of the RGC population and 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 death in the first seven days after ischemia. (3) Between seven and 21 days after ischemia, there was an additional slow cell loss of approximately 25% of the RGC population. Pre-treatment with 0.1% BMD also reduced significantly this slow cell death. These results indicate that the neuroprotective effects of BMD, when administered topically, are dose-dependent and that the 0.1% concentration achieves optimal neuroprotective effects against the early loss of RGCs. Furthermore, this concentration is also effective to diminish the protracted loss of RGCs that occurs with time after transient ischemia.
Dr. M.P. Lafuente, Laboratorio de Oftalmologia Experimental, Departamento de Oftalmologia, Universidad de Murcia, E-30.100 Espinardo, Murcia, Spain
Classification:
11.3.3 Apraclonidine, brimonidine (Part of: 11 Medical treatment > 11.3 Adrenergic drugs)