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Abstract #18376 Published in IGR 3-3

Brimonidine's neuroprotective effects against transient ischaemia-induced retinal ganglion cell death

Vidal-Sanz M; Lafuente MP; Mayor-Torroglosa S; Aguilera ME; Miralles de Imperial J; Villegas-Perez MP
European Journal of Ophthalmology 2001; 11: Suppl 2 S36-S40


PURPOSE: Brimonidine is a pressure-lowering agent currently being used in glaucoma. This chronic degenerative condition is characterized by neuronal death, and as an agent that offers neuroprotection, it may slow down or impede the progression of neuronal cell death. METHODS: The effects of brimonidine (BMD) on the short- and long-term survival of retinal ganglion cells (RGCs) after transient retinal ischemia are reported using a rat model. The fluorescent tracer Fluorogold (FG) was applied to both superior colliculi to retrogradely label RGCs. A 90-minute period of ischemia was induced and densities of surviving RGCs were estimated over time by counting FG-labelled RGCs in 12 standard regions of each retina. RESULTS: Seven days after inducing transient ischaemia, there was loss of approximately half the RGC population. Topical pretreatment with 0.1% or 0.5% BMD prevented ischemia-induced RGC death. CONCLUSIONS: These results indicate that optimal neuroprotective effects against the early loss of RGCs are seen with 0.1% or 0.5% BMD. Ischemia-induced RGC loss continued between days 7 and 21 in the vehicle-treated groups, and amounted to approximately 25% of the RGC population. Topical pretreatment with 0.1% or 0.5% BMD was also effective in reducing the slow loss of RGCs.

Dr M. Vidal-Sanz, Lab. de Oftalmologia Experimental, Departamento de Oftalmologia, Universidad de Murcia, E-30.100 Murcia, Spain. ofmmv01@fcu.um.es


Classification:

11.3.3 Apraclonidine, brimonidine (Part of: 11 Medical treatment > 11.3 Adrenergic drugs)



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