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Elizabeth WoldeMussie, Guadalupe Ruiz, Mercy Wijono, Larry A. Wheeler; Neuroprotection of Retinal Ganglion Cells by Brimonidine in Rats with Laser-Induced Chronic Ocular Hypertension. Invest. Ophthalmol. Vis. Sci. 2001;42(12):2849-2855.
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purpose. To examine the neuroprotective effect of theα 2-adrenergic agonist brimonidine in a chronic ocular
methods. Intraocular pressure (IOP) was elevated by laser photocoagulation of
episcleral and limbal veins. Retinal ganglion cell loss was evaluated
in wholemounted retinas. Brimonidine or timolol was administered,
either at the time of or 10 days after IOP elevation and continued for
3 weeks. Drug-related immunohistochemical changes in glial fibrillary
acidic protein (GFAP) were also determined after 3 weeks.
results. Laser treatment caused a twofold IOP increase over baseline that was
maintained for 2 months. A time-dependent loss of ganglion cells
occurred with elevated IOP. Systemic administration of brimonidine or
timolol caused little decrease in IOP. After 3 weeks of elevated IOP,
ganglion cell loss in control rats was 33% ± 3%. Brimonidine reduced
the progressive loss of ganglion cells to 26% ± 1% and 15% ± 2%
at doses of 0.5 and 1 mg/kg · d, respectively. Timolol had no effect.
Ten days of high IOP resulted in 22% ± 4% ganglion cell loss.
Brimonidine administration initiated 10 days after IOP elevation
prevented any further loss of ganglion cells. In vehicle- or
timolol-treated rats, ganglion cell loss continued to 33%. The
increase in immunoreactivity of GFAP in ocular hypertensive retinas was
attenuated by brimonidine.
conclusions. Systemic application of brimonidine or timolol had little effect on
IOP. Brimonidine, but not timolol, showed significant protection of
retinal ganglion cells when applied at the time of IOP elevation and
prevented further cell loss when applied after IOP was elevated. This
indicates that brimonidine has a neuroprotective activity unrelated to
its effect on ocular hypotension.
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