Abstract
We evaluated the role of topical clonidine on experimental ocular inflammation. Transcorneal diffusion of prostaglandin (PG) E<sub>2</sub>, 7.09 × 10<sup>–2</sup> mmol/l, with the use of a glass cylinder was employed to produce aqueous flare elevation in pigmented rabbits. Clonidine was topically administered and yohimbine was injected intravenously. Aqueous flare was measured with a laser flare cell meter. Topical instillation of 0.25% clonidine inhibited 89% of PGE<sub>2</sub>-induced aqueous flare elevation. Instillation of clonidine at 60 or 30 min before and 10 min after PGE<sub>2</sub> inhibited flare significantly. Pretreatment with intravenous yohimbine decreased the clonidine-induced inhibition of the flare elevation in a dose-dependent manner. It is possible that the anti-inflammatory action of topical clonidine may be mediated partly by α<sub>2</sub>-receptors.
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