Abstract

Tolfenamic acid (TA) was tested in two studies to investigate its value in controlling ocular inflammation in the dog. First, TA was assayed within primary and secondary aqueous humour (AH) and in plasma 0, 4 and 24 hours after a 4 mg/kg subcutaneous injection. Secondly, an experimental ocular surgery model was set up in 10 dogs-five receiving TA two hours before surgery and five left untreated. TA was shown to diffuse into AH, reaching lower levels than in plasma: 1:126 ratio in primary AH and 1:43 in secondary AH. In the model, TA-treated dogs versus untreated dogs showed a significant reduction of miosis (P < 0.05) and a clear trend to a reduced ocular discharge and corneal oedema (P = 0.06). Prostaglandin E2 (PGE2) levels increased significantly less in AH after TA treatment (P < 0.05). These results show that TA, even if the whole concentration measured in AH is lower than in plasma, is able to limit the synthesis of the inflammatory mediator PGE2 in AH and to control ocular inflammatory symptoms induced by corneal surgery.

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