Effects of Tetramethylpyrazine on Prostaglandin E 2- and Prostaglandin E 2 Receptor Agonist-induced Disruption of Blood-Aqueous Barrier in Pigmented Rabbits

Abstract

Purpose: To evaluate the effect of tetramethylpyrazine on the elevation of aqueous flare and intraocular pressure (IOP) induced by prostaglandin (PG) E 2 and PGE 2 receptor (EP) agonists. Methods: PGE 2 or EP agonists (11-deoxy PGE 1, EP 2 agonist; 17-phenyl trinor PGE 2, EP 1 and EP 3 agonist; or sulprostone, EP 1 and EP 3 agonist), 25 μg/mL, were transcorneally administered to pigmented rabbits. Animals were pretreated with tetramethylpyrazine intravenously (10 or 30 mg/kg) or topically (0.1% solution). Aqueous flare was measured using a laser flare-cell meter, and the intensity was expressed as the area under the curve (AUC). Intraocular pressure was measured using a noncontact tonometer. Results: After administration of PGE 2, aqueous flare and IOP increased and then gradually decreased. The AUC of eyes pretreated with tetramethylpyrazine, 10 or 30 mg/kg, intravenously, or topical 0.1% solution, was significantly smaller than that of the controls. The mean Δ IOP of eyes pretreated with tetramethylpyrazine, 30 mg/kg intravenously, was significantly lower than that of the controls. After administration of 11-deoxy PGE 1, aqueous flare increased and then gradually decreased. 17-phenyl trinor PGE 2 and sulprostone did not disrupt the blood-aqueous barrier. The AUC of eyes pretreated with tetramethylpyrazine, 10 or 30 mg/kg, intravenously, before 11-deoxy PGE 1 application was significantly smaller than that of the controls. Conclusion: The results indicated that tetramethylpyrazine inhibited PGE 2- or 11-deoxy PGE 1-induced elevation of aqueous flare and IOP.