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C. Millar, O. A. Candia, R. Gerometta, S. M. Podos; Anecortave Acetate Suppresses and Reduces Corticosteroid-Induced Ocular Hypertension in Sheep. Invest. Ophthalmol. Vis. Sci. 2010;51(13):584.
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To corroborate the ocular hypotensive effects of anecortave acetate (AL-3789, Alcon Research, Ltd.) on an ovine model of steroid-induced ocular hypertension. Eyes of normal sheep exhibited a robust steroid-induced ocular hypertensive response. Recent observations in an uncontrolled, interventional case series indicated that anecortave acetate elicited hypotensive effects when administered as a sub-Tenon depot in the eyes of a small sample of glaucoma patients. We sought to investigate this phenomenon further in sheep.
Intraocular pressure (IOP) was monitored by Perkins applanation tonometry in 16 normal sheep receiving topically administered 0.5% prednisolone acetate in both eyes, three times daily, a protocol that approximately doubled IOP within 12 days. Half of the sheep had received a unilateral sub-Tenon injection of anecortave acetate in one eye prior to initiation of the bilateral prednisolone instillations; while the 8 remaining sheep received the unilateral anecortave acetate sub-Tenon depot after the IOP was maximally elevated by the prednisolone instillations.
In these two sets of experiments, the presence of the anecortave acetate depot prevented the steroid-induced IOP elevation, normally to 26.4+/-0.7mmHg (Mean+/-SEM, n=8, P<1x10-6), and reversed the elevated IOP to baseline levels (10.4+/-0.8mmHg, n=8) respectively. Measurements of aqueous outflow facility indicated that eyes treated by the combined presence of prednisolone plus anecortave acetate exhibited a 5.8-fold higher outflow facility than that of the fellow eyes solely exposed to prednisolone (0.46+/-0.15 microliters/min/mmHg vs. 0.08+/-0.02 microliters/min/mmHg, n=9, P<0.01); indicating that anecortave acetate prevented the increase in outflow resistance produced by the corticosteroid.
Elucidation of the mechanisms of action of anecortave acetate in animal models may prove relevant to the design of novel interventions for the management of primary open-angle glaucoma.
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