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Carol B. Toris, PhD; Guilin Zhan, MD; Carl B. Camras, MD

Arch Ophthalmol. 2004;122:1782-1787.

Objective  To determine the mechanism by which 0.15% unoprostone isopropyl reduces intraocular pressure (IOP) by studying 33 patients with ocular hypertension or primary open-angle glaucoma.

Methods  At baseline, IOP was determined by pneumatonometry, aqueous flow and outflow facility by fluorophotometry, episcleral venous pressure by venomanometry, and uveoscleral outflow by mathematical calculation. Unoprostone was administered to one eye and placebo to the fellow eye of each patient twice daily in a randomized masked fashion. In patients who demonstrated an IOP reduction of 3 mm Hg or more in either eye on day 5 ± 1 (n = 29), determinations were repeated on that day and on day 28 ± 2. Treated eyes were compared with control eyes, and treatment days were compared with baseline by paired t tests.

Results  Compared with baseline, unoprostone significantly (P<.001) reduced IOP by a mean ± SEM of 5.6 ± 0.4 mm Hg and 4.8 ± 0.6 mm Hg on days 5 and 28, respectively. The change from baseline with unoprostone was significantly (P<.001) greater than with placebo by 2.8 ± 0.4 mm Hg on day 5 and by 3.2 ± 0.5 mm Hg on day 28. Compared with baseline, unoprostone significantly (P.001) increased outflow facility by 0.05 ± 0.01 and 0.08 ± 0.02 µL·min^–1·mm Hg^–1 on days 5 and 28, respectively. The baseline-adjusted between-treatment differences were significant (P.04) on day 28 (0.06 ± 0.02 µL·min^–1·mm Hg^–1). Other measures were not different from placebo.

Conclusion  In responsive patients, unoprostone decreased IOP by increasing outflow facility.

Author Affiliation: Department of Ophthalmology, University of Nebraska Medical Center, Omaha.

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