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Carol B. Toris, PhD; Michele L. Gleason, MD; Carl B. Camras, MD; Michael E. Yablonski, MD, PhD

Arch Ophthalmol. 1995;113(12):1514-1517.

Abstract
Objective
To evaluate the mechanism by which brimonidine, a selective ₂-adrenergic agonist, lowers intraocular pressure (IOP) in humans.

Subjects
Twenty-one volunteers with ocular hypertension.

Methods
Brimonidine tartrate (0.2%) was given topically twice daily for 1 week to one eye in a randomized, double-masked study. The fellow eye was similarly treated with brimonidine vehicle. Before (baseline) and after 1 week (day 8) of dosing, IOP, aqueous flow, episcleral venous pressure, and tonographic outflow facility were directly measured. Fluorophotometric outflow facility and uveoscleral outflow were calculated. Brimonidinetreated eyes were compared with vehicle-treated contralateral control eyes and with baseline measurements after 1 week of dosing.

Results
Brimonidine significantly (P<.001, Student's two-tailed t test) reduced IOP mean±SE of 4.7±0.7 and 4.2±0.4 mm Hg compared with the baseline day and with the vehicle-treated contralateral control eyes, respectively. Compared with the baseline day, aqueous flow was reduced by 20% (P=.002) and uveoscleral outflow was increased (P=.04). A slight contralateral decrease in IOP of 1.2±0.6 mm Hg (P=.05) and in aqueous flow of 12% (P=.05) was noted. No significant difference was seen in the outflow facility values or episcleral venous pressure compared with the baseline day or with the contralateral control eye.

Conclusions
The brimonidine-induced reduction in IOP in humans is associated with a decrease in aqueous flow and an increase in uveoscleral outflow. The decrease in IOP and aqueous flow in the contralateral control eye on day 8 compared with the baseline day suggests a mild contralateral effect.

Author Affiliations
From the Department of Ophthalmology, University of Nebraska Medical Center, Omaha. None of the authors has proprietary interests in Allergan Inc, or in brimonidine.

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