Objective: To evaluate the mechanism by which brimonidine, a selective alpha 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. Brimonidine-treated 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.