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Editorial
May 1999

Assessment of Ocular Hypotensive Mechanisms and Additivity of Antiglaucoma Drugs in Humans

Arch Ophthalmol. 1999;117(5):673-674. doi:10.1001/archopht.117.5.673

IN THIS issue of the ARCHIVES, Maus et al1 demonstrate and quantify the effects of single doses of the α2-adrenergic agonists brimonidine tartrate and apraclonidine hydrochloride and the prostaglandin receptor agonist latanoprost on intraocular pressure (IOP) and aqueous humor flow (AHF) in timolol-treated human eyes. The authors interpret their data as indicating that all 3 drugs further reduce "timolol-treated" IOP to a similar extent, apraclonidine and brimonidine doing so essentially exclusively by further suppressing AHF with no effect on aqueous outflow, latanoprost doing so essentially exclusively by enhancing aqueous outflow (presumably uveoscleral) with no effect on AHF. Furthermore, they found the magnitude of the AHF-suppressing effects of apraclonidine and brimonidine to be essentially identical. These data and their interpretation highlight several areas of interest and uncertainty in the clinical physiology of AHF dynamics and glaucoma therapy.

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