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Abstract #5390 Published in IGR 1-2
Assessment of ocular hypotensive mechanisms and additivity of antiglaucoma drugs in humans (editorial; comment)
Kaufman PFArchives of Ophthalmology 1999; 117: 673-674
In this editorial the author comments on a paper by Maus et al. on the comparison of the early effects of brimonidine and apraclonidine as topical ocular hypotensive agents. Their study concerns single dose responses in normotensive subjects. The effects of brimonidine and apraclonidine are compared to latanoprost. The original authors stated that all three drugs further reduce timolol treated IOP to a similar extent, apraclonidine and brimonidine doing so essentially exclusively by further suppressing aqueous humor flow with no effect on aqueous outflow, latanoprost doing so essentially exclusively by enhancing aqueous outflow with no effect on aqueous humor flow. Based on several data the present author concludes that the alpha-2-agonists would have reduced aqueous humor flow by only approximately 10% from baseline. In untreated eyes these compounds reduce aqueous humor flow by up to 30 or 40%. Thus the additivity of alpha-2- adrenergic agonists and beta-2-adrenergic antagonists is incomplete. There may be a commonality of mechanisms at the cellular level. There is no concensus as to whether apraclonidine and brimonidine have sufficiently different alpha-adrenergic receptor selectivities to explain putative differences between the drugs in physiological mechanisms of lowering IOP. Another problem of course is that the methods by which some parameters of ocular hydrodynamics are clinically measured are far from perfect. In another study the Nebraska group reports that brimonidine enhances but apraclonidine reduces uveoscleral outflow after one week or one month of treatment. In contrast the Mayo group feels that there is no outflow enhancement by either alpha-2-adrenergic agonist. There is some difficulty in comparing the two studies as the Mayo group study involved single dosing in normotensive eyes whereas the Nebraska studies involved multiple dosing in ocular hypertensive eyes. Thus, there seems some doubt whether there is a significant second mechanism for the ocular hypotensive effect of brimonidine. The author ends by stating that what is most needed to resolve these issues are non-invasive clinical techniques to accurately and directly measure trabecular and uveoscleral outflow and their resistances in the living human eye.
P.F. Kaufman, Department of Ophthalmology and Visual Sciences, University of Wisconsin Clinical Science Center, 600 Highland Avenue, Madison, WI 53792-3220; USA
Classification:
11.1 General management, indication (Part of: 11 Medical treatment)
