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Paul L. Kaufman, MD
Madison, Wis

Arch Ophthalmol. 1992;110(8):1042.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—The article by Alm and Villumsen¹ indicated that PhXA34, a congener of prostaglandin F₂ isopropyl ester (PGF₂-IE), increased tonographic outflow facility in ocular normotensive humans by approximately one third, accounting for approximately one fourth to one third of the drug-induced intraocular pressure (IOP) decrease. The authors state that, because no effect on aqueous flow was found, and assuming that episcleral venous pressure was unchanged, "an increased uveoscleral outflow, as has been demonstrated for PGF₂-IE in monkeys, is a possible explanation for the remaining pressure reduction." Their use of the word "remaining" implies that the increase in tonographic facility reflected a physiologic process distinct from uveoscleral outflow. Although the authors did not directly so state, most readers would infer from the text that facility of outflow from the anterior chamber into the canal of Schlemm (ie, conventional, trabecular, or true facility) had increased. However, this may well not have . . . [Full Text PDF of this Article]

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