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August 1992

PhXA34-Induced Ocular Hypotension

Author Affiliations

Madison, Wis

Arch Ophthalmol. 1992;110(8):1042. doi:10.1001/archopht.1992.01080200022004

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To the Editor.  —The article by Alm and Villumsen1 indicated that PhXA34, a congener of prostaglandin F isopropyl ester (PGF-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 PGF-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

Alm A, Villumsen J.  PhAX34, a new potent ocular hypotensive drug: a study on dose-response relationship and on aqueous humor dynamics in healthy volunteers . Arch Ophthalmol . 1991;109:1564-1568.Article
Gabelt BT, Kaufman PL.  Prostaglandin F2α increases uveoscleral outflow in the cynomolgus monkey . Exp Eye Res . 1989;49:389-402.Article
Gabelt BT, Kaufman PL.  The effect of prostaglandin F2α on trabecular outflow facility in cynomolgus monkeys . Exp Eye Res . 1990;51:87-91.Article