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PURPOSE: To determine whether exposure of sclera to latanoprost acid alters transscleral permeation by FGF-2. METHODS: Pieces of human sclera were isolated from donor eyes after death, placed in organ culture, and exposed to 50-200 mN latanoprost acid or vehicle for three days. Transscleral permeability was then assessed by placing each scleral piece into a Ussing apparatus and measuring the amount of FGF-2 that moves from the orbital side to the uveal side of the scleral piece. Transscleral permeation by 10-kDa tetramethylrhodamine-dextran was also determined, for comparison. RESULTS: Transscleral permeation by FGF-2 through sclera that had been incubated with vehicle was 1.53 ± 0.86 x 108 cm/sec. Transscleral permeation by 10-kDa tetramethylrhodamine-dextran was 1.04 ± 0.39 x 106 cm/sec. FGF-2 permeation of sclera exposed to 50, 100, and 200 mN latanoprost acid was increased by an average of 48 ± 62%, 100 ± 108%, and 108 ± 79%, respectively, compared with sclera exposed to vehicle (n = 13, p < 0.05). Scleral permeation by 10-kDa dextran after exposure to 50, 100, or 200 mN latanoprost acid was significantly increased by 42 ± 36%, 59 ± 51%, and 65 ± 49%, respectively (n = 14; p < 0.05). The ratio of dextran to FGF-2 permeation was approximately 90 and did not vary with 50, 100, or 200 nM latanoprost acid (p = 0.93, ANOVA). CONCLUSIONS: Exposure of sclera to latanoprost acid increases transscleral permeation by FGF-2 in human scleral organ cultures. Because this increase parallels the increased scleral permeability caused by dextran, it may reflect a general enhancement of permeability, a possibility that future in vivo studies should explore.
Dr R.N. Weinreb, Glaucoma Center, University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0946, USA. weinreb@eyecenter.ucsd.edu
2.3 Sclera (Part of: 2 Anatomical structures in glaucoma)