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C.K. Bahler, K.G. Howell, C.R. Hann, M.P. Fautsch, D.H. Johnson; Prostaglandins Increase Outflow Facility in Cultured Human Anterior Segments . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1845.
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To determine the affect of latanoprost (free acid) and PGE1 on outflow facility in cultured human anterior segments. Although all studies find an increase in pressure insensitive outflow (uveoscleral flow) after prostaglandin treatment, some clinical studies also find an increase in pressure sensitive outflow ("trabecular outflow").
Anterior segments from human eyes were placed in perfusion organ culture within 20 hours of death. One eye received either latanoprost (free acid) or PGE1 by anterior chamber exchange followed by constant perfusion of the drug for 72 hours while the fellow eye received vehicle control (10–7 M final concentration of each drug). Zymography was performed on effluents to measure MMP 2, 3, and 9 activity. Western blots were used to assess MMP 3 levels.
Latanoprost increased facility 67% ± 11% compared with the fellow control eye that increased facility 7% ± 9% (n=4 eyes, p=0.0002). PGE1 was less effective, increasing facility 13% ± 17% vs the fellow eye that increased facility only 1% ± 11% (n=9, p=0.02). MMP activity in effluent media was increased in only 1 latanoprost eye (MMP 3, 9) and none of the PGE1 eyes that were tested (n=3).
Prostaglandins increased outflow facility in perfusion organ culture, with latanoprost more effective than PGE1. Although the results suggest the change in facility is due to an effect on the trabecular meshwork, changes in scleral permeability could also be involved, and will be assessed in future studies.
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