The primary mechanism by which most PGs reduce IOP is by increasing outflow, especially through the uveoscleral outflow pathway (figure 2.2). Numerous animal and human studies have confirmed this mechanism of action.11,12 In several studies, PGs have been demonstrated to increase outflow facility.12-17 PGs do not reduce aqueous production.
The mechanism by which PGs increase uveoscleral outflow is continuing to be elucidated. One mechanism may be the relaxation of the ciliary muscle. This is supported by studies in monkeys that have shown pilocarpine pretreatment blocks the effect of PGs on uveoscleral outflow or IOP.11,12,15 An increase in ciliary body
thickness has been measured by ultrasound biomicroscopy in human eyes treated with latanoprost.18 Additionally, PGs may cause dilated spaces between ciliary muscle bundles. This is thought to result from PG-induced stimulation of collage-nases and other matrix metalloproteinases.11,19 However, other studies, using both light and electron microscopy, have found no evidence of dilated spaces between ciliary muscle bundles or other alterations in the ciliary muscle or other ocular tissues in monkeys treated with PGF2a.20
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