Prostaglandins (PG) are very effective ocular hypotensive agents. It is generally agreed that these drugs reduce intraocular pressure primarily by increasing uveoscleral outflow. They may also increase trabecular outflow facility though available evidence is less convincing. It has been hypothesized that PGs may increase facility of uveoscleral outflow in addition to their other mechanisms, but this has not yet been tested. To help clarify the ocular hypotensive mechanism of action of a derived PG of the A type, cats were treated twice daily for one week with PGA2 (0·01%) to one eye and vehicle to the other. Measurements were made of aqueous flow and outflow facility with fluorophotometry and of intraocular pressure with pneumatonometry. From these values, uveoscleral outflow was calculated. In addition, total outflow facility, uveoscleral outflow, and uveoscleral outflow facility were determined with invasive methods. PGA2 significantly reduced IOP by a mean of at least 4·7 mmHg in all experiments with all P-values less than 0·01. Compared with contralateral vehicle-treated control eyes, uveoscleral outflow in the treated eye was significantly (P < 0·05) increased by at least 50% using two different methods of measurement. Compared with baseline day, PGA2 significantly (P ≤ 0·05) increased aqueous flow by 1·8 μl min-1, fluorophotometric outflow facility by 0·36 μl min-1 mmHg-1 and fluorophotometric uveoscleral outflow by 2·0 μl min-1. Total outflow facility was not significantly different comparing treated with contralateral control eyes. Facility of uveoscleral outflow was ≤ 0·02 μl min-1 mmHg-1 for both control and treated eyes. It is concluded that PGA2 decreases IOP in cats by increasing uveoscleral outflow and trabecular outflow facility as measured with fluorophotometry. A significant increase in aqueous flow reduces the ocular hypotensive effect.
ASJC Scopus subject areas
- Sensory Systems
- Cellular and Molecular Neuroscience