Prostaglandin mediated inflammatory changes induced by alpha-adrenoceptor stimulation in the sympathectomised rabbit eye.

Topical application of 50 microliter of 0.1% noradrenaline or 10% phenylepherine to either a surgically sympathectomised or a guanethidine treated rabbit eye induced a transient increase in intraocular pressure (IOP), between 90 and 150 min, followed by a fall to hypotensive levels. These changes were accompanied by the development of conjunctival and anterior uveal hyperemia and an aqueous flare. Fluorescein angiography and microscopic examination after intravenously injecting colloidal carbon showed that the major site of disruption of the blood-aqueous barrier occurs in the ciliary processes. Slightly elevated levels of protein and prostaglandin-like activity (PG) were detected in aqueous samples withdrawn 3 or 5 h after application of either adrenergic agent. Prior treatment with indomethacin or phentolamine prevented the ocular hypertensive phase as well as the inflammatory changes, suggesting that the inflammatory rebound is mediated by PG and that PG release under such circumstances is closely linked to alpha-adrenoceptor activation. By contrast, the rise in IOP occurring after each of several successive daily applications of an alpha-agonist to a normal rabbit eye was not accompanied by hyperemia or an aqueous flare and was not inhibited by indomethacin pretreatment.