Intracamerally injected platelet activating factor (PAF) induces marked intraocular inflammatory reactions.

An inflammatory response was elicited in the rabbit eye by intracameral injection of platelet activating factor (PAF). PAF induced severe aqueous flare, corneal edema, pupillary constriction and marked biphasic changes in intraocular pressure (IOP) in a dose-dependent manner. All of the responses to PAF were inhibited by the PAF receptor antagonist, BN 52021 (20 mg/kg, i.p.). The cyclooxygenase inhibitor, indomethacin (30 mg/kg, i.p.) caused significant inhibition of the early phase PAF-induced aqueous flare, pupillary constriction and intraocular hypertension, but did not effect PAF-induced corneal edema or intraocular hypotension. NDGA (10 mg/kg, i.p.), a lipoxygenase inhibitor, did not inhibit the inflammatory effects of PAF. PAF-induced chemotactic response was evaluated by tissue chemiluminescence. Intracamerally injected PAF did not significantly increase chemiluminescence in cornea or iris-ciliary body, but intracorneal injection of PAF did cause a chemotactic response in both the conjunctiva and cornea. These data suggest that PAF may be an important mediator of intraocular inflammation and that some PAF-induced effects are prostaglandin dependent, while others may be independent of eicosanoid synthesis and release.