摘要
Objective To evaluate platelet activating factor (PAF) induced aqueous liare, corneai edema, pupillary constriction and btphasic intraocular pressure (IOP) changes in the rabbit eyes. Methods PAF was delivered into anterior chamber by intracameral injection, other antagonists were administered systemically. Results PAF induced responses in a dose - dependent manner. All of the responses to PAF were inhibited by the PAF receptor antagonist, BN 52021 (20mg/kg, i.p.). The cyclooxygenase inhibitor, indomethacin (30mg/kg, i.P.) caused signofcant inhibition of the early phase PAF- induced aqueous flare, pupillary constriction and intraocular hypertension, but did not alfect PAF- induced corneal edema or intraocular hypotension. Nordihydroguaiaretic acid (NDGA) (10mg/kg, ip.), a lipoxygenase inhibitor, did not inhibit the inflammatory effects of PAF. Conclusion These data suggest that PAF may be an important mediator of intraocular inllammation and that some PAF- induced effects are prostaglandin dependent, while others may be independent of eicosanoid synthesis and release.
Objective To evaluate platelet activating factor (PAF) induced aqueous liare, corneai edema, pupillary constriction and btphasic intraocular pressure (IOP) changes in the rabbit eyes. Methods PAF was delivered into anterior chamber by intracameral injection, other antagonists were administered systemically. Results PAF induced responses in a dose - dependent manner. All of the responses to PAF were inhibited by the PAF receptor antagonist, BN 52021 (20mg/kg, i.p.). The cyclooxygenase inhibitor, indomethacin (30mg/kg, i.P.) caused signofcant inhibition of the early phase PAF- induced aqueous flare, pupillary constriction and intraocular hypertension, but did not alfect PAF- induced corneal edema or intraocular hypotension. Nordihydroguaiaretic acid (NDGA) (10mg/kg, ip.), a lipoxygenase inhibitor, did not inhibit the inflammatory effects of PAF. Conclusion These data suggest that PAF may be an important mediator of intraocular inllammation and that some PAF- induced effects are prostaglandin dependent, while others may be independent of eicosanoid synthesis and release.
