Platelet-activating factor (PAF) accumulation correlates with injury in the cornea.

This study reports the accumulation of platelet-activating factor (PAF) in corneas injured with either 0.1 N NaOH or 1 N NaOH. The degree of injury in corneas exposed to alkali for 5, 10, 20, or 60 sec was assessed by light microscopy and scanning electron microscopy. PAF accumulation in vivo increased with time (up to 24 hr) after injury and also according to the severity of the alkali injury. PAF was isolated by high-performance liquid chromatography (HPLC) and assayed by platelet aggregation of the HPLC fraction containing PAF. The specificity of the aggregating bioactivity was ascertained from inhibition of platelet aggregation by selective PAF antagonists. BN 50726, a new synthetic PAF antagonist, applied in vivo topically or subconjunctivally, was effective in inhibiting PAF formation. Because PAF is accumulated in vivo as soon as 30 min after corneal injury, this lipid mediator seems to be synthesized by corneal cells and not be recruited inflammatory cells, since they arrive later. Moreover, if the injury causes stromal edema and endothelial damage, the amount of PAF accumulated is even greater. Results from isolated corneas stimulated in vitro with calcium ionophore A23187 suggest that PAF synthesis is the result of stimulation of phospholipase A2 to form lyso-PAF and subsequent activation of an acetyltransferase.