Corneal injury alters eicosanoid formation in the rabbit anterior segment in vivo.

The author injected [1-14C]arachidonic acid into the anterior chamber of the rabbit eye, and its metabolism was studied in vivo in the various eye tissues. Incorporation of the radioisotope was analyzed in individual phospholipids and neutral lipids, and its conversion to oxygenated metabolites was evaluated in the three corneal layers and the aqueous humor, iris-ciliary body, lens, vitreous, and "rest of eye." Three hours after injection, 30% of the label was in corneal stroma and 25% in iris-ciliary bodies. The posterior part of the eye retained 40%, and the remainder was distributed unequally throughout other eye tissues. A major portion of the label was located in membrane lipids, especially phosphatidylcholine, phosphatidylinositol, and triacylglycerols, with the exception of the lens and vitreous where 45% of the labeled arachidonic acid was free. Two hours after a cryogenic lesion had been applied to the cornea (prelabeled with [1-14C]arachidonic acid), there was an increase in cyclooxygenase and lipoxygenase products in the aqueous humor with a concomitant increase in the iris-ciliary bodies and decrease in the corneal stroma. When animals were pretreated with indomethacin, formation of cyclooxygenase products was inhibited in various eye tissues, and 5-HETE increased in stroma. These results suggest that a cryogenic injury to the cornea not only affects the immediate site of injury but also elicits a response from other eye tissues, and that the arachidonic acid metabolites appearing in the aqueous humor are a result of the response from several tissues (including the corneal stroma) to the injury.