AN EXCESS OF TOPICAL CALCIUM AND MAGNESIUM REVERSES THE THERAPEUTIC EFFECT OF CITRATE ON THE DEVELOPMENT OF CORNEAL ULCERS AFTER ALKALI INJURY

Our purpose was to determine whether chelation of Ca2+ and Mg2+ is the mechanism by which sodium citrate inhibits corneal ulceration in the alkali-injured rabbit eye. The right eyes of 60 albino rabbits (2-2.5 kg) were alkali-injured by filling a 12-mm-diameter plastic well place d on the corneal surface with 0.4 ml of 1 N NaOH. After 35 s the alkal i was aspirated, and the well was rinsed with physiological saline. An imals were randomly distributed to three treatment groups of equal siz e. Two drops of the following topical medications were administered on the hour (14 times per day) for 35 days: physiological saline, 10% ci trate in saline, and 346 mM Ca2+, 346 mM Mg2+, and 10% citrate in sali ne. During the experiment, significantly fewer ulcerations occurred in the citrate-treated eyes (five of 20, 25%) than in the saline-treated eyes (13 of 20, 65%) or in the calcium-magnesium-citrate-treated eyes (15 of 20, 75%). When ulcerations did develop in the citrate group, t hey occurred significantly later and were less severe than those in th e saline and calcium-magneslum-citrate groups. There was a significant increase in the number of eyes with signs of band keratopathy and tra nslucent areas in the calcium-magnesium-citrate group when compared wi th the other two groups. As in previous studies, sodium citrate signif icantly inhibited the development of corneal ulcers after alkali injur y. The annulment of the favorable effect of citrate on ulceration in t he alkali-injured eye by the addition of calcium and magnesium shows t hat the mechanism of action of citrate is the chelation of these dival ent cations.