The ocular hypertensive response following experimental acid burns in the rabbit eye.

Following application of 50 microliter of 2N hydrochloric acid to the rabbit cornea, the intraocular pressure rapidly increases and remains markedly elevated for up to 3 hr. The initial rapid increase in intraocular pressure appears to be the result of acid-induced shrinkage of the outer collagenous coats of the eye. The sustained rise in intraocular pressure is mediated in part by prostaglandin release. Increased prostaglandin-like activity, determined in the aqueous after an acid burn, was greatly inhibited by pretreatment of rabbits with indomethacin and to a much lesser extent by pretreatment with imidazole. Both indomethacin and imidazole essentially abolished the sustained elevation of intraocular pressure after an acid burn. Analysis of changes in pH and protein level in the aqueous implies that the stimulus for prostaglanding release within the eye is the penetration of hydrogen ions into the aqueous humor, with resultant intraocular trauma.