Ascorbic acid prevents corneal ulceration and perforation following experimental alkali burns.
Depressed aqueous humor glucose and ascorbic acid levels returned to control values within 14 days following a 20 sec, 6 mm. diameter, 1N sodium hydroxide burn of the rabbit cornea. These corneas did not ulcerate or perforate. After a 20 sec., 12 mm. diameter, 1N sodium hydroxide burn, aqueous humor glucose levels returned to normal values, but ascorbic acid levels remained significantly depressed for up to 30 days. These corneas became markedly ulcerated in about 60 per cent of animals and frequently perforated. Following 12 mm. alkali burns, rabbits treated daily with 1.5 Gm. of subcutaneous ascorbic acid rarely developed corneal ulcerations and the corneas did not perforate. It is suggested that exogenous maintenance of adequate aqueous humor levels of ascorbic acid overcomes the relatively scorbutic state of the anterior segment induced by a 12 mm. alkali burn, thereby impairing the development of corneal ulceration and perforation. Elevated aqueous humor levels of ascorbic acid had no influence on corneal epithelial cell migration patterns following alkali burns.
D000468:Alkalies / Q000009:adverse effects; D000818:Animals; D001082:Aqueous Humor / Q000032:analysis; D001205:Ascorbic Acid / Q000032:analysis / Q000627:therapeutic use*; D002057:Burns, Chemical / Q000188:drug therapy*; D003320:Corneal Ulcer / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control*; D004195:Disease Models, Animal; D005126:Eye Burns / Q000188:drug therapy*; D005260:Female; D005947:Glucose / Q000032:analysis; D008297:Male; D011817:Rabbits
D000468:Alkalies; D005947:Glucose; D001205:Ascorbic Acid