抗坏血酸可防止实验性碱烧伤后角膜溃疡和穿孔。

Investigative ophthalmology Pub Date : 1976-12-01
R A Levinson, C A Paterson, R R Pfister
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引用次数: 0

摘要

在对兔角膜进行20秒、直径6毫米、1N氢氧化钠烧伤后的14天内,降低的房水葡萄糖和抗坏血酸水平恢复到控制值。这些角膜没有溃烂或穿孔。经过20秒,直径12毫米,1N氢氧化钠烧伤后,房水葡萄糖水平恢复到正常值,但抗坏血酸水平仍然明显下降长达30天。这些角膜在大约60%的动物中明显溃烂,并经常穿孔。在12 mm碱烧伤后,每天皮下注射1.5 gm抗坏血酸治疗的家兔很少出现角膜溃疡,角膜也没有穿孔。这表明外源性维持足够的房水抗坏血酸水平可以克服由12毫米碱烧伤引起的前段相对坏血病状态,从而损害角膜溃疡和穿孔的发展。升高的房水抗坏血酸水平对碱烧伤后角膜上皮细胞的迁移模式没有影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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.

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