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局部过量的钙和镁会逆转柠檬酸盐对碱烧伤后角膜溃疡发展的治疗效果。

An excess of topical calcium and magnesium reverses the therapeutic effect of citrate on the development of corneal ulcers after alkali injury.

作者信息

Haddox J L, Pfister R R, Slaughter S E

机构信息

Eye Research Laboratories, Brookwood Medical Center, Birmingham, Alabama 35209, USA.

出版信息

Cornea. 1996 Mar;15(2):191-5. doi: 10.1097/00003226-199603000-00013.

DOI:10.1097/00003226-199603000-00013
PMID:8925668
Abstract

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 placed on the corneal surface with 0.4 ml of 1 N NaOH. After 35 s the alkali was aspirated, and the well was rinsed with physiological saline. Animals were randomly distributed to three treatment groups of equal size. Two drops of the following topical medications were administered on the hour (14 times per day) for 35 days: physiological saline, 10% citrate in saline, and 346 mM Ca2+, 346 mM Mg2+, and 10% citrate in saline. 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, they occurred significantly later and were less severe than those in the saline and calcium-magnesium-citrate groups. There was a significant increase in the number of eyes with signs of band keratopathy and translucent areas in the calcium-magnesium-citrate group when compared with the other two groups. As in previous studies, sodium citrate significantly inhibited the development of corneal ulcers after alkali injury. The annullment of the favorable effect of citrate on ulceration in the alkali-injured eye by the addition of calcium and magnesium shows that the mechanism of action of citrate is the chelation of these divalent cations.

摘要

我们的目的是确定钙和镁的螯合作用是否是柠檬酸钠抑制碱损伤兔眼角膜溃疡形成的机制。用0.4毫升1N氢氧化钠填充放置在角膜表面的直径12毫米的塑料孔,对60只白化兔(2-2.5千克)的右眼进行碱损伤。35秒后吸出碱液,并用生理盐水冲洗孔。动物被随机分为三个大小相等的治疗组。每小时(每天14次)给予以下局部用药两滴,持续35天:生理盐水、10%柠檬酸盐生理盐水、346 mM钙、346 mM镁和10%柠檬酸盐生理盐水。在实验过程中,柠檬酸盐治疗组的眼睛发生溃疡的数量(20只中的5只,25%)明显少于生理盐水治疗组(20只中的13只,65%)或钙-镁-柠檬酸盐治疗组(20只中的15只,75%)。当柠檬酸盐组出现溃疡时,其发生时间明显更晚,且比生理盐水组和钙-镁-柠檬酸盐组的溃疡程度更轻。与其他两组相比,钙-镁-柠檬酸盐组出现带状角膜病变体征和半透明区域的眼睛数量显著增加。如先前研究一样,柠檬酸钠显著抑制碱损伤后角膜溃疡的发展。通过添加钙和镁消除柠檬酸盐对碱损伤眼溃疡的有利作用,表明柠檬酸盐的作用机制是螯合这些二价阳离子。

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1
An excess of topical calcium and magnesium reverses the therapeutic effect of citrate on the development of corneal ulcers after alkali injury.局部过量的钙和镁会逆转柠檬酸盐对碱烧伤后角膜溃疡发展的治疗效果。
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