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准分子激光治疗后角膜中的氧自由基损伤。

Oxygen free radical damage in the cornea after excimer laser therapy.

作者信息

Hayashi S, Ishimoto S, Wu G S, Wee W R, Rao N A, McDonnell P J

机构信息

Doheny Eye Institute, University of Southern California School of Medicine, Los Angeles, USA.

出版信息

Br J Ophthalmol. 1997 Feb;81(2):141-4. doi: 10.1136/bjo.81.2.141.

Abstract

AIMS/BACKGROUND: To evaluate the extent of oxygen radical damage in the cornea after excimer laser ablation.

METHODS

The 193 nm argon fluoride excimer laser was programmed for an average fluence of 150 mJ/cm2, with a firing rate of 5 Hz and an ablation zone diameter of 6 mm. Phototherapeutic keratectomy was performed to remove 30 microns of epithelium and 50 microns of stroma from the corneas of New Zealand white rabbits. Oxidative tissue damage after laser was determined by measuring oxidised lipids (conjugated dienes and ketodienes) in corneal lipid extracts, and by fast blue B staining to localise the lipid peroxide in the tissue.

RESULTS

Conjugated diene levels were 3.73 (SD 0.56) nmol per hemicornea in ablated corneas and 1.99 (0.33) nmol per hemicornea in normal corneas (p = 0.0044). Ketodiene levels were 2.72 (0.38) nmol per hemicornea in treated corneas and 0.91 (0.12) nmol per hemicornea in normal corneas (p < 0.001). Fast blue B staining disclosed that the tissue damage occurred primarily on the surface of the ablated cornea.

CONCLUSION

The presence of lipid peroxidation in the superficial corneal stroma in excimer laser treated corneas was demonstrated. This lipid peroxidation could be from oxygen free radicals generated by the infiltrating polymorphonuclear cells at the site of tissue damage.

摘要

目的/背景:评估准分子激光消融术后角膜中氧自由基损伤的程度。

方法

将193nm氟化氩准分子激光设定为平均能量密度150mJ/cm²,频率5Hz,消融区直径6mm。对新西兰白兔角膜进行光治疗性角膜切削术,去除30微米的上皮和50微米的基质。通过测量角膜脂质提取物中的氧化脂质(共轭二烯和酮二烯)以及用固蓝B染色来定位组织中的脂质过氧化物,以确定激光治疗后的氧化组织损伤。

结果

消融角膜中每半角膜的共轭二烯水平为3.73(标准差0.56)nmol,正常角膜中为1.99(0.33)nmol(p = 0.0044)。治疗角膜中每半角膜的酮二烯水平为2.72(0.38)nmol,正常角膜中为0.91(0.12)nmol(p < 0.001)。固蓝B染色显示组织损伤主要发生在消融角膜表面。

结论

证实了准分子激光治疗的角膜浅层基质中存在脂质过氧化。这种脂质过氧化可能来自组织损伤部位浸润的多形核细胞产生的氧自由基。

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