Hull D S, Green K, Elijah R D
Acta Ophthalmol (Copenh). 1985 Oct;63(5):513-8. doi: 10.1111/j.1755-3768.1985.tb05237.x.
Oxygen free radicals and their products are known to be elaborated by inflammatory cells during the 'respiratory burst'. Xanthine oxidase combined with hypoxanthine was injected into the anterior chamber of rabbit eyes. This combination is known to result in the production of oxygen free radicals. Iris fluorescein angiography performed 2 h and 24 h following injection of xanthine oxidase and hypoxanthine into the anterior chamber resulted in increased iris vascular permeability. The increased permeability was not modified by either of the prostaglandin inhibitors naproxen or aspirin nor by the free radical scavenger D-penicillamine. This study demonstrates that iris vascular permeability, and possibly blood-aqueous barrier permeability is increased following exposure to chemically generated oxygen free radicals. It is possible that the increased iris vascular permeability that occurs during ocular inflammatory processes may in part be mediated by oxygen free radical products. This model may be useful in developing therapeutic modalities directed at preventing the damaging effect of oxygen free radical products, and this may be of benefit in reducing the untoward effects of ocular inflammatory disorders.
已知炎症细胞在“呼吸爆发”过程中会产生氧自由基及其产物。将黄嘌呤氧化酶与次黄嘌呤注入兔眼的前房。已知这种组合会导致氧自由基的产生。在前房注入黄嘌呤氧化酶和次黄嘌呤后2小时和24小时进行虹膜荧光素血管造影，结果显示虹膜血管通透性增加。萘普生或阿司匹林这两种前列腺素抑制剂以及自由基清除剂D-青霉胺均未改变这种增加的通透性。本研究表明，暴露于化学产生的氧自由基后，虹膜血管通透性以及可能的血-房水屏障通透性会增加。眼部炎症过程中发生的虹膜血管通透性增加可能部分由氧自由基产物介导。该模型可能有助于开发针对预防氧自由基产物损伤作用的治疗方法，这可能有利于减少眼部炎症性疾病的不良影响。
