Olesen S P
Acta Physiol Scand. 1987 Feb;129(2):181-7. doi: 10.1111/j.1748-1716.1987.tb08057.x.
The effect of free oxygen radicals on the electrical resistance of brain venular endothelium was studied in anesthetized frogs. The technique allowed continuous recording of the electrical resistance of the vascular wall reflecting its ionic permeability. The oxygen radicals were generated by an enzymatic reaction between xanthine oxidase and hypoxanthine supplied to the surface of the exposed brain. Electrical resistance of the venular endothelium decreased within 1-2 s after the reaction was initiated. Hypoxanthine (1 mM) and xanthine oxidase at a concentration of 10, 25, 50, 100, and 250 mU ml-1 lowered resistance to 1.0, 0.9, 0.8, 0.5 and 0.2 X control value, respectively, within a 3 min period of administration. The effect induced by 25 and 50 mU ml-1 of xanthine oxidase was readily reversible, whereas that induced by the two highest concentrations was irreversible within the observation time. The response was totally blocked by allopurinol as well as by superoxide dismutase plus catalase. Pretreatment with methylprednisolone or BW755C (an inhibitor of cyclo- and lipoxygenase) did not inhibit the response, nor did removal of calcium or magnesium from the extracellular medium. Free oxygen radicals are powerful agents that rapidly induce dynamic changes in the electrical resistance of brain vessels, supporting the notion that they may be important mediators of vascular endothelial damage in the brain.
在麻醉的青蛙身上研究了游离氧自由基对脑静脉内皮电阻的影响。该技术能够连续记录反映血管壁离子通透性的电阻。氧自由基通过黄嘌呤氧化酶与供应到暴露脑表面的次黄嘌呤之间的酶促反应产生。反应开始后1 - 2秒内，静脉内皮的电阻降低。在给药3分钟内，1 mM次黄嘌呤和浓度为10、25、50、100和250 mU/ml的黄嘌呤氧化酶分别将电阻降低至对照值的1.0、0.9、0.8、0.5和0.2倍。25和50 mU/ml黄嘌呤氧化酶诱导的效应易于逆转，而在观察时间内，两个最高浓度诱导的效应不可逆。别嘌呤醇以及超氧化物歧化酶加过氧化氢酶可完全阻断该反应。用甲基泼尼松龙或BW755C（环氧化酶和脂氧化酶抑制剂）预处理不抑制该反应，从细胞外培养基中去除钙或镁也不抑制该反应。游离氧自由基是能够迅速诱导脑血管电阻动态变化的强效物质，支持了它们可能是脑内血管内皮损伤重要介质的观点。
