Kontos H A, Wei E P, Povlishock J T, Christman C W
Circ Res. 1984 Sep;55(3):295-303. doi: 10.1161/01.res.55.3.295.
Topical application of sodium arachidonate (50-200 micrograms/ml) or bradykinin (0.1-10 micrograms/ml) on the brain surface of anesthetized cats caused dose-dependent cerebral arteriolar dilation. This dilation was blocked by 67-100% in the presence of superoxide dismutase and catalase. These enzymes did not affect the changes in arteriolar diameter caused by alterations in arterial blood PCO2, or the arteriolar dilation from topical acetylcholine. Enzymes inactivated by heat had no effect on the vasodilation from arachidonate or bradykinin. Superoxide dismutase alone or catalase alone reduced the dilation during application of 200 micrograms/ml of arachidonate for 15 minutes; they also completely prevented the residual dilation seen 1 hour after washout, as well as the reduction in the vasoconstrictive effects of arterial hypocapnia observed at this time. The results show that superoxide anion radical and hydrogen peroxide, or radicals derived from them, such as the hydroxyl radical, are mediators of the cerebral arteriolar dilation from sodium arachidonate or bradykinin. These radicals are not the endothelium-derived relaxant factor released by acetylcholine. The presence of both superoxide anion radical and hydrogen peroxide is required for the production of the vascular damage seen during prolonged application of high concentrations of sodium arachidonate.
在麻醉猫的脑表面局部应用花生四烯酸钠（50 - 200微克/毫升）或缓激肽（0.1 - 10微克/毫升）可引起剂量依赖性的脑小动脉扩张。在超氧化物歧化酶和过氧化氢酶存在的情况下，这种扩张被阻断了67% - 100%。这些酶并不影响由动脉血PCO2改变引起的小动脉直径变化，也不影响局部应用乙酰胆碱引起的小动脉扩张。经加热失活的酶对花生四烯酸或缓激肽引起的血管舒张没有影响。单独使用超氧化物歧化酶或单独使用过氧化氢酶可减少在应用200微克/毫升花生四烯酸15分钟期间的扩张；它们还完全阻止了冲洗1小时后出现的残余扩张，以及此时观察到的动脉低碳酸血症血管收缩作用的减弱。结果表明，超氧阴离子自由基和过氧化氢，或由它们衍生的自由基，如羟基自由基，是花生四烯酸钠或缓激肽引起脑小动脉扩张的介质。这些自由基不是乙酰胆碱释放的内皮源性舒张因子。长时间应用高浓度花生四烯酸钠期间出现的血管损伤的产生需要超氧阴离子自由基和过氧化氢同时存在。
