OXYGEN RADICALS IN CEREBRAL-ISCHEMIA
OXYGEN RADICALS IN CEREBRAL-ISCHEMIA
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DOI：
10.1152/ajpheart.1992.263.5.h1356
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发表时间：
1992-11-01
影响因子：
--
通讯作者：
MOSKOWITZ, MA
中科院分区：
文献类型：
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作者：
NELSON, CW;WEI, EP;MOSKOWITZ, MA
超氧化物歧化酶（SOD）-硝基四氮唑蓝（NBT）减少后，脑缺血-再灌注猫配备了颅窗的超氧化物歧化酶（SOD）的可降解部分测量。在再灌注早期发现了显着的超氧化物产生，并持续超过1小时后缺血。在未经受缺血的对照动物、缺血期间和再灌注120分钟时未检测到超氧化物。缺血后，对动脉性低碳酸血症的血管收缩反应降低。这种影响被阻止预处理SOD加过氧化氢酶或去铁胺。缺血后，对局部乙酰胆碱的反应转化为血管收缩。再灌注120分钟时，正常的血管舒张反应又自发出现。血管舒张反应乙酰胆碱保存在动物预处理SOD加过氧化氢酶。缺血后血脑屏障对标记白蛋白和辣根过氧化物酶的通透性增加。用SOD和过氧化氢酶预处理可使这些影响最小化。我们的结论是，超氧化物的产生发生在脑缺血后再灌注相当长的一段时间，超氧化物及其衍生物负责至少部分的血管舒张和异常反应，以及增加血脑屏障通透性的大分子缺血后看到。此外，研究结果表明，负责血管异常的代理是通过铁催化的Haber-Weiss反应产生的羟基自由基。
Superoxide production was measured as the superoxide dismutase (SOD)-inhibitable portion of nitro blue tetrazolium (NBT) reduction after cerebral ischemia-reperfusion in anesthetized cats equipped with cranial windows. Significant superoxide production was found in the early reperfusion period and continued for more than 1 h after ischemia. Superoxide was not detected in control animals not subjected to ischemia, during ischemia, and at 120 min of reperfusion. After ischemia, the vasoconstrictor response to arterial hypocapnia was reduced. This effect was prevented by pretreatment with SOD plus catalase or by deferoxamine. The response to topical acetylcholine was converted to vasoconstriction after ischemia. The normal vasodilator response reappeared spontaneously at 120 min of reperfusion. The vasodilator response to acetylcholine was preserved in animals pretreated with SOD plus catalase. Blood-brain barrier permeability to labeled albumin and horseradish peroxidase was increased after ischemia. These effects were minimized by pretreatment with SOD and catalase. We conclude that superoxide generation occurs during reperfusion after cerebral ischemia for a fairly long period and that superoxide and its derivatives are responsible at least in part for the vasodilation and the abnormal reactivity as well as for the increase in blood-brain barrier permeability to macromolecules seen after ischemia. Furthermore, the findings suggest that the agent responsible for the vascular abnormalities is hydroxyl radical generated via the iron-catalyzed Haber-Weiss reaction.