Mitochondrial generation of reactive oxygen species after brain ischemia in the rat
Mitochondrial generation of reactive oxygen species after brain ischemia in the rat
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DOI：
10.1161/01.str.27.2.327
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发表时间：
1996-02-01
期刊：
影响因子：
8.3
通讯作者：
Zhang, J
中科院分区：
文献类型：
--
作者：
Piantadosi, CA;Zhang, J
背景和目的脑缺血后，当呼吸链的组分减少而分子氧存在时，脑线粒体具有产生活性氧的能力。我们测试的假设，脑线粒体在体内产生活性氧物种后，缺血/再灌注（IR）在大鼠足以逃避内源性抗氧化剂defenses.Methods缺血依赖性生产的羟基自由基在麻醉大鼠的海马监测与使用脑内微透析。通过双侧颈动脉闭塞和出血性低血压至35 mm Hg的平均动脉压持续15分钟，随后再灌注60分钟来产生短暂性全脑缺血：在实验过程中，将水杨酸注入海马，观察其羟基化产物2，3-二羟基苯甲酸的恢复情况。（2，3-DHBA），将来自对照组动物的羟基化数据与来自在单独的线粒体复合物I抑制剂或抑制剂治疗期间经历IR的动物的数据进行比较。结果短暂性脑缺血1h后，微透析法测定的2，3-DHBA回收率较对照组增加5倍（P
Background and Purpose Brain mitochondria have a substantial capacity to generate reactive oxygen species after ischemia when the components of the respiratory chain are reduced and molecular oxygen is present. We tested the hypothesis that brain mitochondria in vivo produce reactive oxygen species after ischemia/reperfusion (IR) in rats at a rate sufficient to escape endogenous antioxidant defenses.Methods Ischemia-dependent production of hydroxyl radical in the hippocampus of the anesthetized rat was monitored with the use of intracerebral microdialysis. Transient global ischemia was produced by bilateral carotid artery occlusion and hemorrhagic hypotension to a mean arterial pressure of 35 mm Hg for 15 minutes followed by reperfusion for 60 minutes: Salicylic acid was infused into the hippocampus during the experiments, and changes in the recovery of its hydroxylated product, 2,3-dihydroxybenzoic acid (2,3-DHBA), were used to assess the effects of inhibitors of mitochondrial complex I on formation of hydroxyl radical during IR. Hydroxylation data from control groups of animals were compared with data from animals undergoing IR during treatment with either a mitochondrial complex I inhibitor alone or the inhibitor plus succinic acid.Results Transient ischemia led to a fivefold increase in the recovery of 2,3-DHBA by microdialysis after 1 hour relative to control animals (P