INCREASED LIPID-PEROXIDATION IN VULNERABLE BRAIN-REGIONS AFTER TRANSIENT FOREBRAIN ISCHEMIA IN RATS
INCREASED LIPID-PEROXIDATION IN VULNERABLE BRAIN-REGIONS AFTER TRANSIENT FOREBRAIN ISCHEMIA IN RATS
复制标题
DOI：
10.1161/01.str.20.7.918
复制
发表时间：
1989-07-01
期刊：
影响因子：
8.3
通讯作者：
BRALET, J
中科院分区：
文献类型：
--
作者：
BROMONT, C;MARIE, C;BRALET, J
我们研究了脑脂质过氧化反应，估计由硫代巴比妥酸试验，在大鼠大脑区域后30分钟的严重前脑缺血和再循环期长达72小时。脂质过氧化物水平保持不变，在所有的脑区域在缺血期间，在第一个小时的再循环，但选择性增加8和72小时之间的再循环在海马，纹状体和皮质的缺血敏感区域。在再循环48小时时观察到最明显的增加（30-37%）。相比之下，脂质过氧化物水平不变，在梗死的脑区域后24小时颈动脉注射微球，表明缺血性脑的再氧合是液体过氧化的先决条件。我们评估了脂质过氧化能力的脑匀浆获得缺血和再循环大鼠通过测量有氧孵育后的脂质过氧化物的生产。暴露于30分钟的缺血或1小时的再循环大鼠的匀浆并不更容易过氧化。然而，在再循环8-48小时时，海马、纹状体和皮质中脂质过氧化物的产生选择性增加，表明抗氧化系统的功效丧失。这些结果表明，在缺血敏感的大脑区域发生的脂质过氧化反应的延迟和持久的增加，并平行于神经元坏死的发展，支持的假设，自由基过程参与缺血后神经元损伤。
We examined cerebral lipid peroxidation, estimated by a thiobarbituric acid test, in rat brain regions after 30 minutes of severe forebrain ischemia and at recirculation periods of up to 72 hours. The lipid peroxide levels remained unaltered in all brain regions during ischemia and during the first hour of recirculation but were selectively increased between 8 and 72 hours of recirculation in the ischemia-sensitive regions of the hippocampus, striatum, and cortex. The most pronounced increases (30-37%) were seen at 48 hours of recirculation. In contrast, lipid peroxide levels were unchanged in infarcted brain regions 24 hours after intracarotid injection of microspheres, indicating that reoxygenation of the ischemic brain is a prerequisite for liquid peroxidation. We assessed the lipid peroxidation capacity of cerebral homogenates obtained from rats subjected to ischemia and recirculation by measuring the production of lipid peroxides after aerobic incubation. The homogenates from rats exposed to 30 minutes of ischemia or to 1 hour of recirculation were not more susceptible to peroxidation. However, the production of lipid peroxides was selectively increased in the hippocampus, striatum, and cortex at 8-48 hours of recirculation, suggesting a loss of efficacy of the antioxidant systems. These results showing a delayed and long-lasting increase in lipid peroxidation that occurs in ischemia-sensitive brain regions and parallels the development of neuronal necrosis, support the hypothesis that free radical processes participate in postischemic neuronal damage.