Free Radical Reaction and Biological Defense Mechanism in the Pathogenesis of Prolonged Vasospasm in Experimental Subarachnoid Hemorrhage
Free Radical Reaction and Biological Defense Mechanism in the Pathogenesis of Prolonged Vasospasm in Experimental Subarachnoid Hemorrhage
复制标题
实验性蛛网膜下腔出血长期血管痉挛发病机制中的自由基反应和生物防御机制
DOI：
10.1038/jcbfm.1988.1
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发表时间：
1988
影响因子：
6.3
通讯作者：
S. Takeda
中科院分区：
文献类型：
--
作者：
S. Sakaki;S. Ohta;Hisashi Nakamura;S. Takeda
研究了自由基反应及其防御机制在实验性蛛网膜下腔出血（SAH）后延长血管痉挛发病机制中的关系。脑脊液（CSF）中脂质过氧化物浓度在SAH后第8天显著升高；动脉壁和蛛网膜下腔血凝块所在的颞叶灰质浓度均升高（p < 0.01）。另一方面，到SAH后第8天，超氧化物歧化酶（SOD）活性显著降低（p < 0.01），脑脊液中谷胱甘肽过氧化物酶（GSH-px）逐渐升高。动脉壁超氧化物歧化酶（SOD）活性轻微降低（p < 0.01）， GSH-px活性显著降低（p < 0.01），谷胱甘肽浓度显著降低（p < 0.01），直至SAH后第8天。综上所述，动脉壁脂质过氧化与脑脊液中脂质过氧化的生物防御机制不足，可能参与了SAH后血管痉挛延长的发生。
The relationship between free radical reactions and the defense mechanisms against them was investigated in the pathogenesis of prolonged vasospasm following experimental subarachnoid hemorrhage (SAH) in dogs. The concentration of lipid peroxides in the cerebro spinal fluid (CSF) increased markedly up to the eighth day following SAH; the concentrations also rose in the arterial wall (p < 0.01) and the gray matter of the temporal lobe where the subarachnoid blood clots were (p < 0.01). On the other hand, the activity of superoxide dismutase (SOD) decreased significantly up to the eighth day after SAH (p < 0.01), and there was a gradual increase of glutathione peroxidase (GSH-px) in the CSF. In the arterial wall, there was a slight decrease in the activity of SOD, a significant decrease in the activity of GSH-px (p < 0.01), and also a significant decrease in the concentration of glutathione (p < 0.01) up to the eighth day following SAH. In conclusion, lipid peroxidation with insufficient biological defense mechanisms against it in the arterial wall, concomitant with that in the CSF, might take part in the genesis of prolonged vasospasm following SAH.