摘要
沙土鼠双侧颈总动脉结扎1小时后,于高氧环境中再灌流2小时,脑MDA含量(4.39±0.26nmol/mg蛋白)与空气对照组(2.63±0.50nmol/mg蛋白)、高氧对照组(3.07±0.52nmol/mg蛋白)、缺血组(2.96±0.41nmol/mg蛋白)及空气中再灌流组(2.79±0.59nmol/mg蛋白)相比较,差异均具有高度显著性(P<0.01)。大脑皮层TXB_2含量增加,6-Keto-PGF_(1α)含量减少,水、钠含量明显增加。但上述各指标与缺血后在大气环境中再灌流组相比,差异均无显著性。作者推测,高浓度氧导致脂质过氧化作用增强的机理可能源于异常的线粒体电子传递链功能。
Exposure of gerbils 120 min to a high concentration oxygen (HCO)atmosphere after 60 min cerebral ischemia resulted in a marked increase in cerebral malondialdehyde (MDA, 4.39±0.26 nmol/mg protein). Much less cerebral MDA was among the other groups (2.63±0.50 nmol/mg protein in sham-operated controls; 3.07±0.52 nmol/mg protein in gerbils exposed to HCO without ischemia; 2.96±0.41nmol/mg protein in ger. bils subjected to 60 min ischemia; 2.79±0.59nmol/mg protein in gerbils subjected to 60 min ischemia and 120 min reperfusion). The contents of cerebral water, sodium, increassd after 60 mln cerebral ischemia. The contents of TXB_2 increased, 6-Keto-PGF_(1α) decreased, the elevation of cerebral water and sodium were more obvious after 120 min repefusion following ischemia. There was no difference in these items except for MDA between the reperfusion groups within air and within HCO.
The authors proposed the mechanism that HCO elevates the contents of cerebral MDH might be due to abnormal function of election transport chain of mitochondria.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1990年第6期506-509,共4页
Chinese Journal of Pathophysiology
基金
国家自然科学基金
关键词
过氧化脂质
脑缺血
沙土鼠科
Lipid peroxides
Cerebral ischemia
Gerbillinae
