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目的探讨一氧化氮（ＮＯ）、超氧化物歧化酶（ＳＯＤ）和丙二醛（ＭＤＡ）在急性脑缺血时血与脑中的含量变化及其作用。方法４６只Ｗｉｓｔａｒ大鼠分为假手术组和缺血组。假手术组颈部正中切口，分离两侧颈总动脉；缺血组，结扎大鼠双侧颈总动脉，对缺血不同时相血清、脑皮层和丘脑组织中的ＮＯ、ＳＯＤ和ＭＤＡ含量进行测定。结果大鼠脑缺血１０分钟血清、脑组织ＮＯ浓度增高，３０分钟血清和脑组织中ＮＯ浓度最高，于６０分钟血清和脑组织中ＮＯ浓度下降至脑缺血１０分钟时的水平；而缺血１８０分钟血清和脑组织中ＮＯ浓度最低，并于３６０分钟后血清和脑组织中ＮＯ浓度回升，且较对照组升高但无显著性差异（Ｐ＞０．０５）。脑缺血１０，３０与６０分钟大鼠血清、脑组织中ＮＯ显著高于对照组（Ｐ＜０．０１和Ｐ＜０．００１）。脑缺血３０，６０，１８０与３６０分钟，大鼠ＳＯＤ活力显著低于对照组（Ｐ＜０．０５，Ｐ＜０．０１和Ｐ＜０．００１）；而ＭＤＡ显著高于对照组（Ｐ＜０．０５，Ｐ＜０．０１和Ｐ＜０．００１）。结论脑缺血时间越长ＳＯＤ酶活力越低而ＭＤＡ含量越高，长时间将大量产生释放具有神经毒性及细胞毒性作用的ＮＯ，可引起神经元死亡及细胞和组织损伤。
Objective To investigate the changes of blood and brain contents of nitric oxide (NO), superoxide dismutase (SOD) and malondialdehyde (MDA) in acute cerebral ischemia and their effects. Methods 46 Wistar rats were divided into sham operation group and ischemia group. In the sham-operated group, the carotid artery was excised from both sides of the neck and the common carotid arteries were separated. The bilateral common carotid arteries were ligated in ischemic group. The content of NO, SOD and MDA in the serum, cortex and thalamus at different phases Determination. Results NO concentration in serum and brain tissue increased at 10 minutes after cerebral ischemia in rats, and the highest concentration of NO was observed in serum and brain tissue at 30 minutes. The concentration of NO in serum and brain tissue at 60 minutes decreased to 10 minutes after cerebral ischemia. The concentration of NO in serum and brain tissue was the lowest in 180 minutes of blood, and NO level in serum and brain tissue rebounded after 360 minutes, which was higher than that in control group (P> 0.05). The levels of NO in serum and brain of rats at 10, 30 and 60 minutes after cerebral ischemia were significantly higher than those of the control group (P <0.01 and P <0.001). At 30, 60, 180 and 360 minutes after cerebral ischemia, the activity of SOD in rats was significantly lower than that in the control group (P <0.05, P <0.01 and P <0.001) <0.05, P <0.01 and P <0.001). Conclusions The longer the cerebral ischemia time, the lower the activity of SOD and the higher the content of MDA, the more the release of NO with neurotoxicity and cytotoxicity will be produced in large quantities for a long time, which can cause neuronal death and cell and tissue damage.