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目的 探讨一氧化氮在全脑缺血 2 0min后再灌注大鼠脑损害中的作用。方法 雄性Wistar大鼠 84只 ,体重 (2 2 0± 2 0 )g ,随机分为对照组 (12只 )和缺血组 (72只 ) ,后者设 8、2 4、48、72、96、16 8h 6个时相点。参照Pulsinelli等的方法制作大鼠全脑缺血 2 0min再灌注模型 ,于再灌注后 8、2 4、48、72、96、16 8h活杀取血及海马组织 ,对照组施行麻醉及手术 ,但不缺血 ,观察 72h后取血及海马组织 ,测定血清NSE、海马NO含量及海马CA1区锥体神经元 (Pyramidalneuron ,PN)密度。结果 ①海马NO含量于缺血再灌注后 48h明显升高 ,72h达峰值 (与对照组比较P均 <0 .0 1) ,以后逐渐下降 (96h仍明显高于对照组水平 ,P <0 .0 5 ) ,16 8h降至接近对照组 ;②缺血组各时相点血清NSE含量均显著高于对照组 (P 均 <0 .0 1) ;③缺血组海马CA1区PN密度呈明显的逐渐减少趋势 ,自 48h后均明显低于对照组 (P均 <0 .0 1) ,再灌注后 16 8h仅为对照组水平的 2 2 .8% ;④缺血再灌注后海马NO含量与血清NSE水平的变化呈显著的线性正相关 (r =0 .90 2 2 ,P <0 .0 1)。结论 NO在全脑缺血再灌注损伤中起着重要作用 ,是引起海马CA1区锥体神经元DND发生的主要因素之一。
Objective To investigate the role of nitric oxide in brain damage after reperfusion in rats with global cerebral ischemia 2 0min. Methods Eighty-four male Wistar rats weighing 220 ± 20 g were randomly divided into control group (n = 12) and ischemic group (n = 72). The latter group consisted of 8,2,48,72,96 , 16 8h 6 time points. According to the method of Pulsinelli et al., A rat model of global cerebral ischemia 20 min reperfusion was established. Blood was taken and killed in the hippocampus at 8,2 4,48,72,96,168 h after reperfusion. The control group was anesthetized and operated, However, no ischemia was observed. Blood and hippocampus tissue were observed after 72 hours. Serum NSE, NO content in hippocampus and pyramidal neuron (PN) density of hippocampal CA1 area were measured. Results ① The content of NO in hippocampus increased significantly at 48h after ischemia-reperfusion and peaked at 72h (P <0.01), then decreased gradually after 96h (P <0.01). (P <0.05). The serum NSE levels in ischemic group at each time point were significantly higher than those in control group (all P <0.01). ③The density of PN in hippocampal CA1 area of ischemic group was significantly higher than that of control group (P <0.01) after 48h, only 22.8% of the control group at 168h after reperfusion; ④The content of NO in hippocampus after ischemia-reperfusion And serum NSE levels showed a significant linear positive correlation (r = 0.9022, P <0.01). Conclusion NO plays an important role in global cerebral ischemia-reperfusion injury and is one of the main factors that cause DND in pyramidal neurons of hippocampal CA1 region.