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目的为研究脑缺血和缺血再灌注对各脑区一氧化氮（ＮＯ）的变化，以及一氧化氮合成酶（ＮＯＳ）抑制剂ＷＮ－硝基左旋精氨酸（Ｌ－ＮＮＡ）对脑缺血和缺血再灌注时各脑区ＮＯ生成的影响。方法采用四动脉阻断的全脑缺血模型，通过组化方法、荧光方法和放射免疫方法，观察脑缺血５ｍｉｎ、１０ｍｉｎ、１５ｍｉｎ、３０ｍｉｎ和６０ｍｉｎ，以及脑缺血１０ｍｉｎ再灌注１５ｍｉｎ、缺血３０ｍｉｎ再灌注１５ｍｉｎ，大脑皮质、海马、纹状体和小脑组织中ＮＯＳ表达、ＮＯＳ活性、ＮＯ２和ｃＧＭＰ的变化；同时观察了Ｌ－ＮＮＡ对脑缺血１０ｍｉｎ、缺血１０ｍｉｎ再灌注１５ｍｉｎ，各脑区ＮＯ２生成量的影响。每组大鼠８～１０只。结果（１）大鼠四个脑区ＮＯＳ表达、ＮＯＳ活性、ＮＯ２和ｃＧＭＰ的含量，在缺血５～１５ｍｉｎ明显高于假手术组（Ｐ＜０．０５或Ｐ＜０．０１），在缺血３０～６０ｍｉｎ开始下降。（２）在缺血１０ｍｉｎ、３０ｍｉｎ再灌注１５ｍｉｎ，它们的含量可明显增加，与单纯缺血组相比，有显著性差异（Ｐ＜０．０１）。（３）Ｌ－ＮＮＡ可使脑缺血１０ｍｉｎ和缺血１０ｍｉｎ再灌注１５ｍｉｎ，各脑区ＮＯ２的生成量明显减少（Ｐ＜０．０５或Ｐ＜０．０１）；左旋精氨酸可部分逆?
Objective To investigate the changes of nitric oxide (NO) in cerebral regions and the effect of NOS inhibitor WN-L-NNA on brain Effects of NO production in various brain regions during ischemia and reperfusion. Methods The model of global cerebral ischemia was established by four-artery occlusion. The cerebral ischemia was observed at 5 min, 10 min, 15 min, 30 min and 60 min, and reperfusion 15 min after cerebral ischemia 10 min by fluorescence, radioimmunoassay. The expression of NOS, NOS activity, NO2 and cGMP in cerebral cortex, hippocampus, striatum and cerebellum were observed after 30min reperfusion for 30min. The effects of L-NNA on cerebral ischemia 10min, ischemia 10min 15min, NO2 production area of the impact. 8 to 10 rats in each group. Results (1) NOS expression, NOS activity, NO2 and cGMP contents in the four brain regions in rats were significantly higher than those in the sham-operated group (P <0.05 or P <0.01) Blood 30 ~ 60min began to decline. (2) Compared with the ischemia group, there was a significant difference (P <0.01) in the content of 10 min ischemia, 30 min reperfusion 15 min. (3) L-NNA can make cerebral ischemia 10 min and ischemia 10 min reperfusion 15 min, the production of NO 2 in each brain area decreased significantly (P <0.05 or P <0.01); L-arginine could be partially reversed ?