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目的观察缺血预处理提高脑组织对缺血再灌注损伤的耐受性（即脑缺血预适应）过程中，脑血管内皮细胞台成及释放ＮＯ功能的变化。方法取健康成年雄性Ｗｉｓｔａｒ大鼠，采用Ｐｕｌｓｉｎｅｌｌｉ四血管阻断法制备前脑缺血模型。动物随机分为两组．（１）单纯缺血再灌注组（ＩＲ组，ｎ＝１５）。在假手术３ｄ后给予８ｍｉｎ致死性缺血再灌注７ｄ．分别在缺血前、再灌注后１ｈ、１ｄ、３ｄ及７ｄ采集脑血液，用硝酸还原酶法测定血浆ＮＯ含量。并在再灌注后１ｈ和７ｄ行海马ＣＡ_１区电镜与光镜组织学检查。（２）缺血预处理组（ＩＰＣ组．ｎ＝１５），先给予一次３ｍｉｎ短暂非致死性缺血预处理，３ｄ后再给于８ｍｉｎ致死性缺血及再灌注７ｄ，检测指标同 ＩＲ组。结果 （１） ＩＲ组，缺血再灌注后脑血液中 ＮＯ含量持续下降，于再灌注１ｈ，Ｎｏ含量由对照值１５１±８μｍｏｌ／Ｌ降至 １３７±１５μｍｏｌ／Ｌ， １ｄ时为１５６±１５μｍｏｌ／Ｌ， ３ｄ时为 １４５上１７μｍｏｌ／Ｌ，于 ７ｄ时进一步下降至 １２４±１２μｍｏｌ／Ｌ（Ｐ／０． ０５）。ＩＰＣ组缺血再灌注后７ｄ内，脑血液中ＮＯ含量显著高于对照值和ＩＲ组各相应时间点的ＮＯ含量值（均为Ｐ＜Ｏ．０１）。于再灌注后１ｈ由对照?
OBJECTIVE: To observe the role of ischemic preconditioning (IC) in improving cerebral function and cerebral ischemia-reperfusion injury (ICAO) in cerebral ischemic preconditioning. Methods Healthy adult male Wistar rats were used to establish forebrain ischemia model by Pulsinelli four-vessel occlusion method. Animals were randomly divided into two groups. (1) ischemia-reperfusion group (IR group, n = 15). Three days after sham operation, 8-month lethal ischemia-reperfusion was given for 7 days. Cerebral blood was collected before ischemia, 1h, 1d, 3d and 7d after reperfusion, respectively. Plasma NO was measured by nitrate reductase method. Electron microscopy and light microscopy examination of hippocampal CA1 area were performed at 1h and 7d after reperfusion. (2) In ischemic preconditioning group (IPC group, n = 15), a 3-min transient non-lethal ischemic preconditioning was given. 3d was followed by lethal ischemia and reperfusion for 8 min. . Results (1) In the IR group, the content of NO in the brain blood decreased after ischemia-reperfusion, and the content of No decreased from 151 ± 8μmol / L to 137 ± 15μmol / L at 1h after reperfusion and 156 ± 15μmol / L 145 at 17 μmol / L at day 3 and 124 ± 12 μmol / L at day 7 (P = 0.05). Within 7 days after ischemia-reperfusion in IPC group, the content of NO in brain blood was significantly higher than that in control group and the corresponding time point in IR group (both P <0.01). 1h after reperfusion by the control?