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目的 研究大鼠脑缺血再灌流后大脑皮层、海马、纹状体和小脑组织一氧化氮合酶 (NOS)的变化。 方法 采用放射免疫法检测脑组织中 NOS的活性。 结果 大鼠脑缺血后 5 min,各脑区结构型 NOS(c NOS)活性明显升高 ,持续到脑缺血 30 m in,脑缺血 30～ 6 0 min开始下降 ;诱导型 NOS(i NOS)活性在脑缺血后 10～ 15 m in开始升高 ,并持续到脑缺血 6 0 min;脑缺血 30 min再灌流 15 min,各脑区 c NOS和 i NOS活性明显高于缺血 30 m in(P<0 .0 5或 P<0 .0 1)。 结论 提示脑缺血再灌流时脑组织 NOS活性增强 ,采用特异 NOS抑制剂可能有助于阻断脑缺血再灌流时由一氧化氮 (NO)介导的脑损伤作用。
Objective To investigate the changes of nitric oxide synthase (NOS) in cerebral cortex, hippocampus, striatum and cerebellum after cerebral ischemia and reperfusion in rats. Methods Radioimmunoassay was used to detect the activity of NOS in brain tissue. Results At 5 min after cerebral ischemia, the activity of structural NOS (c NOS) in each brain region was significantly increased and continued to decrease 30 min after cerebral ischemia. The cerebral ischemia began to decrease 30 min to 60 min. The inducible NOS (i NOS activity began to increase 10 ~ 15 mins after cerebral ischemia and continued to cerebral ischemia 60 min; 30 min after cerebral ischemia and reperfusion 15 min, c NOS and i NOS activity in each brain was significantly higher than the lack of Blood was 30 mins (P <0. 05 or P <0. 01). The results suggest that NOS activity in brain tissue increases after cerebral ischemia and reperfusion, and the use of specific inhibitors of NOS may be helpful to block brain injury induced by nitric oxide (NO) during cerebral ischemia and reperfusion.