诱生型一氧化氮合酶与脑缺血后期损伤

脑缺血后期敏感细胞受缺血局部产生的某些细胞因子以及血管切变力、氧化还原状态的改变等因素所诱导，表达活性诱生型一氧化氮合酶（ｉｎｄｕｃｉｂｌｅｎｉｔｒｉｃｏｘｉｄｅｓｙｎｔｈａｓｅ，ｉＮＯＳ）并持续催化大量的ＮＯ。后者通过干扰细胞正常代谢、形成自由基等途径产生强大的神经细胞毒性。脑缺血损伤后２４ｈ应用选择性的ｉＮＯＳ抑制剂仍能明显减少实验动物的脑缺血梗死区面积，提示ｉＮＯＳ选择性抑制剂有望成为极有价值的脑缺血损伤治疗药物。

Relationship between iNOS and the late-phase cerebral ischemia

During the late-phase of cerebral ischemia iNOS is expressed in susceptible cells,induced by some cytokines or by the changes of redox and shear.stress in local vessels.The activeiNOS then catalyzes Larginine and produce a large amount of NO which contributes to severeneuronal cytoxicity. 24h after the ischemic injury, administration of selective iNOS inhibitors tothe experimental animals can significantly reduce the infarct volume of the ischemic brain tissue.Itsuggests that the selective iNOS inhibitors may well represent a kind of valuble drugs to developfor the management of ischemic stroke.