兔MCAO后脑组织NOS活性的变化

Alteration of brian NOS activity after focal cerebral ischemia in rabbits

一氧化氮（ＮＯ）与脑缺血关系密切，对缺血性脑损害可能有直接的影响。一氧化氮合成酶（ＮＯＳ）是ＮＯ生物合成的限速酶。本文在建立兔ＭＣＡＯ局灶脑缺血模型基础上，测定缺血后不同时间缺血区和正常脑组织的ＮＯＳ活性。结果证实缺血后早期（ＭＣＡＯ后１ｈ内）ＮＯＳ活性突然升高。

There is increasing evidence that nitric oxide(NO) is and important molecule messenger involved in a wide variety of biological processes. Recent data suggest that NO is also involved in cerebral ischemia, and affect ischemic insult. NOS catalyzes the conversion of L-arginine to citrulline and NO.We measured brain NOS activity 10 min, 30min and 2 hour after cerebral ischemia in rabbits.Compared with one of controls,brain NOS activity was increased as early as 10 min after the onset of ischemia and its amplitude reached a maximum at 30 min (1.1982±0.2271 vs 0.6218± 2. 007 ,P<0. 01, mean ±SD). These results support that brain NOS activity is sharp transient increased during the first hour of cerebral ischemia,which leads to a burst in NO production