一氧化氮在大鼠脑缺血及再灌注损伤中的作用

目的：研究一氧化氮（NO）在大鼠脑缺血及再灌注损伤中的作用和梗死侧大脑半球内一氧化氮合酶（NOS）活性的变化。方法：运用线栓法建立大鼠脑缺血及再灌注模型，采用液体闪烁法检测NOS活性和计算机图像分析技术测量海马CAI区梗死灶体积，并运用t检验对数据结果进行分析。结果：脑缺血2h后，NOS活性较正常大鼠明显增高（P＜0．01），腹腔注射L－硝酸精氨酸（L－NA，60mg/kg）后，NOS活性显著降低，海马CA1区梗死灶体积缩小（P＜0．01）。缺血再灌注2h后，NOS活性和缺血2h时相比再次增高（P＜0．01），注射L－NA后，NOS活性明显受到抑制，海马CA1区梗死灶体积扩大（P＜0．01）。结论：NO可能具有双重作用，既可以加重缺血性脑损伤，又对缺血后的脑损伤具有保护作用。

Effect of nitric oxide on cerebral ischemia and reperfusion injury in rats

Objective: To explore the effect of nitric oxide ( NO) on cerebral ischemia and reperfusion injury in the rats as well as the chan ges of nitric oxide synthase (NOS) activity in the infarcted cerebral hemisphere . Methods: The model of cerebral ischemia and reperfus ion in rats were established by intraluminal suture method. The NOS activities were determined by the liquid scintillation spectroscopy and the hippocampus CA 1 infarct volume was measured by the computerized image, and the data were ana lyzed with t test. Results: The NOS activities were significantly higher than that of the normal rats 2 hours after ischemia ( P <0.01). However, the NOS activities were significantly decreased after an i ntraperitoneal injection of L nitroarginine (L NA, 60 mg/kg), and the CA1 i nfarct size decreased ( P < 0.01 ). Two hours after ischemic reperfusion, N OS activities as compared with the 2 hour ischemia in the rats increased once m ore ( P <0.01). But this dramatically decreased after the injection of L NA, and the infarct size enlarged in CA1 ( P <0.01). Conclus ion: The present results suggest that NO may have double actions, i .e., either aggravating the ischemic cerebral injury, or having a protective eff ect on the cerebral injury after ischemia.