Balkan E, Balkan S, Ozben T, Serteser M, Gümüslü S, Oguz N
Department of Otorhinolaryngology, Faculty of Medicine, Akdeniz University, Antalya, Turkey.
Int J Neurosci. 1997 Jan;89(1-2):61-77. doi: 10.3109/00207459708988465.
Recent evidence in primary neuronal cell culture implicates NO as a mediator of glutamatergic neurotoxicity acting via N-methyl-D-aspartate (NMDA) receptors. In this study, we investigated the effects of inhibition of NOsynthase activity in focal cerebral ischemia in rats. Focal cerebral ischemia was produced by permanent occlusion of right MCA in urethane anesthetized rats. A number of indicators of brain NO production, nitrite and cGMP were determined in ipsilateral and contralateral cerebral cortex and cerebellum after 0, 10 and 60 minutes of focal cerebral ischemia. The same parameters were measured in rats pre- and posttreated with the potent Nitric oxide synthase (NOS) inhibitor, NW-nitro-L-arginine methyl ester (L-NAME).
近期原代神经元细胞培养实验的证据表明,一氧化氮(NO)作为一种通过N-甲基-D-天冬氨酸(NMDA)受体发挥作用的谷氨酸能神经毒性介质。在本研究中,我们调查了抑制大鼠局灶性脑缺血中一氧化氮合酶活性的作用。通过在氨基甲酸乙酯麻醉的大鼠中永久性闭塞右侧大脑中动脉(MCA)来制造局灶性脑缺血。在局灶性脑缺血0、10和60分钟后,测定同侧和对侧大脑皮层及小脑中脑NO生成、亚硝酸盐和环磷酸鸟苷(cGMP)的多项指标。在使用强效一氧化氮合酶(NOS)抑制剂Nω-硝基-L-精氨酸甲酯(L-NAME)进行预处理和后处理的大鼠中测量相同参数。