N-ω-硝基-L-精氨酸甲酯抑制蒙古沙鼠短暂性全脑缺血后的皮层电活动恢复。
N omega-nitro-L-arginine-methyl ester inhibits electrocortical recovery subsequent to transient global brain ischemia in Mongolian gerbil.
作者信息
Sancesario G, Iannone M, D'Angelo V, Nisticò G, Bernardi G
机构信息
Department of Public Health and Molecular Biology, University of Rome Tor Vergata, Italy.
出版信息
Funct Neurol. 1992 Mar-Apr;7(2):123-7.
Electrocorticographic (ECoG) activity remains isoelectric for about 15 min after transient (10 min) bilateral carotid arteries occlusion in mongolian gerbils. In this model of global forebrain ischemia N omega-Nitro-L-arginine methyl ester (L-NAME), a nitric oxide (NO) synthase inhibitor, significantly delays the recovery of ECoG amplitude. Thus, the present experiments suggest that NO is involved in the cerebrovascular physiological response to brain ischemia.
在蒙古沙鼠中，短暂性（10分钟）双侧颈动脉闭塞后，皮层脑电图（ECoG）活动会保持约15分钟的等电位状态。在这种全脑缺血模型中，一氧化氮（NO）合酶抑制剂Nω-硝基-L-精氨酸甲酯（L-NAME）会显著延迟ECoG振幅的恢复。因此，本实验表明NO参与了脑血管对脑缺血的生理反应。
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