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NG-硝基-L-精氨酸会加重沙鼠短暂性前脑缺血后的神经元死亡。

NG-nitro-L-arginine enhances neuronal death following transient forebrain ischemia in gerbils.

作者信息

Weissman B A, Kadar T, Brandeis R, Shapira S

机构信息

Department of Pharmacology, Israel Institute for Biological Research, Ness Ziona.

出版信息

Neurosci Lett. 1992 Nov 9;146(2):139-42. doi: 10.1016/0304-3940(92)90062-c.

Abstract

Experiments were performed with Mongolian gerbils to study the effect of the specific nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine (L-NNA) on ischemic brain damage induced by 5 min bilateral carotid occlusion. A single i.p. injection of L-NNA did not result in any neuronal loss in the central nervous system. In animals undergoing ischemia, a selective destruction of hippocampal CA1 cells was observed whereas pretreatment with 50 mg/kg L-NNA 4 h before administration of ischemia produced significantly more extensive cell damage in the hippocampus and other brain regions. These findings demonstrate that in this model inhibition of nitric oxide generation augments ischemia-induced neuronal cell injury in the brain.

摘要

用蒙古沙鼠进行实验,以研究特异性一氧化氮(NO)合酶抑制剂NG-硝基-L-精氨酸(L-NNA)对5分钟双侧颈动脉闭塞诱导的缺血性脑损伤的影响。单次腹腔注射L-NNA未导致中枢神经系统任何神经元损失。在经历缺血的动物中,观察到海马CA1细胞的选择性破坏,而在缺血给药前4小时用50mg/kg L-NNA预处理在海马和其他脑区产生了明显更广泛的细胞损伤。这些发现表明,在该模型中,一氧化氮生成的抑制增强了脑缺血诱导的神经元细胞损伤。

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