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一氧化氮在缺血性脑损伤发病机制中的作用。

Role of nitric oxide in pathogenesis underlying ischemic cerebral damage.

作者信息

Matsui T, Nagafuji T, Kumanishi T, Asano T

机构信息

Department of Neurosurgery, Saitama Medical Center/School, Japan.

出版信息

Cell Mol Neurobiol. 1999 Feb;19(1):177-89. doi: 10.1023/a:1006985112459.

Abstract
  1. Based upon the intriguing report that nitric oxide synthase (NOS) inhibitor dose-dependently reverses N-methyl-D-aspartate (NMDA)-induced neurotoxicity observed in primary cortical cell cultures, many laboratories have investigated whether NOS inhibition is beneficial as a treatment for cerebral ischemia. 2. Although the results are variable, it is likely thought that nitric oxide plays a key role in pathomechanism underlying ischemic brain damage. 3. We review the experimental studies on effects of NOS inhibition on cerebral ischemia and measuring nitric oxide produced in the brain subjected to cerebral ischemia. 4. Finally, the possibility of NOS inhibitors as a therapeutical tool is discussed.
摘要
  1. 基于一氧化氮合酶(NOS)抑制剂能剂量依赖性地逆转在原代皮质细胞培养物中观察到的N-甲基-D-天冬氨酸(NMDA)诱导的神经毒性这一有趣报告,许多实验室已研究NOS抑制作为脑缺血治疗方法是否有益。2. 尽管结果各异,但人们普遍认为一氧化氮在缺血性脑损伤的发病机制中起关键作用。3. 我们综述了关于NOS抑制对脑缺血影响以及测量脑缺血时脑内产生的一氧化氮的实验研究。4. 最后,讨论了NOS抑制剂作为治疗工具的可能性。

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