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Role of neuronal and endothelial nitric oxide synthase in nitric oxide generation in the brain following cerebral ischemia.神经元型和内皮型一氧化氮合酶在脑缺血后大脑中一氧化氮生成中的作用。
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Nitric oxide mediates cerebral ischemic tolerance in a neonatal rat model of hypoxic preconditioning.一氧化氮在新生大鼠缺氧预处理的脑缺血耐受模型中介导脑缺血耐受。
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Ischemia-induced taurine release is modified by nitric oxide-generating compounds in slices from the developing and adult mouse hippocampus.在发育中和成年小鼠海马体切片中,一氧化氮生成化合物可改变缺血诱导的牛磺酸释放。
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本文引用的文献

1
N omega-nitro-L-arginine attenuates early ischemic neuronal damage of prolonged focal cerebral ischemia and recirculation in rats.N-ω-硝基-L-精氨酸减轻大鼠长时间局灶性脑缺血再灌注早期的缺血性神经元损伤。
Neurol Res. 1997 Apr;19(2):192-203. doi: 10.1080/01616412.1997.11740795.
2
Neuronal (type I) nitric oxide synthase regulates nuclear factor kappaB activity and immunologic (type II) nitric oxide synthase expression.神经元型(I型)一氧化氮合酶调节核因子κB活性和免疫型(II型)一氧化氮合酶表达。
Proc Natl Acad Sci U S A. 1997 Mar 18;94(6):2676-80. doi: 10.1073/pnas.94.6.2676.
3
ARL 17477, a potent and selective neuronal NOS inhibitor decreases infarct volume after transient middle cerebral artery occlusion in rats.ARL 17477,一种强效且选择性的神经元型一氧化氮合酶抑制剂,可减少大鼠短暂性大脑中动脉闭塞后的梗死体积。
J Cereb Blood Flow Metab. 1996 Jul;16(4):599-604. doi: 10.1097/00004647-199607000-00009.
4
Enlarged infarcts in endothelial nitric oxide synthase knockout mice are attenuated by nitro-L-arginine.硝基-L-精氨酸可减轻内皮型一氧化氮合酶基因敲除小鼠的梗死灶扩大。
J Cereb Blood Flow Metab. 1996 Sep;16(5):981-7. doi: 10.1097/00004647-199609000-00023.
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Cerebroprotective effects of aminoguanidine in a rodent model of stroke.氨基胍在啮齿动物中风模型中的脑保护作用。
Stroke. 1996 Aug;27(8):1393-8. doi: 10.1161/01.str.27.8.1393.
6
Inducible nitric oxide synthase gene expression in vascular cells after transient focal cerebral ischemia.短暂性局灶性脑缺血后血管细胞中诱导型一氧化氮合酶基因的表达
Stroke. 1996 Aug;27(8):1373-80. doi: 10.1161/01.str.27.8.1373.
7
Nitroprusside improves blood flow and reduces brain damage after focal ischemia.硝普钠可改善局部缺血后的血流并减少脑损伤。
Neuroreport. 1993 May;4(5):559-62. doi: 10.1097/00001756-199305000-00024.
8
Nitric oxide measured by a porphyrinic microsensor in rat brain after transient middle cerebral artery occlusion.用卟啉微传感器测量大鼠大脑中动脉短暂闭塞后的一氧化氮。
J Cereb Blood Flow Metab. 1993 May;13(3):355-8. doi: 10.1038/jcbfm.1993.48.
9
Nitric oxide synthesis and regional cerebral blood flow responses to hypercapnia and hypoxia in the rat.大鼠体内一氧化氮合成及局部脑血流对高碳酸血症和低氧的反应
J Cereb Blood Flow Metab. 1993 Jan;13(1):80-7. doi: 10.1038/jcbfm.1993.10.
10
A redox-based mechanism for the neuroprotective and neurodestructive effects of nitric oxide and related nitroso-compounds.一种基于氧化还原的机制,用于解释一氧化氮及相关亚硝基化合物的神经保护和神经破坏作用。
Nature. 1993 Aug 12;364(6438):626-32. doi: 10.1038/364626a0.

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.

DOI:10.1023/a:1006985112459
PMID:10079976
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11545421/
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。