Nitric oxide and cerebral blood flow: an update.

L D Watkins
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Abstract

This article focuses on the key concept that a basal production of nitric oxide (NO) is required as a background for biological modulation, although an excess can be cytotoxic. Studies of ischaemia and neurodegeneration have tended to emphasise detrimental effects of excess NO, but this review contrasts the emerging importance of diminished NO or interference with its action in vasospasm following subarachnoid haemorrhage (SAH) in ageing and in atherosclerosis. Clinical intervention in cerebral ischaemia will require specificity of action, since NO appears to be protective or detrimental depending on the time, source, and distribution of its production. It may be possible to utilise targeted action on the different forms of NO synthase or the specific redox forms of NO in different tissue areas.

一氧化氮和脑血流:最新进展。
这篇文章着重于一个关键的概念,即一氧化氮(NO)的基础生产是作为生物调节的背景所必需的,尽管过量的一氧化氮可能具有细胞毒性。缺血和神经退行性变的研究倾向于强调过量NO的有害影响,但本综述对比了NO减少或干扰其在老龄化和动脉粥样硬化中蛛网膜下腔出血(SAH)后血管痉挛中的作用。脑缺血的临床干预将需要特异性的作用,因为一氧化氮的保护或有害作用取决于其产生的时间、来源和分布。有可能利用针对不同形式的NO合成酶或不同组织区域中NO的特定氧化还原形式的靶向作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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