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一氧化氮介导的血流调节受吸烟和尼古丁的影响。

Nitric oxide-mediated blood flow regulation as affected by smoking and nicotine.

机构信息

Toyama Institute for Cardiovascular Research, 7-13, 1-Chome, Azuchi-machi, Chuo-ku, Osaka 541-0052, Japan.

出版信息

Eur J Pharmacol. 2010 Dec 15;649(1-3):1-13. doi: 10.1016/j.ejphar.2010.09.042. Epub 2010 Sep 21.

DOI:10.1016/j.ejphar.2010.09.042
PMID:20868673
Abstract

Cigarette smoking is a major risk factor for atherosclerosis, cerebral and coronary vascular diseases, hypertension, and diabetes mellitus. Chronic smoking impairs endothelial function by decreasing the formation of nitric oxide and increasing the degradation of nitric oxide via generation of oxygen free radicals. Nitric oxide liberated from efferent nitrergic nerves is also involved in vasodilatation, increased regional blood flow, and hypotension that are impaired through nitric oxide sequestering by smoking-induced factors. Influence of smoking on nitric oxide-induced blood flow regulation is not necessarily the same in all organs and tissues. However, human studies are limited mainly to the forearm blood flow measurement that assesses endothelial function under basal and stimulated conditions and also determination of penile tumescence and erection in response to endothelial and neuronal nitric oxide. Therefore, information about blood flow regulation in other organs, such as the brain and placenta, has been provided mainly from studies on experimental animals. Nicotine, a major constituent of cigarette smoke, acutely dilates cerebral arteries and arterioles through nitric oxide liberated from nitrergic neurons, but chronically interferes with endothelial function in various vasculatures, both being noted in studies on experimental animals. Cigarette smoke constituents other than nicotine also have some vascular actions. Not only active but also passive smoking is undoubtedly harmful for both the smokers themselves and their neighbors, who should bear in mind that they can face serious diseases in the future, which may result in lengthy hospitalization, and a shortened lifespan.

摘要

吸烟是动脉粥样硬化、脑和冠状动脉血管疾病、高血压和糖尿病的主要危险因素。慢性吸烟通过减少一氧化氮的形成和通过生成氧自由基增加一氧化氮的降解来损害内皮功能。从传出性含氮能神经释放的一氧化氮也参与血管舒张、增加局部血流和低血压,这些都通过吸烟引起的因素对一氧化氮的隔离而受损。吸烟对一氧化氮诱导的血流调节的影响在所有器官和组织中不一定相同。然而,人体研究主要限于前臂血流测量,该测量评估基础和刺激条件下的内皮功能,以及评估阴茎勃起和勃起对内皮和神经元一氧化氮的反应。因此,关于大脑和胎盘等其他器官的血流调节的信息主要来自于实验动物的研究。尼古丁是香烟烟雾的主要成分,通过从含氮能神经元释放的一氧化氮急性扩张脑血管和小动脉,但在实验动物的研究中也发现,尼古丁慢性干扰各种血管的内皮功能。除尼古丁以外的香烟烟雾成分也具有一些血管作用。不仅主动吸烟,被动吸烟对吸烟者本身及其邻居也是有害的,他们应该记住,他们将来可能会面临严重的疾病,这可能导致长时间住院和寿命缩短。

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