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吸烟对呼出一氧化氮的急性和慢性影响。

Acute and chronic effects of cigarette smoking on exhaled nitric oxide.

作者信息

Kharitonov S A, Robbins R A, Yates D, Keatings V, Barnes P J

机构信息

Department of Thoracic Medicine, National Heart and Lung Institute, London, United Kingdom.

出版信息

Am J Respir Crit Care Med. 1995 Aug;152(2):609-12. doi: 10.1164/ajrccm.152.2.7543345.

DOI:10.1164/ajrccm.152.2.7543345
PMID:7543345
Abstract

Cigarette smoking is associated with an increased risk of respiratory tract infections, chronic airway disease, and cardiovascular diseases, all of which may be modulated by endogenous nitric oxide (NO). We have investigated whether cigarette smoking reduces the production of endogenous NO. We compared exhalations of 41 current cigarette smokers with normal lung function and 73 age-matched non-smoking controls. Peak exhaled NO levels were measured by a modified chemiluminescence analyzer. The effects of inhaling a single cigarette in smokers were also measured. In control subjects we also measured the effects of inhalation of NO itself and carbon monoxide, both constituents of tobacco smoke. Peak exhaled NO concentrations were significantly reduced in smokers (42 +/- 3.9 compared with 88 +/- 2.7 parts per billion in nonsmokers, p < 0.01), with a significant relation between the exhaled NO and cigarette consumption (r = 0.77, p < 0.001). Smoking a single cigarette also significantly (p < 0.02), but transiently, reduced exhaled NO. Inhalation of carbon monoxide and NO had no effect on exhaled NO in normal subjects. Cigarette smoking decreased exhaled NO, suggesting that it may inhibit the enzyme NO synthase. Since endogenous NO is important in defending the respiratory tract against infection, in counteracting bronchoconstriction and vasoconstriction, and in inhibiting platelet aggregation, this effect may contribute to the increased risks of chronic respiratory and cardiovascular disease in cigarette smokers.

摘要

吸烟与呼吸道感染、慢性气道疾病及心血管疾病风险增加相关,而内源性一氧化氮(NO)可能对这些疾病具有调节作用。我们研究了吸烟是否会减少内源性NO的生成。我们比较了41名肺功能正常的当前吸烟者和73名年龄匹配的非吸烟对照者的呼气情况。采用改良的化学发光分析仪测量呼出NO的峰值水平。我们还测量了吸烟者吸入一支香烟后的影响。在对照受试者中,我们也测量了吸入烟草烟雾的两种成分——NO本身和一氧化碳后的影响。吸烟者呼出NO的峰值浓度显著降低(吸烟者为42±3.9,而非吸烟者为88±2.7十亿分之一,p<0.01),呼出的NO与香烟消费量之间存在显著相关性(r = 0.77,p<0.001)。吸一支烟也会显著(p<0.02)但短暂地降低呼出的NO。吸入一氧化碳和NO对正常受试者呼出的NO没有影响。吸烟会降低呼出的NO,这表明吸烟可能抑制了NO合酶。由于内源性NO在保护呼吸道免受感染、对抗支气管收缩和血管收缩以及抑制血小板聚集方面很重要,这种作用可能导致吸烟者患慢性呼吸道和心血管疾病的风险增加。

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