ACUTE AND CHRONIC EFFECTS OF CIGARETTE-SMOKING ON EXHALED NITRIC-OXIDE
ACUTE AND CHRONIC EFFECTS OF CIGARETTE-SMOKING ON EXHALED NITRIC-OXIDE
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DOI：
10.1164/ajrccm.152.2.7543345
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发表时间：
1995-08-01
影响因子：
24.7
通讯作者：
BARNES, PJ
中科院分区：
文献类型：
--
作者：
KHARITONOV, SA;ROBBINS, RA;BARNES, PJ
吸烟与呼吸道感染、慢性气道疾病和心血管疾病的风险增加有关，所有这些都可能由内源性一氧化氮（NO）调节。我们研究了吸烟是否会减少内源性NO的产生。我们比较了41名肺功能正常的吸烟者和73名年龄匹配的非吸烟者的呼出量。用改进的化学发光分析仪测量呼出的峰值NO水平。吸烟者吸入一根香烟的影响也被测量。在对照组中，我们还测量了吸入一氧化氮和一氧化碳的影响，这两种物质都是烟草烟雾的成分。吸烟者呼出的NO峰值浓度显著降低（42 +/- 3.9，非吸烟者为88 +/- 2.7,p < 0.01），呼出的NO与香烟消费量之间存在显著关系（r = -0.77, p < 0.001）。吸烟也显著（p < 0.02），但短暂地减少了呼出的NO。正常受试者吸入一氧化碳和一氧化氮对呼出一氧化氮无影响。吸烟使呼出的NO减少，表明吸烟可能抑制NO合成酶。由于内源性一氧化氮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具有重要作用，因此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。
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 nonsmoking 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.