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鼻腔一氧化氮与生活方式中烟草烟雾暴露

Nasal nitric oxide and lifestyle exposure to tobacco smoke.

作者信息

Zhou Haibo, Zou Baiming, Hazucha Milan, Carson Johnny L

机构信息

Center for Environmental Medicine, Asthma, and Lung Biology, the Department of Biostatistics, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7310, USA.

出版信息

Ann Otol Rhinol Laryngol. 2011 Jul;120(7):455-9. doi: 10.1177/000348941112000706.

DOI:10.1177/000348941112000706
PMID:21859054
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3193610/
Abstract

OBJECTIVES

Nitric oxide (NO) is a reactive gas generated by inflammatory cells and mucosal epithelial cells of the nose and paranasal sinuses and is an important mediator in nonspecific host defense against infectious agents. However, NO also mediates physiologic events such as vasodilation, mucus hypersecretion, and mucosal disruption that are associated with inflammatory conditions, and it is a regulator of ciliary beat frequency. In the present study, we hypothesized that lifestyle exposure to tobacco smoke, whether through active smoking or by inadvertent exposure to secondhand tobacco smoke, would result in higher detectable levels of nasal NO (nNO) than are found in well-documented nonsmokers.

METHODS

Nasal NO measurements were obtained concomitant with assays of urine cotinine from well-documented nonsmokers, active smokers, and individuals exposed by lifestyle to secondhand smoke. These parameters were statistically analyzed to determine whether increasing levels of tobacco smoke exposure yield higher concentrations of nNO.

RESULTS

Our results and subsequent statistical analyses imply that active smokers who exhibit high urine cotinine levels exhibit significant increases in nNO levels in comparison to both nonsmokers and nonsmokers exposed to secondhand smoke.

CONCLUSIONS

There is an increased level of nNO associated with tobacco smoke exposure that may contribute to the inflammatory processes characteristic of disease pathogenesis in smokers.

摘要

目的

一氧化氮(NO)是一种由鼻腔和鼻窦的炎症细胞及黏膜上皮细胞产生的活性气体,是机体对感染因子非特异性宿主防御中的重要介质。然而,NO也介导诸如血管舒张、黏液分泌亢进和黏膜破坏等与炎症状态相关的生理过程,并且它是纤毛摆动频率的调节因子。在本研究中,我们推测,无论是主动吸烟还是不经意间接触二手烟,生活方式中接触烟草烟雾都会导致可检测到的鼻腔一氧化氮(nNO)水平高于有充分记录的非吸烟者。

方法

对有充分记录的非吸烟者、主动吸烟者以及生活方式上接触二手烟的个体,在检测尿可替宁的同时进行鼻腔NO测量。对这些参数进行统计分析,以确定烟草烟雾暴露水平的增加是否会产生更高浓度的nNO。

结果

我们的结果及后续统计分析表明,与非吸烟者和接触二手烟的非吸烟者相比,尿可替宁水平高表明为主动吸烟者的nNO水平显著升高。

结论

与烟草烟雾暴露相关的nNO水平升高可能会促使吸烟者疾病发病机制中具有特征性的炎症过程发生发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07f8/3193610/05da0366be15/nihms329674f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07f8/3193610/e2be156fdbe3/nihms329674f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07f8/3193610/05da0366be15/nihms329674f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07f8/3193610/e2be156fdbe3/nihms329674f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07f8/3193610/05da0366be15/nihms329674f2.jpg

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Role of nitric oxide and its metabolites as potential markers in lung cancer.一氧化氮及其代谢产物在肺癌中作为潜在标志物的作用。
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