Chambers D C, Tunnicliffe W S, Ayres J G
Birmingham Heartlands Hospital, Birmingham B9 5SS, UK.
Thorax. 1998 Aug;53(8):677-9. doi: 10.1136/thx.53.8.677.
Cigarette smoking is associated with a number of common pulmonary diseases including chronic airflow limitation and bronchial carcinoma. Lower respiratory tract (LRT) nitric oxide (NO) concentrations are reduced in habitual cigarette smokers between cigarettes, and although this finding has been implicated in the pathogenesis of smoking related disease, the underlying mechanisms are unclear. A study was undertaken to determine the nature and time course for changes in LRT NO concentrations following acute inhalation of cigarette smoke.
Twenty four healthy habitual smokers were studied. The concentration of LRT NO in exhaled breath before, one and ten minutes after smoking a single cigarette was measured using chemiluminescence.
LRT NO concentrations increased in all subjects from a mean (SE) of 2.6 (0.27) to 4.8 (0.26) ppb (p < 0.0001) at one minute, and at 10 minutes remained significantly raised above the baseline level at 3.2 (0.25) ppb (p = 0.003). The mean (95% CI) increases in NO concentrations were 2.2 (1.7 to 2.7) and 0.6 (0.2 to 1.0) ppb, respectively.
These findings were unexpected in both their direction and time course. They suggest a novel mechanism for the handling of NO in the human lung. We hypothesise that NO is trapped in the epithelial lining fluid (ELF) of the normal human respiratory tract in bioequivalent forms such as S-nitrosothiols or peroxynitrite and that this trapping mechanism is sensitive to the redox state of the ELF. LRT NO concentrations will thus increase with oxidant exposure and decline as pulmonary antioxidant defence mechanisms take effect. These findings may have implications for the pathogenesis and diagnosis of oxidant mediated pulmonary disease.
吸烟与多种常见肺部疾病相关，包括慢性气流受限和支气管癌。在习惯性吸烟者中，两次吸烟期间下呼吸道（LRT）一氧化氮（NO）浓度会降低，尽管这一发现与吸烟相关疾病的发病机制有关，但其潜在机制尚不清楚。开展了一项研究以确定急性吸入香烟烟雾后LRT NO浓度变化的性质和时间进程。
对24名健康的习惯性吸烟者进行了研究。使用化学发光法测量吸一支烟之前、之后1分钟和10分钟时呼出气中LRT NO的浓度。
所有受试者的LRT NO浓度在1分钟时从平均（标准误）2.6（0.27）ppb增加到4.8（0.26）ppb（p < 0.0001），在10分钟时仍显著高于基线水平，为3.2（0.25）ppb（p = 0.003）。NO浓度的平均（95%可信区间）增加分别为2.2（1.7至2.7）和0.6（0.2至1.0）ppb。
这些发现无论在方向还是时间进程上都出乎意料。它们提示了人类肺部处理NO的一种新机制。我们假设NO以生物等效形式如S-亚硝基硫醇或过氧亚硝酸盐被困在正常人呼吸道的上皮衬液（ELF）中，并且这种捕获机制对ELF的氧化还原状态敏感。因此，LRT NO浓度将随着氧化剂暴露而增加，并在肺部抗氧化防御机制起作用时下降。这些发现可能对氧化介导的肺部疾病的发病机制和诊断有影响。
