Ganas K, Loukides S, Papatheodorou G, Panagou P, Kalogeropoulos N
Thoracic Medicine Department, Athens Army General Hospital, Greece.
Respir Med. 2001 Aug;95(8):649-54. doi: 10.1053/rmed.2001.1117.
Production of nitric oxide (NO) is generally increased during inflammatory diseases including asthma. The eventual fate of NO is oxidation to nitrite (NO2) and nitrate (NO3), both of which are end-products of NO metabolism. Hydrogen Peroxide (H2O2) is increased in exhaled breath condensate of asthmatic subjects and may be used as a non-invasive marker of oxidative stress. NO has in some cases been shown to attenuate oxidant-induced lung injury. Total NO2/NO3 concentration and H2O2 levels were measured in expired breath condensate in 50 clinically stable asthmatics [all males, all atopics, mean age 22 (3) SD yrs, forced expiratory volume in 1 sec (FEV1) 91 (10)% predicted, PD20 to histamine 0.262 (0.16) mg 20 on inhaled steroids, 20 smokers, all steroid-naive] and in 10 normal, non-atopic subjects [all males, age 23 (4) yrs, FEV1 101 (14)% predicted, PD20 to histamine 1.3 (0.55) mg]. NO2/NO3 levels were significantly higher in patients with asthma than in normal subjects (1.08, 95% CI 0.86-1.3 microM vs. 0.6; 95% CI 0.46-0.8, P < 0.001). Patients who were on inhaled steroids had significantly ower values compared to steroid-naive (0.71, 95% CI 0.55-0.87 microM vs. 133, 95% CI 1-1.65 microM, P < 0.001). Similar results were observed between smokers and non-smokers (1.11, 95% CI 0.74-1.47 microM vs. 1.77, 95% CI 1.1-24 microM, P < 0.0001). There was a significant positive correlation between NO2/NO3 levels and H2O2 concentration in expired breath condensate (r = 0.48, P < 0.0001). No correlation was observed between NO2/NO3 levels, airway obstruction and bronchial hyper-reactivity as assessed by PD20 to histamine. Total NO2/NO3 levels in expired breath condensate are raised in patients with stable asthma and are significantly related to oxidative stress as assessed by H2O2 concentration. Measurement of expired breath NO2/NO3 and H2O2 levels may be clinically useful in the management of oxidation and inflammation mediated lung injury.
在包括哮喘在内的炎症性疾病中，一氧化氮（NO）的生成通常会增加。NO的最终归宿是氧化为亚硝酸盐（NO2）和硝酸盐（NO3），这两者都是NO代谢的终产物。过氧化氢（H2O2）在哮喘患者呼出气冷凝物中增加，可作为氧化应激的非侵入性标志物。在某些情况下，NO已被证明可减轻氧化剂诱导的肺损伤。对50例临床稳定的哮喘患者[均为男性，均为特应性体质，平均年龄22（3）标准差岁，第1秒用力呼气量（FEV1）为预测值的91（10）%，吸入糖皮质激素时组胺激发试验的PD20为0.262（0.16）mg，20例吸烟者，均未使用过糖皮质激素]和10例正常非特应性受试者[均为男性，年龄23（4）岁，FEV1为预测值的101（14）%，组胺激发试验的PD20为1.3（0.55）mg]的呼出气冷凝物中的NO2/NO3总量和H2O2水平进行了测量。哮喘患者的NO2/NO3水平显著高于正常受试者（1.08，95%可信区间0.86 - 1.3微摩尔/升对0.6；95%可信区间0.46 - 0.8，P < 0.001）。与未使用糖皮质激素的患者相比，使用吸入糖皮质激素的患者的值显著更低（0.71，95%可信区间0.55 - 0.87微摩尔/升对1.33，95%可信区间1 - 1.65微摩尔/升，P < 0.001）。吸烟者和非吸烟者之间观察到类似结果（1.11，95%可信区间0.74 - 1.47微摩尔/升对1.77，95%可信区间1.1 - 2.4微摩尔/升，P < 0.0001）。呼出气冷凝物中NO2/NO3水平与H2O2浓度之间存在显著正相关（r = 0.48，P < 0.0001）。通过组胺激发试验的PD20评估，未观察到NO2/NO3水平、气道阻塞和支气管高反应性之间的相关性。稳定期哮喘患者呼出气冷凝物中的NO2/NO3总量升高，且与通过H2O2浓度评估的氧化应激显著相关。测量呼出气中的NO2/NO3和H2O2水平在氧化和炎症介导的肺损伤管理中可能具有临床应用价值。
