Ho L P, Innes J A, Greening A P
Scottish Adult Cystic Fibrosis Service, Western General Hospital NHS Trust, Edinburgh, UK.
Thorax. 1998 Aug;53(8):680-4. doi: 10.1136/thx.53.8.680.
Nitric oxide (NO) is released by activated macrophages, neutrophils, and stimulated bronchial epithelial cells. Exhaled NO has been shown to be increased in patients with asthma and has been put forward as a marker of airways inflammation. However, we have found that exhaled NO is not raised in patients with cystic fibrosis, even during infective pulmonary exacerbation. One reason for this may be that excess airway secretions may prevent diffusion of gaseous NO into the airway lumen. We hypothesised that exhaled NO may not reflect total NO production in chronically suppurative airways and investigated nitrite as another marker of NO production.
Breath condensate nitrite concentration and exhaled NO levels were measured in 21 clinically stable patients with cystic fibrosis of mean age 26 years and mean FEV1 57% and 12 healthy normal volunteers of mean age 31 years. Breath condensate was collected with a validated method which excluded saliva and nasal air contamination and nitrite levels were measured using the Griess reaction. Exhaled NO was measured using a sensitive chemiluminescence analyser (LR2000) at an exhalation rate of 250 ml/s. Fourteen patients with cystic fibrosis had circulating plasma leucocyte levels and differential analysis performed on the day of breath collection.
Nitrite levels were significantly higher in patients with cystic fibrosis than in normal subjects (median 1.93 microM compared with 0.33 microM). This correlated positively with circulating plasma leucocytes and neutrophils (r = 0.6). In contrast, exhaled NO values were not significantly different from the normal range (median 3.8 ppb vs 4.4 ppb). There was no correlation between breath condensate nitrite and lung function and between breath condensate nitrite and exhaled NO.
Nitrite levels in breath condensate were raised in stable patients with cystic fibrosis in contrast to exhaled NO. This suggests that nitrite levels may be a more useful measure of NO production and possibly airways inflammation in suppurative airways and that exhaled NO may not reflect total NO production.
一氧化氮（NO）由活化的巨噬细胞、中性粒细胞及受刺激的支气管上皮细胞释放。已证实哮喘患者呼出的NO增加，且其被视为气道炎症的标志物。然而，我们发现囊性纤维化患者即使在肺部感染加重期呼出的NO也未升高。其原因之一可能是气道分泌物过多会阻碍气态NO扩散至气道管腔。我们推测呼出的NO可能无法反映慢性化脓性气道中NO的总生成量，并研究了亚硝酸盐作为NO生成的另一种标志物。
对21名平均年龄26岁、平均第一秒用力呼气容积（FEV1）为57%的临床稳定的囊性纤维化患者及12名平均年龄31岁的健康正常志愿者测量呼气冷凝液中的亚硝酸盐浓度和呼出的NO水平。采用一种经验证可排除唾液和鼻腔空气污染的方法收集呼气冷凝液，并使用格里斯反应测量亚硝酸盐水平。使用灵敏的化学发光分析仪（LR2000）以250 ml/s的呼气速率测量呼出的NO。14名囊性纤维化患者在收集呼气当天进行了循环血浆白细胞水平及分类分析。
囊性纤维化患者的亚硝酸盐水平显著高于正常受试者（中位数为1.93 μM，而正常受试者为0.33 μM）。这与循环血浆白细胞和中性粒细胞呈正相关（r = 0.6）。相比之下，呼出的NO值与正常范围无显著差异（中位数为3.8 ppb对4.4 ppb）。呼气冷凝液亚硝酸盐与肺功能之间以及呼气冷凝液亚硝酸盐与呼出的NO之间均无相关性。
与呼出的NO不同，临床稳定的囊性纤维化患者呼气冷凝液中的亚硝酸盐水平升高。这表明亚硝酸盐水平可能是化脓性气道中NO生成以及可能的气道炎症更有用的指标，且呼出的NO可能无法反映NO的总生成量。
