Grasemann H, Ioannidis I, Tomkiewicz R P, de Groot H, Rubin B K, Ratjen F
Department of Paediatrics, University of Essen, Germany.
Arch Dis Child. 1998 Jan;78(1):49-53. doi: 10.1136/adc.78.1.49.
Although the activity of nitric oxide (NO) synthases are increased in lung tissue of patients with cystic fibrosis, the concentrations of nasal and exhaled NO have recently been found to be decreased in cystic fibrosis. This could either be due to reduced NO formation or metabolism of NO within airway fluids. In this study, the stable NO metabolites, nitrate and nitrite, were determined in the saliva and sputum of 18 stable cystic fibrosis patients, 21 cystic fibrosis patients during a pulmonary exacerbation, and in saliva and endotracheal secretions of normal controls. Median saliva concentrations of NO metabolites (nitrate plus nitrite) were 704 mumol/l (95% confidence interval (CI) 419 to 1477) in stable cystic fibrosis patients, 629 mumol/l (95% CI 382 to 1392) in cystic fibrosis patients presenting with pulmonary exacerbation, and 313 mumol/l (95% CI 312 to 454) in controls. Median sputum NO metabolite concentration in stable cystic fibrosis was 346 mumol/l (95% CI 311 to 504). This was not significantly different from cystic fibrosis patients presenting with pulmonary exacerbation (median 184 mumol/l, 95% CI 249 to 572), but significantly higher than in endotracheal secretions of controls (median 144 mumol/l, 95% CI 96 to 260). Sputum NO metabolite concentration in cystic fibrosis pulmonary exacerbation significantly increased during antibiotic treatment. A positive correlation was observed between sputum NO metabolites and lung function in stable cystic fibrosis, suggesting less airway NO formation in cystic fibrosis patients with more severe lung disease. These data indicate that decreased exhaled NO concentrations in cystic fibrosis patients may be due to retention and metabolism of NO within the airway secretions. However, sputum NO metabolites are not a useful marker of airway inflammation in cystic fibrosis lung disease.
尽管囊性纤维化患者肺组织中一氧化氮(NO)合酶的活性增加,但最近发现囊性纤维化患者鼻腔和呼出的NO浓度降低。这可能是由于气道液体内NO生成减少或NO代谢所致。在本研究中,测定了18例稳定期囊性纤维化患者、21例肺部加重期囊性纤维化患者的唾液和痰液以及正常对照者的唾液和气管内分泌物中稳定的NO代谢产物硝酸盐和亚硝酸盐。稳定期囊性纤维化患者唾液中NO代谢产物(硝酸盐加亚硝酸盐)的中位数浓度为704μmol/l(95%置信区间(CI)419至1477),肺部加重期囊性纤维化患者为629μmol/l(95%CI 382至1392),对照组为313μmol/l(95%CI 312至454)。稳定期囊性纤维化患者痰液中NO代谢产物的中位数浓度为346μmol/l(95%CI 311至504)。这与肺部加重期囊性纤维化患者无显著差异(中位数184μmol/l,95%CI 249至572),但显著高于对照组气管内分泌物中的浓度(中位数144μmol/l,95%CI 96至260)。囊性纤维化肺部加重期患者在抗生素治疗期间痰液中NO代谢产物浓度显著增加。在稳定期囊性纤维化患者中,观察到痰液中NO代谢产物与肺功能呈正相关,提示肺部疾病较严重的囊性纤维化患者气道内NO生成较少。这些数据表明囊性纤维化患者呼出的NO浓度降低可能是由于气道分泌物中NO的潴留和代谢所致。然而,痰液中NO代谢产物并非囊性纤维化肺病气道炎症的有用标志物。