Markers of nitric oxide metabolism in sputum and exhaled air are not increased in chronic obstructive pulmonary disease

被引:94
作者
Rutgers, SR
van der Mark, TW
Coers, W
Moshage, H
Timens, W
Kauffman, HF
Koëter, GH
Postma, DS [1 ]
机构
[1] Univ Groningen Hosp, Dept Pulmonol, NL-9700 RB Groningen, Netherlands
[2] Univ Groningen Hosp, Dept Pathol, NL-9700 RB Groningen, Netherlands
[3] Univ Groningen Hosp, Dept Gastroenterol & Hepatol, NL-9700 RB Groningen, Netherlands
[4] Univ Groningen Hosp, Dept Allergol, NL-9700 RB Groningen, Netherlands
关键词
sputum; exhaled nitric oxide; smoking; chronic obstructive pulmonary disease;
D O I
10.1136/thx.54.7.576
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
Background-Nitric oxide (NO) is involved in inflammation and host defence of the lung. It has been found in increased concentrations in the airways in asthmatic subjects but its levels in patients with chronic obstructive pulmonary disease (COPD) have not been investigated. A study was undertaken to determine whether markers of NO metabolism (NO in exhaled air, iNOS expression in sputum cells, and nitrite + nitrate (NO2-/NO3-) in sputum supernatant) are increased in subjects with COPD, and whether they correlate with inflammatory indices in induced sputum. The associations of these markers with smoking were also assessed. Methods-Sixteen subjects with COPD (median age 66 years, median forced expiratory volume in one second (FEV,) 63% predicted, eight current smokers) and 16 healthy subjects (median age 63 years, median FEV1 113% predicted, eight current smokers) participated in the study. NO was measured during tidal breathing and sputum was induced by inhalation of hypertonic saline. Results-No differences were observed between subjects with COPD and healthy controls in exhaled NO excretion rate (median 5.15 and 6.25 nmol/min), sputum macrophage iNOS expression (14% and 12%), and sputum supernatant NO2-/NO3-, (46 and 73 mu M) NO in exhaled air correlated with the percentage of sputum eosinophils in patients with COPD (rho 0.65, p = 0.009) but not in healthy individuals. Exhaled NO and supernatant NO2-/NO3- levels were lower in healthy smokers than in healthy non/ex-smokers. Conclusions-Our findings indicate that NO metabolism is not increased in patients with stable COPD. The close association between exhaled NO levels and sputum eosinophils suggests a role for NO in airway inflammation in COPD. Studies performed during exacerbations may clarify this role.
引用
收藏
页码:576 / 580
页数:5
相关论文
共 20 条
  • [1] ALVING K, 1993, EUR RESPIR J, V6, P1368
  • [2] [Anonymous], 1987, AM REV RESPIR DIS, V136, P225
  • [3] THE NITRIC-OXIDE DONORS, AZIDE AND HYDROXYLAMINE, INHIBIT THE PROGRAMMED CELL-DEATH OF CYTOKINE-DEPRIVED HUMAN EOSINOPHILS
    BEAUVAIS, F
    MICHEL, L
    DUBERTRET, L
    [J]. FEBS LETTERS, 1995, 361 (2-3) : 229 - 232
  • [4] delPozo V, 1997, J IMMUNOL, V158, P859
  • [5] Inhibition of eosinophil chemotaxis by chronic blockade of nitric oxide biosynthesis
    Ferreira, HHA
    Medeiros, MV
    Lima, CSP
    Flores, CA
    Sannomiya, P
    Antunes, E
    DeNucci, G
    [J]. EUROPEAN JOURNAL OF PHARMACOLOGY, 1996, 310 (2-3) : 201 - 207
  • [6] THE BIOLOGY OF NITROGEN-OXIDES IN THE AIRWAYS
    GASTON, B
    DRAZEN, JM
    LOSCALZO, J
    STAMLER, JS
    [J]. AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1994, 149 (02) : 538 - 551
  • [7] INDUCTION OF NITRIC-OXIDE SYNTHASE IN ASTHMA
    HAMID, Q
    SPRINGALL, DR
    RIVEROSMORENO, V
    CHANEZ, P
    HOWARTH, P
    REDINGTON, A
    BOUSQUET, J
    GODARD, P
    HOLGATE, S
    POLAK, JM
    [J]. LANCET, 1993, 342 (8886-7) : 1510 - 1513
  • [9] REPRODUCIBILITY AND COMPARISON OF RESPONSES TO INHALED HISTAMINE AND METHACHOLINE
    JUNIPER, EF
    FRITH, PA
    DUNNETT, C
    COCKCROFT, DW
    HARGREAVE, FE
    [J]. THORAX, 1978, 33 (06) : 705 - 710
  • [10] Increased levels of nitric oxide derivatives in induced sputum in patients with asthma
    Kanazawa, H
    Shoji, S
    Yamada, M
    Fujii, T
    Kawaguchi, T
    Kudoh, S
    Hirata, K
    Yoshikawa, J
    [J]. JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 1997, 99 (05) : 624 - 629