Increased exhaled nitric oxide in patients with stable chronic obstructive pulmonary disease

Abstract

Background-Nitric oxide (NO) plays an important role as an inflammatory mediator in the airways. Since chronic obstructive pulmonary disease (COPD) is characterised by airway inflammation, a study was undertaken to determine NO levels in the exhaled air of patients with COPD. Methods-Two groups of patients with clinically stable COPD were studied, 10 current smokers and 10 ex-smokers. Two control groups of healthy subjects consisting of 10 current smokers and 20 nonsmokers were also studied. Exhaled NO levels were measured by the collection bag technique and NO chemiluminescence analyser. Results-Mean (SE) levels of exhaled NO in ex-smokers and current smokers with COPD (25.7 (3.0) ppb and 10.2 (1.4) ppb, respectively) were significantly higher than in non-smoker and current smoker control subjects (9.4 (0.8) ppb and 4.6 (0.4) ppb, respectively). In current smokers with COPD exhaled levels of NO were significantly lower than in ex-smokers. In this latter group of patients there was a significant negative correlation between smoking history (pack years) and levels of exhaled NO (r = -0.8, p = 0.002). A positive correlation was seen between forced expiratory volume in one second (FEV 1 ) and levels of exhaled NO (r = 0.65, p = 0.001) in patients with COPD. Conclusions-These data show that exhaled NO is increased in patients with stable COPD, both current and exsmokers, compared with healthy control subjects.

Smoking is associated with an age-related decline in exhaled nitric oxide

“…Consistent with prior studies [1][2][3][4][5][6][7][8], it was found that FeNO levels were significantly lower in smokers compared with nonsmokers (geometric mean¡SD): 13.9¡18.0 ppb versus 20.5¡21.3 ppb (p,0.0001); difference56.6 ppb (confidence interval (CI) 4.1-9.2). As shown in figure 2, there was an association of FeNO levels with serum cotinine levels in smokers; serum cotinine levels were inversely correlated with FeNO levels in smokers (r 2 50.13; p50.0003), suggesting that lower FeNO levels were associated with increased levels of tobacco smoke exposure.…”

“…However, given the significant association of cigarette smoking with lower FeNO levels [1][2][3][4][5][6][7][8], ATS questionnaire data on smoking [34] were collected and serum cotinine levels were measured [36,37] as a way to rigorously exclude smoking as a potential confounder of FeNO levels. To confirm the validity of using serum cotinine levels as a surrogate marker of cigarette smoking, cotinine levels were compared in subjects who selfreported cigarette smoking on the ATS questionnaire with subjects that did not report smoking.…”

“…FeNO levels are lower in otherwise healthy subjects who habitually smoke tobacco compared with nonsmokers [1][2][3][4][5][6][7][8], and FeNO levels decrease in nonsmokers and smokers acutely after smoking a cigarette and after passive smoke exposure [1,5,9]. There is an inverse relationship between the number of cigarettes smoked per day and FeNO levels [1].…”

Airway function, oedema, cell infiltration and nitric oxide generation in conscious ozone‐exposed guinea‐pigs: effects of dexamethasone and rolipram

“…Exposure of asthmatic subjects to antigen (Alving et al, 1993) and exacerbations in individuals with COPD (Bhowmik et al, 1998;Corradi et al, 1999) are associated with increases in levels of exhaled nitric oxide (NO). Derived from the nitric oxide synthase (NOS) conversion of L-arginine to L-citrulline, a basal level of the free radical, NO, maintains bronchodilatory airway tone, suppresses leukocyte activation and inhibits microvascular leakage (Barnes et al, 1999;Colasanti & Suzuki, 2000).…”

Exhaled nitric oxide, systemic inflammation, and the spirometric response to inhaled fluticasone propionate in severe chronic obstructive pulmonary disease: A prospective study

“…When compared to persons without COPD, patients with COPD have increased numbers of inflammatory cells in bronchoalveolar lavage and lung biopsy samples [Baraldo et al 2004;Hogg et al 2004;Turato et al 2002], elevated cytokine levels in induced sputum [Vernooy et al 2002;Keatings et al 1996], and elevated fractions of nitric oxide (F E NO) in exhaled breath [Montuschi et al 2001;Corradi et al 1999;Kanazawa et al 1998;Maziak et al 1998]. Many patients with COPD also show evidence of systemic inflammation, as evidenced by elevated serum levels of proinflammatory cytokines and C-reactive protein (CRP) [Mannino et al 2003;Dentener et al 2001;Eid et al 2001;Mendall et al 2000;Takabatake et al 2000;Schols et al 1996].…”