Increased production of endogenous nitric oxide in patients with bronchial asthma and chronic obstructive pulmonary disease

Kanazawa, Hiroshi; Shoji, Seiichi; Yoshikawa, Takahiro; Hirata, Kazuto; Yoshikawa, Junichi

doi:10.1046/j.1365-2222.1998.00342.x

Cited by 42 publications

(23 citation statements)

References 22 publications

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“…In COPD, the measurement of exhaled eNO as a noninvasive marker of inflammation has previously been investigated [24][25][26][27][28][29]. In the present study, eNO levels were elevated in COPD and were not influenced by steroid treatment, in accordance with previously published data [24].…”

Section: Discussionsupporting

confidence: 82%

Slower rise of exhaled breath temperature in chronic obstructive pulmonary disease

Paredi¹,

Caramori²,

Cramer³

et al. 2003

Eur Respir J

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In chronic obstructive pulmonary disease (COPD) there is decreased vascularity of the bronchi and inflammation of the airways that may have opposite effects on the regulation of heat loss.Exhaled air temperature increase (DeuT) was measured in 23 patients with moderate COPD (18 male, mean age¡SEM 70¡1 yrs; forced expiratory volume in one second (FEV1) 45¡3%, FEV1/forced vital capacity 54¡4%) and 16 normal volunteers (64¡4 yr) and compared to exhaled nitric oxide (eNO) and inflammatory cells in induced sputum as a marker of airway inflammation. DeuT was measured during a flowand pressure-controlled single exhalation with a fast-response thermometer.DeuT was reduced in patients with COPD (1.86¡0.15 DuC?s -1 ) compared to normal subjects (4.00¡0.26 DuC?s -1 ). There was no difference in DeuT between patients treated with inhaled steroids and those who were steroid naïve. DeuT was correlated with eNO (r=0.60) but not with sputum neutrophilia. In COPD patients, DeuT was increased (2.26¡0.16 DuC?s -1 ) after the inhalation of 200 mg of albuterol, which is a known vasodilator, indicating that DeuT and bronchial blood flow may be correlated.Exhaled temperature increase is reduced in chronic obstructive pulmonary disease patients and is increased by the inhalation of vasodilators and therefore may be related to changes of bronchial blood flow and tissue remodelling.

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Section: Discussionsupporting

confidence: 82%

Slower rise of exhaled breath temperature in chronic obstructive pulmonary disease

Paredi¹,

Caramori²,

Cramer³

et al. 2003

Eur Respir J

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“…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].…”

Section: Introductionmentioning

confidence: 99%

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

Kunisaki

Rice

Janoff

et al. 2008

Ther Adv Respir Dis

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Background:A subset of patients with chronic obstructive pulmonary disease (COPD) may respond more favorably to inhaled corticosteroids (ICS), but no simple method is currently utilized to predict the presence or absence of ICS responses in patients with COPD. We evaluated the ability of exhaled nitric oxide (F E NO) and serum inflammatory markers (C-reactive protein [CRP], interleukin-6 [IL-6], and interleukin-8 ) to independently predict spirometric responses to ICS in patients with COPD. Methods: Among 60 ex-smokers with severe COPD (mean FEV 1 1.07 L, 36% of predicted), we conducted a single-arm, open-label study. Participants spent four weeks free of any ICS, followed by four weeks of ICS use (fluticasone propionate 500 mcg twice daily). F E NO, CRP, IL-6, IL-8, and pre-bronchodilator spirometry were measured immediately before and after the four weeks of ICS use. Results: Baseline F E NO, CRP, IL-6, and IL-8 showed no correlations to FEV 1 responses to ICS. ICS responders (increase in FEV 1 ≥ 200 mL after four weeks of ICS) did have significantly higher baseline F E NO levels compared with non-responders (46.5 parts per billion [ppb] vs. 25 ppb, p = 0.028). The receiver operating characteristic curve for F E NO to discriminate responders from non-responders had an area under curve of 0.72. Baseline serum inflammatory markers did not differ between responders and non-responders. Conclusion:In ex-smokers with severe COPD, a measure of local pulmonary inflammation, F E NO, may be more closely associated with FEV 1 responses to four weeks of ICS than are standard markers of systemic inflammation, serum CRP, IL-6, and IL-8 Keywords: Androstadienes / tu (therapeutic use), anti-inflammatory agents / tu (therapeutic use), breath tests, C-reactive protein, inflammation / bl (blood), interleukin-6 / bl (blood), interleukin-8 / bl (blood), nitric oxide / du (diagnostic use), pulmonary disease, chronic obstructive Abbreviations ATS = American Thoracic Society AUC = area under curve COPD = chronic obstructive pulmonary disease CRP = C-reactive protein F E NO = fraction of exhaled nitric oxide FEV 1 = forced expiratory volume in one second FVC = forced vital capacity ICS = inhaled corticosteroid IL-6 = interleukin-6 IL-8 = interluekin-8 IQR = interquartile range ppb = parts per billion

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“…Different effects were discussed as the result of the application of l -arginine, the supposed precursor of NO. After oral applications of l -arginine, Kanazawa and colleagues [16] found an increased NO production in healthy subjects and Kharitonow and associates [17] in asthmatic subjects. Sapienza and colleagues [6] detected higher, arginine dose± dependent NO concentrations in the breath of asthmatic subjects after the inhalation of unlabeled l -arginine, but no effects in healthy subjects.…”

Section: Discussionmentioning

confidence: 97%

“…According to literature data and our own investigations, asthmatic subjects produce more endogenous NO than healthy subjects as long as there is no external induction [6,13,16]. Different effects were discussed as the result of the application of l -arginine, the supposed precursor of NO.…”

Section: Discussionmentioning

confidence: 98%

[ 15 N 2 ]Arginine as a First Potential Inhaled Diagnostic Agent to Characterize Respiratory Diseases

Krumbiegel

Denk

Russow

et al. 2002

Experimental Lung Research

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Conventional diagnosis of the pulmonary tract uses physical methods such as spirometry and oscillometry. However, the inhalation of a chemical diagnostic agent ought to provide novel ways of more specific diagnosis, for instance of inflammatory states of the bronchial and lung mucosa. The stable isotope technique using a (15)N-labeled substrate appears to be a suitable tool for this application. In a pilot study, defined amounts of the amino acid L-[guanidino-(15)N(2)]arginine monohydrochloride (aqueous solution, 20 atom % (15)N) were inhaled as a diagnostic agent by healthy volunteers and pulmonary patients suffering from asthma bronchiale. The amino acid is resorbed and partly metabolized to (15)NO. The exhaled air was collected under defined conditions in 10-L breath bags and analyzed for NO using chemiluminescence. Under standardized test conditions, healthy persons (n = 6) exhaled 0.97 +/- 0.08 micromol NO/m(3) and asthmatic patients (n = 7) 1.17 +/- 0.14 micromol NO/m(3). A better distinction was expected comparing the (15)NO exhalation. The (15)N abundance of NO was determined using a Cryotrap gas chromatography - mass spectrometry set-up. Between 30 and 80 minutes after inhaling 700 mg [(15)N]arginine, a maximum with a plateau of the (15)NO abundance was found in the exhaled air. At this time, healthy and asthmatic subjects exhibited clear differences in their exhaled (15)NO amounts. Under standardized test conditions, the healthy persons (n = 6) exhaled 102.3 +/- 6.7 nmol (15)NO/m(3), whereas asthmatic patients (n = 7) exhaled only 76.1 +/- 10.9 nmol (15)NO/m(3). It is concluded that (15)NO yielded after the inhalation of (15)N-labeled arginine could be a potential marker for demonstrating pathophysiological changes in the lung epithelium. This method could pave a new diagnostic principle of "inhalative breath test."

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Increased production of endogenous nitric oxide in patients with bronchial asthma and chronic obstructive pulmonary disease

Abstract: We conclude the increased production of endogenous NO in patients with asthma and COPD, and that NO derivatives in induced sputum are more valuable than exhaled NO in assessing airway inflammation in patients with COPD.

Cited by 42 publications

References 22 publications

Slower rise of exhaled breath temperature in chronic obstructive pulmonary disease

Slower rise of exhaled breath temperature in chronic obstructive pulmonary disease

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

[ 15 N 2 ]Arginine as a First Potential Inhaled Diagnostic Agent to Characterize Respiratory Diseases

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