Central and peripheral airway nitric oxide in patients with stable and exacerbated chronic obstructive pulmonary disease

Zsófia Lázár, Agnes Kelemen, Gabriella Gálffy, G. Losonczy, I. Horváth, András Bikov

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2 Citations (Scopus)

Abstract

Nitrative stress pathways are involved in airway inflammation characterizing chronic obstructive pulmonary disease (COPD). Extended nitric oxide (NO) analysis allows the partitioned measurement of nitrative stress in the conducting bronchi and peripheral airways/alveolar spaces. However, pulmonary NO production at these two sites has not been systemically studied in stable and exacerbated COPD. Twenty-eight patients with stable COPD, 34 patients during an exacerbation, and 15 smoking controls were recruited. Exhaled NO was measured at constant flow rates of 50 ml s-1 (for FENO50) and 100-150-200-250 ml s-1 (for the extended NO analysis). Clinical variables, including lung function, white blood cell count, C-reactive protein concentration, blood gas values and symptom score (COPD assessment test) were collected. The measurements were repeated in 26 patients with an exacerbation during convalescence. The exhaled NO parameters were analysed with non-parametric tests. The alveolar NO (CANO) was higher in stable COPD (median (interquartile range), 4.24 (2.35-6.09) ppb, p < 0.01) and in patients with an exacerbation (3.83 (2.31-6.62) ppb, p < 0.05) than in the controls (2.05 (1.77-2.80) ppb), but no difference was found between the stable and exacerbated disease (p > 0.05). The CANO correlated with the blood eosinophil percentage in all COPD patients (r = 0.29, p = 0.02). The total flux of bronchial NO (JawNO) increased in an exacerbation (exacerbated: 1.01 (0.45-2.44) nl s-1 versus stable: 0.47 (0.16-0.81) nl s-1, p < 0.01; exacerbated versus control: 0.38 (0.27-0.80) nl s-1, p < 0.05), and it was reduced in convalescence after therapy (0.50 (0.31-0.96) nl s-1, p = 0.01). Neither CANO and JawNO or their change were related to the clinical variables or the length of hospital stay in COPD. JawNO-correlated with FENO50 during exacerbation (r = 0.80, p < 0.001). Extended NO analysis is a feasible method to monitor nitrative stress at different anatomical sites within the airways in stable and exacerbated COPD patients. Our results suggest that nitrative stress is constantly elevated in the small airways in COPD and increases in the conducting airways during an exacerbation.

Original languageEnglish
Article number036017
JournalJournal of Breath Research
Volume12
Issue number3
DOIs
Publication statusPublished - May 28 2018

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Chronic Obstructive Pulmonary Disease
Nitric Oxide
Length of Stay
Lung
Bronchi
Leukocyte Count
Eosinophils
C-Reactive Protein
Gases
Smoking
Inflammation

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Central and peripheral airway nitric oxide in patients with stable and exacerbated chronic obstructive pulmonary disease. / Lázár, Zsófia; Kelemen, Agnes; Gálffy, Gabriella; Losonczy, G.; Horváth, I.; Bikov, András.

In: Journal of Breath Research, Vol. 12, No. 3, 036017, 28.05.2018.

Research output: Contribution to journalArticle

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abstract = "Nitrative stress pathways are involved in airway inflammation characterizing chronic obstructive pulmonary disease (COPD). Extended nitric oxide (NO) analysis allows the partitioned measurement of nitrative stress in the conducting bronchi and peripheral airways/alveolar spaces. However, pulmonary NO production at these two sites has not been systemically studied in stable and exacerbated COPD. Twenty-eight patients with stable COPD, 34 patients during an exacerbation, and 15 smoking controls were recruited. Exhaled NO was measured at constant flow rates of 50 ml s-1 (for FENO50) and 100-150-200-250 ml s-1 (for the extended NO analysis). Clinical variables, including lung function, white blood cell count, C-reactive protein concentration, blood gas values and symptom score (COPD assessment test) were collected. The measurements were repeated in 26 patients with an exacerbation during convalescence. The exhaled NO parameters were analysed with non-parametric tests. The alveolar NO (CANO) was higher in stable COPD (median (interquartile range), 4.24 (2.35-6.09) ppb, p < 0.01) and in patients with an exacerbation (3.83 (2.31-6.62) ppb, p < 0.05) than in the controls (2.05 (1.77-2.80) ppb), but no difference was found between the stable and exacerbated disease (p > 0.05). The CANO correlated with the blood eosinophil percentage in all COPD patients (r = 0.29, p = 0.02). The total flux of bronchial NO (JawNO) increased in an exacerbation (exacerbated: 1.01 (0.45-2.44) nl s-1 versus stable: 0.47 (0.16-0.81) nl s-1, p < 0.01; exacerbated versus control: 0.38 (0.27-0.80) nl s-1, p < 0.05), and it was reduced in convalescence after therapy (0.50 (0.31-0.96) nl s-1, p = 0.01). Neither CANO and JawNO or their change were related to the clinical variables or the length of hospital stay in COPD. JawNO-correlated with FENO50 during exacerbation (r = 0.80, p < 0.001). Extended NO analysis is a feasible method to monitor nitrative stress at different anatomical sites within the airways in stable and exacerbated COPD patients. Our results suggest that nitrative stress is constantly elevated in the small airways in COPD and increases in the conducting airways during an exacerbation.",
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AU - Gálffy, Gabriella

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AU - Horváth, I.

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