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NO is released by activated macrophages, neutrophils and epithelial cells in vitro and is elevated in the exhaled breath of asthmatics. Exhaled NO has thus been put forward as a marker of airways inflammation. However, we have found that, in contrast to asthma, exhaled NO is not elevated in the inflammatory airways diseases of bronchiectasis and cystic fibrosis (CF)1. We, therefore, questioned if exhaled NO reflected an accurate measure of NO production in the airways, particularly in chronically suppurative airways. We explored this by measuring nitrite, a stable end product of NO oxidation in breath condensate as a surrogate marker of NO production. Methods: 1.5 mls of breath condensate were collected over 6 minutes with subjects exhaling from total lung capacity against a resistance created by 0.5 mm diameter Teflon tubing immersed in ice. Nitrite was assayed using the Griess reaction. 21 clinically stable CF patients (mean age 25.4 y; mean FEV1 53.9%) and 11 normal subjects (mean age 28.8) were studied. Nitrite levels in breath condensate were then compared to exhaled NO levels, measured using the chemiluminescence analyser (Logan Research), and FEV1. Results: We found nitrite levels in CF patients to be significantly higher than normal subjects - median: 1.93 μM v 0.33 μM, p<0.001 by Mann Whitney Rank sum test. In contrast their exhaled NO values were not significantly different from normals1. There was no correlation between nitrite levels and exhaled NO or nitrite and FEV1. (Graph Presented). Conclusion: These results suggest that exhaled NO may not reflect total NO production, particularly in chronically suppurative airways. Exhaled NO does not give an indication of the source of NO production,. Possibly, the majority of NO is produced by inflammatory cells rather than epithelial cells and reacts close to its site of production and therefore not detected as free gas in the breath.


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