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a Department of
Pulmonology, b Department of
Pathology, c Department of Gastroenterology and Hepatology, d Department
of Allergology, e University
Hospital, 9700 RB Groningen, The Netherlands
Correspondence to: Dr D S Postma.
Received 16 July 1998; Returned to authors 28 October 1998; Revised version received 18 January 1999; Accepted for publication 4 February 1999
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 (FEV1) 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 µM). 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.
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