Measurement of exhaled nitric oxide by three different techniques.

The purpose of the study was to compare exhaled nitric oxide (NO) determined by three techniques. Ninety-one subjects performed a slow vital capacity maneuver: (1) through the mouth directly into a NO chemiluminescence analyzer (peak oral NO), (2) through the mouth into a collection bag (mean oral NO), and (3) through the nose into a collection bag (mean nasal NO). Peak oral NO was higher in patients with asthma (n = 18, 174.2 +/- 27.0 ppb), but lower in smokers (n = 36, 39.6 +/- 4.8 ppb) compared with nonsmoking control subjects (n = 23, 105.5 +/- 8.4 ppb, p < 0.05 both comparisons). Mean oral NO levels were significantly lower than peak oral NO levels (p < 0.05), but still higher in patients with asthma in comparison with nonsmoking healthy control subjects and asymptomatic smokers (27.2 +/- 3.5 versus 14.5 +/- 1.1 and 7.3 +/- 0.7 ppb, respectively, p < 0.05). In contrast, there was no significant difference in mean nasal NO levels between the three groups. Peak oral NO and mean oral NO levels correlated (r = 0.772, p < 0.0001). Determination of exhaled oral NO levels is qualitatively independent of the technique used, but nasal exhalation may affect NO determination in conditions associated with airway inflammation.

[1]  T. Higenbottam,et al.  Nature and site of action of endogenous nitric oxide in vasculature of isolated pig lungs. , 1997, Journal of applied physiology.

[2]  D. Yates,et al.  Acute and chronic effects of cigarette smoking on exhaled nitric oxide. , 1995, American journal of respiratory and critical care medicine.

[3]  T. Higenbottam,et al.  Exhaled nitric oxide in isolated pig lungs. , 1995, Journal of applied physiology.

[4]  R. Rossaint,et al.  Autoinhalation of nitric oxide after endogenous synthesis in nasopharynx , 1994, The Lancet.

[5]  J. Stamler,et al.  The biology of nitrogen oxides in the airways. , 1994, American journal of respiratory and critical care medicine.

[6]  P. J. Barnes,et al.  Increased nitric oxide in exhaled air of asthmatic patients , 1994, The Lancet.

[7]  O. Zetterström,et al.  Single-breath nitric oxide measurements in asthmatic patients and smokers , 1994, The Lancet.

[8]  P. Howarth,et al.  Induction of nitric oxide synthase in asthma , 1993, The Lancet.

[9]  J. Stamler,et al.  Biochemistry of nitric oxide and its redox-activated forms. , 1992, Science.

[10]  S Moncada,et al.  Endogenous nitric oxide is present in the exhaled air of rabbits, guinea pigs and humans. , 1991, Biochemical and biophysical research communications.

[11]  P. Barnes,et al.  New concepts in the pathogenesis of bronchial hyperresponsiveness and asthma. , 1989, The Journal of allergy and clinical immunology.

[12]  T. Higenbottam,et al.  A simultaneous single breath measurement of pulmonary diffusing capacity with nitric oxide and carbon monoxide. , 1989, The European respiratory journal.

[13]  L. Ignarro,et al.  Endothelium-derived relaxing factor produced and released from artery and vein is nitric oxide. , 1987, Proceedings of the National Academy of Sciences of the United States of America.

[14]  S. Moncada,et al.  Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor , 1987, Nature.