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1 Dept of Physiology and Pharmacology, Karolinska Institutet, Stockholm, 2 Dept of Woman and Child Health, Uppsala University Hospital, Uppsala and 3 Dept of Medicine, Karolinska Hospital, Stockholm, Sweden
CORRESPONDENCE: W. Zetterquist, Dept of Physiology and Pharmacology, Karolinska Institutet, SE-171, 77 Stockholm, Sweden. Fax: 46 8332278. E-mail: wilhelm.zetterquist@fyfa.ki.se
Keywords: allergic rhinitis, asthma, carbon monoxide, cystic fibrosis, exhaled air, nitric oxide
Received: May 15, 2001
Accepted February 3, 2002
This study was supported by The Swedish Research Council (grant no. 10354), The Swedish Heart and Lung Foundation, The Swedish Foundation for Health Care Science and Allergy Research, and The Swedish Asthma and Allergy Association's Research Foundation.
Increased levels of exhaled carbon monoxide (fractional concentration of CO in expired gas (FE,CO)), measured with an electrochemical sensor, have been reported in patients with inflammatory airway disorders, such as asthma, rhinitis and cystic fibrosis. This study aimed to evaluate these findings by using a fast-response nondisperse infrared (NDIR) analyser, and to compare these measurements with the fractional concentration of nitric oxide in exhaled air (FE,NO).
Thirty-two steroid-naïve asthmatics, 24 steroid-treated asthmatics (16 patients with allergic rhinitis, nine patients with cystic fibrosis), and 30 nonsmoking healthy controls were included. CO measurements with the NDIR analyser were performed simultaneously with nitric oxide (NO) analysis (chemiluminescence technique). After 15 s of breath-hold, single-breath exhalations over 10 s were performed at two flow rates and end-tidal plateau concentrations were registered. An electrochemical CO sensor was used independently with an exhalation to residual volume, after a 15 s breath-hold.
None of the two CO analysers gave a significant increase in FE,CO in the groups of patients with inflammatory airway disorders compared to controls. FE,NO was significantly elevated in steroid-naïve asthmatics and subjects with allergic rhinitis, but not in steroid-treated asthmatics and subjects with cystic fibrosis. Reducing exhalation flow rate by 50% gave a two-fold increase in FE,NO, while FE,CO was unaffected. A significant increase was seen in FE,CO, but not in FE,NO, when comparing with and without a 10 s breath-hold.
In conclusion, the fractional concentration of carbon monoxide in expired gas was not increased in any of the patient groups, while the fractional concentration of nitric oxide in expired gas was significantly elevated in patients with steroid-naïve asthma and allergic rhinitis. Moreover, carbon monoxide was unaffected by flow rate but increased with breath-hold, suggesting an origin in the alveoli rather than the conducting airways.
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