2010/03/31 by Julian King, Karl Unterkofler, Gerald Teschl +4 · 3 citations
Biochemistry, Genetics and Molecular Biology · Engineering · Medicine · #Advanced Chemical Sensor Technologies #Cardiovascular and exercise physiology #Obstructive Sleep Apnea Research #msc:92C35 #msc:92C45 #msc:93B07 #msc:93C10 #q-bio.QM
paper · pdf · doi:10.1007/s00285-010-0398-9
published as J. Math. Biol. 63, 959-999 (2011) · 38 pages
openalex publication_date 2011/01/13 · crossref created 2011/01/13 · crossref issued 2011/01/14 · crossref published 2011/01/14 · crossref published-online 2011/01/14 · arxiv created 2011/01/27 · crossref published-print 2011/11/01 · arxiv updated 2015/03/13 · openalex created_date 2016/06/24 · crossref deposited 2020/06/15 · crossref indexed 2026/05/09 · openalex updated_date 2026/07/28
Recommended standardized procedures for determining exhaled lower respiratory nitric oxide and nasal nitric oxide have been developed by task forces of the European Respiratory Society and the American Thoracic Society. These recommendations have paved the way for the measurement of nitric oxide to become a diagnostic tool for specific clinical applications. It would be desirable to develop similar guidelines for the sampling of other trace gases in exhaled breath, especially volatile organic compounds (VOCs) which reflect ongoing metabolism. The concentrations of water-soluble, blood-borne substances in exhaled breath are influenced by: (i) breathing patterns affecting gas exchange in the conducting airways; (ii) the concentrations in the tracheo-bronchial lining fluid; (iii) the alveolar and systemic concentrations of the compound. The classical Farhi equation takes only the alveolar concentrations into account. Real-time measurements of acetone in end-tidal breath under an ergometer challenge show characteristics which cannot be explained within the Farhi setting. Here we develop a compartment model that reliably captures these profiles and is capable of relating breath to the systemic concentrations of acetone. By comparison with experimental data it is inferred that the major part of variability in breath acetone concentrations (e.g., in response to moderate exercise or altered breathing patterns) can be attributed to airway gas exchange, with minimal changes of the underlying blood and tissue concentrations. Moreover, it is deduced that measured end-tidal breath concentrations of acetone determined during resting conditions and free breathing will be rather poor indicators for endogenous levels. Particularly, the current formulation includes the classical Farhi and the Scheid series inhomogeneity model as special limiting cases.