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• W2022802282 abstract "The endogenous vasodilator nitric oxide (NO) is synthesized enzymatically from the amino acid L-arginine by three isoforms of NO synthase (NOS). Two are expressed constuitively in neuronal (nNOS) and in endothelial cells (eNOS), but the expression of the third is induced (iNOS) by cytokines and inflammatory mediators in macrophages and other nucleated mammalian cells, including vascular smooth muscle and hepatocytes. It is now clear that NO is a constituent of normal exhaled human breath,1Borland C Cox Y Higgenbottam T. Measurement of exhaled nitric oxide in man.Thorax. 1993; 48: 1160-1162Crossref PubMed Scopus (140) Google Scholar,2Gustafsson LE Leone AM Persson MG et al.Endogenous nitric oxide is present in exhaled air of rabbits, guinea-pigs and humans.Biochem Biophys Res Commun. 1991; 181: 852-857Crossref PubMed Scopus (819) Google Scholar but the biologic significance of this phenomenon remains unclear. Thus, although the modulation of pulmonary3Liu SF Crawley DG Barnes PJ et al.Endothelium-derived relaxant factor modulates hypoxic pulmonary vasoconstriction in isolated blood-perfused rat lungs.Am Rev Respir Dis. 1991; 143: 32-37Crossref PubMed Scopus (154) Google Scholar and systemic4Stammler JS Loh E Roddy M et al.Nitric oxide regulates broad systemic and pulmonary vascular resistance in normal humans.Circulation. 1994; 89: 2035-2040Crossref Scopus (477) Google Scholar tone may depend in part upon eNOS under physiologic circumstances, and be modulated by iNOS expression during conditions such as systemic sepsis,5Liu SF Adcock IM Old RW et al.Lipoplysaccharide treatment in vivo induces widespread tissue expression of inducible nitric oxide synthase mRNA.Biochem Biophys Res Commun. 1993; 196: 1208-1213Crossref PubMed Scopus (266) Google Scholar,6Petros A Bennett D Vallance P. Effects of nitric oxide synthase inhibitors on hypotension in patients with septic shock.Lancet. 1991; 338: 1557-1558Abstract PubMed Scopus (758) Google Scholar how such activity relates to variations in expired NO concentration is uncertain. Moreover, whether the quantification of exhaled NO is likely to prove clinically useful depends in part upon the origin of the gas. Details of a variety of experiments designed to locate the source of exhaled NO have now been published,7Gerlach H Roissant R Pappert D et al.Autoinhalation of nitric oxide after endogenous synthesis in nasopharynx.Lancet. 1994; 343: 518-519Abstract PubMed Scopus (238) Google Scholar, 8Lundberg JON Weitzburg E Nordvall SL et al.Primarily nasal origin of exhaled nitric oxide and absence in Kartgagener's syndrome.Eur Respir J. 1994; 7: 1501-1504Crossref PubMed Scopus (363) Google Scholar, 9Lundberg JON Farkas-Szallasi T Wetzberg E et al.High nitric oxide production in human paranasal sinuses.Nat Med. 1995; 1: 370-373Crossref PubMed Scopus (545) Google Scholar, 10Schedin U Frostell C Persson MG et al.Contribution from upper and lower airways to exhaled endogenous nitric oxide in humans.Acta Anaesthesiol Scand. 1995; 39: 327-332Crossref PubMed Scopus (115) Google Scholar and a picture is beginning to emerge. The article by Dillon and colleagues published in this issue of CHEST (see page 930) represents a significant addition to this literature. The investigation was designed to locate the sites of NO formation in the respiratory system, and to assess the contributions of iNOS and respiratory tract bacterial flora to its production. Exhaled gas was sampled from a variety of sites in the respiratory system using chemiluminescence. Many workers have expressed concern regarding the accuracy of such measurements of airway-derived NO; to this end, Dillon and colleagues included a conscientious validation of methods in their investigation. Topical steroids and systemic antibiotics were employed to influence iNOS formation and the contribution of bacterial-derived NO respectively. The results support the hypothesis that iNOS is at least partially responsible for the production of exhaled NO. Furthermore, the data are in accord with other published works showing that while NO is undoubtedly present in the lower respiratory tract, most of the exhaled gas originates from the nasal or paranasal structures.7Gerlach H Roissant R Pappert D et al.Autoinhalation of nitric oxide after endogenous synthesis in nasopharynx.Lancet. 1994; 343: 518-519Abstract PubMed Scopus (238) Google Scholar, 8Lundberg JON Weitzburg E Nordvall SL et al.Primarily nasal origin of exhaled nitric oxide and absence in Kartgagener's syndrome.Eur Respir J. 1994; 7: 1501-1504Crossref PubMed Scopus (363) Google Scholar, 9Lundberg JON Farkas-Szallasi T Wetzberg E et al.High nitric oxide production in human paranasal sinuses.Nat Med. 1995; 1: 370-373Crossref PubMed Scopus (545) Google Scholar, 10Schedin U Frostell C Persson MG et al.Contribution from upper and lower airways to exhaled endogenous nitric oxide in humans.Acta Anaesthesiol Scand. 1995; 39: 327-332Crossref PubMed Scopus (115) Google Scholar Some reservations should be expressed regarding this generally excellent study. First, the lack of a detectable effect of antibiotic therapy on exhaled NO concentrations may reflect incomplete sterilization of the upper respiratory tract. Second, it should be possible to employ selective pharmacologic agents administered by inhalation to block NOS activity in a more specific fashion than can be achieved by using antibiotics alone, thereby teasing out the potential contributions of constitutive and inducible forms of NOS to NO production.11Griffiths MJD Messent M MacAllister RJ et al.Aminoguanidine selectively inhibits inducible nitric oxide synthase.Br J Pharmacol. 1993; 110: 963-968Crossref PubMed Scopus (388) Google Scholar,12Yates DH Kharatanov SA Worsdell M et al.Exhaled nitric oxide is decreased after inhalation of a specific inhibitor of inducible nitric oxide synthase, in asthmatics but not in normal subjects.Am J Respir Crit Care Med. 1995; : 15LA699Google Scholar Despite these limitations, such data suggest that iNOS localized to epithelial cells is an important source of airway NO, both constitutively and in conditions of bronchial inflammation,13Robbins RA Springall DR Warren JB et al.Inducible nitric oxide synthase is increased in murine lung epithelial cells by cytokine stimulation.Biochem Biophys Res Commun. 1994; 198: 1027-1033Crossref PubMed Scopus (172) Google Scholar,14Guo FH DeRaeve HR Rice TW et al.Continuous nitric oxide synthesis in normal human airway epithelium in vivo..Proc Natl Acad Sci USA. 1995; 92: 7809-7813Crossref PubMed Scopus (449) Google Scholar although whether it plays a part in modulating airway physiology, or merely represents a by-product of neurotransmission or bronchial vascular control mechanisms is unknown. Alternatively, NO inspired from such sources may be important as an endogenous inhaled vasodilator modulating pulmonary ventilation/perfusion matching. NO may be important in a host defense. The high levels apparently produced by the nasal sinuses are some three orders of magnitude greater than the concentrations estimated to be detectable in the distal airways. At these levels NO has bacteriostatic15Mancinelli RL McKay CP. Effects of nitric oxide and nitrogen dioxide on bacterial growth.Appl Environ Microbiol. 1983; 46: 198-202Crossref PubMed Google Scholar and antiviral16Croen KD. Evidence for an antiviral effect of nitric oxide.J Clin Invest. 1993; 91: 2446-2452Crossref PubMed Scopus (433) Google Scholar properties, which may explain the fact that the sinuses are normally sterile. NO also alters ciliary beat frequency.17Jain B Rubenstein I Robbins RA et al.Modulation of airway epithelial cell ciliary beat frequency by nitric oxide.Biochem Biophys Res Commun. 1993; 191: 83-88Crossref PubMed Scopus (336) Google Scholar Patients with immotile cilia syndrome/primary ciliary dyskinesia8Lundberg JON Weitzburg E Nordvall SL et al.Primarily nasal origin of exhaled nitric oxide and absence in Kartgagener's syndrome.Eur Respir J. 1994; 7: 1501-1504Crossref PubMed Scopus (363) Google Scholar have very low levels of nasal NO and are prone to chronic sinusitis. The induction of iNOS in inflammatory states is now established, and elevated levels of exhaled NO have been reported previously in asthmatics.18Alving K Weitzberg E Lundberg JM. Increased amount of nitric oxide in exhaled air of asthmatics.Eur Respir J. 1993; 6: 1368-1370Crossref PubMed Google Scholar,19Kharatanov SA Yates D Robbins RA et al.Increased nitric oxide in exhaled air of asthmatic patients.Lancet. 1994; 343: 133-135Abstract Scopus (1318) Google Scholar These levels then fall following the administration of inhaled corticosteroid therapy.20Kharatanov SA Yates DH Barnes PJ. Inhaled glucocorticoids decrease nitric oxide in exhaled air of asthmatic patients.Am J Respir Crit Care Med. 1996; 153: 454-457Crossref Scopus (527) Google Scholar The iNOS mRNA expression is transcriptionally regulated and has been shown to be suppressed by steroid administration.5Liu SF Adcock IM Old RW et al.Lipoplysaccharide treatment in vivo induces widespread tissue expression of inducible nitric oxide synthase mRNA.Biochem Biophys Res Commun. 1993; 196: 1208-1213Crossref PubMed Scopus (266) Google Scholar In this sense, if the measurement of exhaled NO proves to be practical in the clinical setting, it may represent a useful tool in monitoring the response to therapy of patients with inflammatory airway diseases. Unfortunately, the measurement of endogenous airway NO that is most reproducible and representative of disease activity is uncertain. NO concentrations in nasal air, peak or plateau expired NO concentrations, and end-tidal NO concentrations may provide differing and even conflicting information about the same pathologic process or coexisting disease states such as asthma and airway infection. The work of Dillon and colleagues represents an important advance in our understanding of the clinical significance of measurements of exhaled NO concentrations. Much work remains to be done before a new and exciting means of monitoring airway disease activity can be announced.21Barnes PJ Kharatanov SA. Exhaled nitric oxide: a new lung function test.Thorax. 1996; 51: 233-237Crossref PubMed Scopus (218) Google Scholar" @default.
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