ORIGINS OF BREATH NITRIC-OXIDE IN HUMANS

Study objectives: Nitric oxide (NO) exists in the human breath, but li ttle is known about its site of origin or enzyme source. The aims of t his study were to locate the main site of NO release into human breath and to decide whether the inducible isoform of NO synthase (iNOS) and nasal bacteria contribute to breath NO. Design: Using a chemiluminesc ence assay, NO levels were measured in air exhaled from the nose, mout h, trachea, and distal airway. The susceptibility of breath NO to trea tment with a topical corticosteroid (to inhibit iNOS; intranasal beclo methasone dipropionate for 2 weeks) and with antibiotics (systemic amo xicillin plus clavulanic acid and intranasal bacitracin zinc, 5 to 10 days) was also tested. Participants: Twenty-one healthy subjects, 9 in tubated patients, and 7 patients undergoing bronchoscopy. All subjects were nonsmokers free of pneumonia, rhinitis, and bronchitis. Measurem ents and results: Breath NO levels, collected. in the gas sampling bag s, were greater (p<0.05) in the nose (25+/-2 parts per billion [ppb]) than in the mouth (6+/-1 ppb), trachea (3+/-1 ppb), or distal airway ( 1+/-2 ppb), Similar results were obtained when NO was sampled directly by cannula from nose or mouth during resting breathing, Nasal breath NO signal increased sharply during 30 s of breath-holding. Beclomethas one, but not antibiotics, decreased nasal NO levels without changing o ral breath NO. Conclusions: Most NO in normal human breath derives loc ally from the nose where it can reach high levels during breath-holdin g. NO is synthesized, at least in part, by a steroid-inhibitable, nonb acterial, NO synthase, presumably iNOS.