Nasal Nitric Oxide Research

- Updated on November 10, 2021

Abnormal NO production and its availability are now associated with hypertension, heart failure, stroke, obesity, diabetes (both type I and II), atherosclerosis, rheumatism, aging, and dyslipidemias (particularly hypercholesterolemia and hypertriglyceridemia).

Heart patients, who often breathe through the mouth, may notice that their heart problems have a tendency to appear when do so. Apart from all CO2-related effects, they do not normally utilize own NO (nitric oxide) generated in the nasal passages. During the First World War it was noticed that people who worked with explosives had abnormally low blood pressure. Later, the chemical became one of the popular pills to reduce blood pressure, nitro-glycerine. The main effect of this chemical is to produce NO. Hence, if these patients close their mouth, their medication needs can be reduced.

Some relevant abstracts about nitric oxide and nasal breathing

T�rnberg DC, Marteus H, Schedin U, Alving K, Lundberg JO, Weitzberg E,

Nasal and oral contribution to inhaled and exhaled nitric oxide: a study in tracheotomized patients,

European Respiratory Journal. 2002 May; 19(5): p.859-864.

Dept of Anaesthesiology and Intensive Care, Karolinska Hospital, Stockholm, Sweden

Nitric oxide (NO) is produced at different sites in the human airways and may have several physiological effects. Orally-produced NO seems to contribute to the levels found in exhaled air. Autoinhalation of nasal NO increases oxygenation and reduces pulmonary artery pressure in humans. The aim of this study was to measure the concentration and output of NO during nasal, oral and tracheal controlled exhalation and inhalation. Ten tracheotomized patients and seven healthy subjects were studied. The mean+/-SEM fraction of exhaled NO from the nose, mouth and trachea was 56+/-8, 14+/-4 and 6+/-1 parts per billion (ppb), respectively. During single-breath nasal, oral and tracheal inhalation the fraction of inhaled NO was 64+/-14, 11+/-3 and 4+/-1, respectively. There was a marked flow dependency on nasal NO output in the healthy subjects, which was four-fold greater at the higher flow rates, during inhalation when compared to exhalation. There is a substantial contribution of nasal and oral nitric oxide during both inhalation and exhalation. Nasal nitric oxide output is markedly higher during inhalation, reaching levels similar to those that are found to have clinical effects in the trachea. These findings have implications for the measurement of nitric oxide in exhaled air and the physiological effects of autoinhaled endogenous nitric oxide.

Dillon WC, Hampl V, Shultz PJ, Rubins JB, Archer SL,

Origins of breath nitric oxide in humans,

Chest 1996 Oct; 110(4): p.930-938.

Department of Medicine, VA Medical Center, Minneapolis, MN, USA

STUDY OBJECTIVES: Nitric oxide (NO) exists in the human breath, but little is known about its site of origin or enzyme source. The aims of this 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 chemiluminescence assay, NO levels were measured in air exhaled from the nose, mouth, trachea, and distal airway. The susceptibility of breath NO to treatment with a topical corticosteroid (to inhibit iNOS; intranasal beclomethasone dipropionate for 2 weeks) and with antibiotics (systemic amoxicillin plus clavulanic acid and intranasal bacitracin zinc, 5 to 10 days) was also tested. PARTICIPANTS: Twenty-one healthy subjects, 9 intubated patients, and 7 patients undergoing bronchoscopy. All subjects were nonsmokers free of pneumonia, rhinitis, and bronchitis. MEASUREMENTS AND RESULTS: Breath NO levels, collected in the gas sampling bags, 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. Beclomethasone, but not antibiotics, decreased nasal NO levels without changing oral breath NO. CONCLUSIONS: Most NO in normal human breath derives locally from the nose where it can reach high levels during breath-holding. NO is synthesized, at least in part, by a steroid-inhibitable, nonbacterial, NO synthase, presumably iNOS.