Nasal Nitric Oxide Research
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
Some relevant abstracts about nitric oxide and nasal breathing
Törnberg DC, Marteus H, Schedin U, Alving K, Lundberg JO, Weitzberg E,
Nasal and oral contribution to inhaled and exhaled nitric oxide: a study in
European Respiratory Journal. 2002 May; 19(5): p.859-864.
Dept of Anaesthesiology and Intensive Care, Karolinska Hospital, Stockholm,
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.