Nasal Nasal Nitric Oxide Research Articles

Normal adult values, diurnal variation, and repeatability of nasal nitric oxide measurement.

Reports of elevated nasal nitric oxide (NO) levels in allergic rhinitis suggest that nasal NO levels could be a valuable marker of upper airway inflammation, provided that the reproducibility of nasal NO measurement is acceptable. The aims of this study were to evaluate the precision with which nasal NO levels can be measured at single point in time, and to quantify within-day and between-day variation. Nasal NO was measured using a modified chemiluminescence analyzer. Population data were normally distributed, as judged by testing for skewness and kurtosis. NO levels were not related to age or gender, and there was no evidence of diurnal variation. Sampling rates of 250 mL/minute and 500 mL/minute at a single point in time had acceptable reproducibility (coefficients of variation 10.2% and 6.6%, respectively). However, within-day variation (coefficient of variation 13.4%) and between-day variation (coefficient of variation 11.8%), at a sampling rate of 500 L/minute, were substantially higher. These findings highlight the importance of taking measurement variation into account, in the interpretation of NO levels, in clinical research and, potentially, in routine practice. In individual patients, an alteration of 20-25% in NO levels is required, to ensure that change is genuine and not ascribable to the noise of measurement.

Nasal nitric oxide is independent of nasal cavity volume.

This study was performed to evaluate the relationship between nasal nitric oxide (NO) and changes in nasal cavity volume resulting from the topical application of xylometazoline and saline and between upright and supine posture. Nasal NO was measured using a fixed high flow technique that avoids contamination with lower airways NO. In nine healthy subjects nasal NO concentration was measured by a rapid response chemiluminescent analyzer. A tapered tube was inserted in one nostril, into which room air was insufflated to produce a constant flow of 100 mL/second; another tube was inserted into the opposite nostril for NO sampling (air exit side). Subjects were instructed to keep the vellum closed while NO was sampled through a sideport connected to the analyzer. Nasal cavity volume was measured by acoustic rhinometry from a segment of the acoustic pathway, 2 to 5 cm from the nostril. Nasal cavity volume and NO measurements were made at baseline, 15 minutes, and 60 minutes after intervention (administration of saline 0.9%, xylometazoline or posture changes on 3 consecutive days). Xylometazoline produced a significant increase in nasal cavity volume, together with a significant reduction in NO level at 15 and 60 minutes after intervention. In addition, the change from seated to supine position decreased the total nasal volume significantly, but without changes in nasal NO. No correlation was found between the magnitudes of changes in nasal NO and the changes in nasal volume. Topical application of xylomethazoline resulted in increased nasal cavity volume and reduced NO output. In contrast to previous published reports, a technique using high flow rate insufflation demonstrated an abscence of correlation between the magnitudes of changes in nasal NO and nasal cavity volume brought about by decongestant, saline, or posture.

Effects of topical alpha 1- and beta 2-adrenoceptor stimulants on nasal nitric oxide level

The effects of locally administered alpha 1- and beta 2-stimulants (naphazoline and salbutamol) on the nasal nitric oxide (NO) level were investigated. Twenty-four healthy volunteers (except nasal allergy) were subjected to the examination. First, nasal cavity air was sampled continuously from the right nostril for 20 seconds at the rate of 3.5 l/m, and NO-free air was supplied passively to the left nostril. During the sampling time, subjects were made to hold their breath at deep inspiration, which obviated the effect of lower airways by closing their glottises. The sampled air was analyzed using a chemiluminescence technique for NO detection. In addition, nasal airway resistances (NAR) were estimated by a rhinomanometer, and minimum cross-section area (MCA) and nasal cavity volume (NCV) were estimated by an acoustic rhinometer. After these estimations, 12 subjects received naphazoline nitrate 15 micrograms per nostril, and the other 12 subjects received salbutamol sulfate 100 micrograms per nostril. Finally, after 15 minutes rest, these four parameters were reviewed. The results demonstrated that naphazoline significantly decreased NO concentration and NAR, and increased NCV. Furthermore, salbutamol significantly increased NO concentration and NAR, and decreased MCA and NCV. The changes in NAR, MCA and NCV indicated that nasal mucosa became contracted and swollen by topical naphazoline and salbutamol application. Naphazoline, a nasal decongestant, contract nasal vessels by stimulating alpha 1-adrenoceptors, whereas salbutamol dilates then by stimulating beta 2-adrenoceptors, and this vasodilation does not intervene NO and cyclic GMP. Thus, nasal NO concentration is significantly affected by the change of blood supply caused simply by vasocontraction and vasodilation. In conclusion, it appeared that nasal NO concentration was possibly altered by the change of nasal blood supply, moreover, by the change in the supply of NO substrate.

Low nitric oxide concentrations in exhaled gas and nasal airways of mammals without paranasal sinuses.

To investigate whether relevant levels of nasal nitric oxide (NO) are produced in the absence of paranasal sinuses, we studied 17 healthy baboons, mammals without any paranasal sinuses. The animals were anesthetized with ketamine hydrochloride and breathed spontaneously. While the baboons breathed through a face mask (mouths closed) connected to a respirator, NO concentrations in exhaled gas were sampled from the expiratory limb and analyzed by chemiluminescence. While the animals were breathing ambient air, nasal gas was sampled via a thin plastic tube and analyzed for NO concentrations by chemiluminescence. Mean NO concentration in the exhaled gas was 1.00 +/- 0.59 parts/billion, and NO release was 4.28 +/- 2.72 nl/min. A NO concentration of 4.79 +/- 2.08 parts/billion was found in the nasal gas (NO release: 7.18 +/- 3.13 nl/min). An age-dependent increase in nasal NO levels was not observed. Exhaled and nasal NO concentrations in baboons were markedly lower than in mammals with paranasal sinuses, suggesting that paranasal sinuses might be an anatomic requirement for production of relevant nasal NO levels.

Effect of arginine on mucociliary function in primary ciliary dyskinesia

Primary ciliary dyskinesia (PCD) is a genetic disease characterised by defective motility of cilia and abnormally low nasal nitric oxide (NO)1 which has a key role in host defence and in up-regulation of ciliary motility in vitro.2 Inhibitors of NO synthesis decrease ciliary beating in airway epithelium.3 We investigated whether arginine, a precursor of NO synthesis,3 could increase nasal NO and improve ciliary beat frequency and nasal mucociliary clearance in patients with and without PCD.

Low Levels of Nasal Nitric Oxide (NO) Correlate to Impaired Mucociliary Function in the Upper Airways

Findings in previous studies have suggested nitric oxide (NO) to be a regulator of mucociliary activity in the upper airways. The aim of the present investigation was to study whether a correlation exists between the nasal NO concentration and mucociliary function in patients suffering from respiratory tract diseases such as chronic sinusitis or recurrent pneumonia. Nasal NO was measured with a chemiluminescence analyser, 100 ppb (parts per billion) being adopted as the lower limit of the normal range on the basis of findings in an earlier study of healthy subjects. Mucociliary function was evaluated by measurements of ciliary beat frequency (CBF) in nasal brush samples, and the saccharin transport test. A subnormal level of nasal NO was found in 50% (9/18) of the patients. This correlated with a significantly impaired mucociliary function, regarding both CBF and the saccharin transport time. The median CBF was 10.6 Hz in the group with normal levels of nasal NO, as compared to 8.4 Hz in the subnormal NO group. AH patients with a normal nasal NO concentration had a mean CBF of s9.0 Hz in their nasal brush samples, but in the subnormal group the same measurements yielded a CBF of ≥9.0 Hz in only 22% (2/9) of the cases. As measured with the saccharin test, mucociliary transport was normal in 78% (7/9) in the normal nasal NO group, but the saccharin test was normal only in 11% (1/9) of the subnormal nasal NO group. Nasal NO levels were found to correlate with both CBF measurements (Spearman's rho, 0.80) and the saccharin transport test results (Spearman's rho, -0.61). The results of the present study provide further support for the view that NO is an important regulator of mucociliary function in the upper airways, and that measurements of the nasal NO concentration should be included in investigations of the mucociliary system.