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Journal articles on the topic 'Exhaled nitric oxide'

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Published: 4 June 2021

Last updated: 20 February 2023

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1

Smith, Andrew D., Jan O. Cowan, Karen P. Brassett, Sue Filsell, Chris McLachlan, Gabrielle Monti-Sheehan, G. Peter Herbison, and D. Robin Taylor. "Exhaled Nitric Oxide." American Journal of Respiratory and Critical Care Medicine 172, no. 4 (August 15, 2005): 453–59. http://dx.doi.org/10.1164/rccm.200411-1498oc.

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2

Taylor, D. Robin. "Exhaled Nitric Oxide." American Journal of Respiratory and Critical Care Medicine 179, no. 2 (January 15, 2009): 88–89. http://dx.doi.org/10.1164/rccm.200810-1605ed.

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3

Kharitonov, Sergei A., and Peter J. Barnes. "Exhaled nitric oxide." Current Opinion in Anaesthesiology 9, no. 6 (December 1996): 542–48. http://dx.doi.org/10.1097/00001503-199609060-00017.

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4

Kharitonov, Sergei A., and Peter J. Barnes. "Exhaled nitric oxide." Current Opinion in Anaesthesiology 9, no. 6 (December 1996): 542–48. http://dx.doi.org/10.1097/00001503-199612000-00017.

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5

Stempel, David A. "EXHALED NITRIC OXIDE." Annals of Allergy, Asthma & Immunology 92, no. 3 (March 2004): 381. http://dx.doi.org/10.1016/s1081-1206(10)61581-5.

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6

Leung, Donald Y. M., Harold S. Nelson, Stanley J. Szefler, and William W. Busse. "Exhaled nitric oxide." Journal of Allergy and Clinical Immunology 112, no. 5 (November 2003): 817. http://dx.doi.org/10.1016/j.jaci.2003.09.004.

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7

Stewart, Lora, and Rohit Katial. "Exhaled Nitric Oxide." Immunology and Allergy Clinics of North America 27, no. 4 (November 2007): 571–86. http://dx.doi.org/10.1016/j.iac.2007.09.002.

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8

Stewart, Lora, and Rohit K. Katial. "Exhaled Nitric Oxide." Immunology and Allergy Clinics of North America 32, no. 3 (August 2012): 347–62. http://dx.doi.org/10.1016/j.iac.2012.06.005.

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9

Hoyte, Flavia C. L., Lara M. Gross, and Rohit K. Katial. "Exhaled Nitric Oxide." Immunology and Allergy Clinics of North America 38, no. 4 (November 2018): 573–85. http://dx.doi.org/10.1016/j.iac.2018.06.001.

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10

Fazel, Fatimah. "Exhaled Nitric Oxide Measurement." Journal of Asthma & Allergy Educators 2, no. 2 (April 2011): 99–100. http://dx.doi.org/10.1177/2150129711404414.

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11

Manaker, Scott. "Fractional Exhaled Nitric Oxide." Chest 149, no. 5 (May 2016): 1123–25. http://dx.doi.org/10.1016/j.chest.2015.12.007.

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12

Kotsiou, Ourania S., and Konstantinos I. Gourgoulianis. "Fractional exhaled nitric oxide." Annals of Allergy, Asthma & Immunology 120, no. 3 (March 2018): 340. http://dx.doi.org/10.1016/j.anai.2017.12.001.

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13

Suresh, Vinod, David A. Shelley, Hye-Won Shin, and Steven C. George. "Effect of heterogeneous ventilation and nitric oxide production on exhaled nitric oxide profiles." Journal of Applied Physiology 104, no. 6 (June 2008): 1743–52. http://dx.doi.org/10.1152/japplphysiol.01355.2007.

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Elevated exhaled nitric oxide (NO) in the breath of asthmatic subjects is thought to be a noninvasive marker of lung inflammation. Asthma is also characterized by heterogeneous bronchoconstriction and inflammation, which impact the spatial distribution of ventilation in the lungs. Since exhaled NO arises from both airway and alveolar regions, and its level in exhaled breath depends strongly on flow, spatial heterogeneity in flow patterns and NO production may significantly affect the exhaled NO signal. To investigate the effect of these factors on exhaled NO profiles, we developed a multicompartment mathematical model of NO exchange using a trumpet-shaped central airway segment that bifurcates into two similarly shaped peripheral airway segments, each of which empties into an alveolar compartment. Heterogeneity in flow alone has only a minimal impact on the exhaled NO profile. In contrast, placing 70% of the total airway NO production in the central compartment or the distal poorly ventilated compartment can significantly increase (35%) or decrease (−10%) the plateau concentration, respectively. Reduced ventilation of the peripheral and acinar regions of the lungs with concomitant elevated NO production delays the rise of NO during exhalation, resulting in a positive phase III slope and reduced plateau concentration (−11%). These features compare favorably with experimentally observed profiles in exercise-induced asthma and cannot be simulated with single-path models. We conclude that variability in ventilation and NO production in asthmatic subjects impacts the shape of the exhaled NO profile and thus impacts the physiological interpretation.

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14

Taruya, T., S. Takeno, K. Kubota, A. Sasaki, T. Ishino, and K. Hirakawa. "Comparison of arginase isoform expression in patients with different subtypes of chronic rhinosinusitis." Journal of Laryngology & Otology 129, no. 12 (October 21, 2015): 1194–200. http://dx.doi.org/10.1017/s0022215115002728.

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AbstractObjective:Although human paranasal sinuses are critical organs for nitric oxide production, little information is available regarding the role of arginase in alterations of arginine metabolism and nasal nitric oxide levels that may be informative for classifying chronic rhinosinusitis subtypes.Methods:The expression and localisation of arginase and nitric oxide synthase isoforms in paranasal sinus mucosa were examined, and the fractional exhaled nitric oxide was measured in chronic rhinosinusitis without nasal polyps (n=18) and chronic rhinosinusitis with nasal polyps (n = 27) patients.Results:Increased arginase-2 activities in chronic rhinosinusitis without nasal polyps patients were associated with significantly lower levels of nasal fractional exhaled nitric oxide. Chronic rhinosinusitis with nasal polyps patients showed significant NOS2 messenger RNA upregulation with concomitant higher levels of oral and nasal fractional exhaled nitric oxide.Conclusion:These results indicate that fractional exhaled nitric oxide is a valid marker for differentiating chronic rhinosinusitis phenotypes based on a delicate balance between arginase and nitric oxide synthase activities in nitric oxide production.

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15

Torretta, S., P. Marchisio, L. Drago, P. Capaccio, E. Baggi, and L. Pignataro. "The presence of biofilm-producing bacteria on tonsils is associated with increased exhaled nitric oxide levels: preliminary data in children who experience recurrent exacerbations of chronic tonsillitis." Journal of Laryngology & Otology 129, no. 3 (February 6, 2015): 267–72. http://dx.doi.org/10.1017/s0022215115000031.

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AbstractBackground:It has been suggested that bacterial biofilms may be a causative factor in the aetiopathogenesis of chronic tonsillitis. Involvement of exhaled nitric oxide has been previously considered, with conflicting findings.Objective:A pilot study was performed to investigate the relationship between exhaled nitric oxide levels and the presence of tonsillar biofilm-producing bacteria in children with chronic tonsillitis.Method:Tonsillar biofilm-producing bacteria on bioptic specimens taken during tonsillectomy were assessed by means of spectrophotometry.Results:Analysis was based on 24 children aged 5–10 years (median, 7.5 years). Biofilm-producing bacteria were found in 40.9 per cent of specimens. The median exhaled nitric oxide level was 11.6 ppb (range, 3.2–22.3 ppb). There was a significant relationship between the presence of biofilm-producing bacteria and increased exhaled nitric oxide levels (p = 0.03). Children with exhaled nitric oxide levels of more than 8 ppb were at three times greater risk of developing tonsillar biofilm-producing bacteria than those with lower levels.Conclusion:Our findings suggest the possibility of discriminating children with chronic biofilm-sustained tonsillar infections on the basis of exhaled nitric oxide levels.

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16

Moos, Łukasz, Magdalena Zajac, and Zenon Brzoza. "Exhaled Nitric Oxide Level in Pharynx Angioedema." Journal of Clinical Medicine 11, no. 3 (January 27, 2022): 637. http://dx.doi.org/10.3390/jcm11030637.

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Airway inflammation is related to increased nitric oxide production. It can be assessed noninvasively with exhaled nitric oxide measurement. As airway inflammation was supposed to be present in chronic urticaria and angioedema patients we hypothesized increased exhaled nitric oxide in this group. Twenty-six symptomatic chronic urticaria patients with an acute episode of pharynx angioedema (17 women and 9 men, median age 35) were included in the study group. None of the patients reported a history of asthma, allergic rhinitis or cigarette smoking. The control group consisted of 29 non-smoking healthy subjects (19 women and 10 men, median age 22) without any history of atopy. Exhaled nitric oxide measurement was performed in all subjects. Exhaled nitric oxide levels in the angioedema group did not differ statistically significantly from those detected in healthy subjects (15.5 ppb and 17.0 ppb respectively). Our results indicate the lack of airway inflammation in chronic urticaria patients with pharynx angioedema.

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17

Oguzulgen, I. Kivilcim. "Measurement of Exhaled Nitric Oxide." Turkish Thoracic Journal/Türk Toraks Dergisi 14 (August 26, 2013): 37–40. http://dx.doi.org/10.5152/ttd.2013.50.

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18

Sheel, A. William, Jeremy Road, and Donald C. McKenzie. "Exhaled Nitric Oxide During Exercise." Sports Medicine 28, no. 2 (1999): 83–90. http://dx.doi.org/10.2165/00007256-199928020-00003.

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19

Bikov, Andras, Martina Meszaros, and Zsofia Lazar. "Exhaled Nitric Oxide in COPD." Current Respiratory Medicine Reviews 15, no. 2 (December 10, 2019): 71–78. http://dx.doi.org/10.2174/1573398x14666181025150537.

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Chronic obstructive pulmonary disease (COPD) is a common and progressive disorder which is characterised by pathological abnormalities driven by chronic airway inflammation. The assessment of airway inflammation in routine clinical practice in COPD is limited to surrogate blood markers. Fractional exhaled nitric oxide (FENO) is a marker of eosinophilic airway inflammation in asthma, and it can predict steroid responsiveness and help tailor corticosteroid treatment. The clinical value of FENO in COPD is less evident, but some studies suggest that it may be a marker of the eosinophilic endotype. More importantly, mathematical methods allow investigation of the alveolar/small airway production of NO which potentially better reflects inflammatory changes in anatomical sites, most affected by COPD. This review summarises the pathophysiological role of nitric oxide in COPD, explains the methodology of its measurement in exhaled air and discusses clinical findings of FENO in COPD.

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20

Ricciardolo, Fabio L. M., and Philip E. Silkoff. "Perspectives on exhaled nitric oxide." Journal of Breath Research 11, no. 4 (September 27, 2017): 047104. http://dx.doi.org/10.1088/1752-7163/aa7f0e.

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21

Lundberg, J. O. N., E. Weitzberg, J. M. Lundberg, and K. Alving. "Nitric oxide in exhaled air." European Respiratory Journal 9, no. 12 (December 1, 1996): 2671–80. http://dx.doi.org/10.1183/09031936.96.09122671.

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22

Salonen, Iiris, Kati Huttunen, Maija-Riitta Hirvonen, Juhani Dufva, Kaj Groundstroem, Hilkka Dufva, and Raimo O. Salonen. "Exhaled nitric oxide and atherosclerosis." European Journal of Clinical Investigation 42, no. 8 (March 16, 2012): 873–80. http://dx.doi.org/10.1111/j.1365-2362.2012.02662.x.

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23

Taylor, D. R., and J. Dummer. "Exhaled nitric oxide and COPD." European Respiratory Journal 36, no. 3 (August 31, 2010): 692. http://dx.doi.org/10.1183/09031936.00058310.

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24

Thébaud, B., J. F. Arnal, J. C. Mercier, and A. T. Dinh-Xuan. "Inhaled and exhaled nitric oxide." Cellular and Molecular Life Sciences CMLS 55, no. 8 (July 1999): 1103–12. http://dx.doi.org/10.1007/s000180050360.

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25

Menzies, Daniel, Arun Nair, and Brian J. Lipworth. "Portable Exhaled Nitric Oxide Measurement." Chest 131, no. 2 (February 2007): 410–14. http://dx.doi.org/10.1378/chest.06-1335.

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26

Olivieri, Mario, Massimo Corradi, and Mario Malerba. "Gender and Exhaled Nitric Oxide." Chest 132, no. 4 (October 2007): 1410. http://dx.doi.org/10.1378/chest.07-0741.

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27

Olin, Anna-Carin, Björn Bake, and Kjell Toren. "Exhaled Nitric Oxide and Gender." Chest 132, no. 4 (October 2007): 1410. http://dx.doi.org/10.1378/chest.07-1701.

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28

Grob, Natalia M., and Raed A. Dweik. "Exhaled Nitric Oxide in Asthma." Chest 133, no. 4 (April 2008): 837–39. http://dx.doi.org/10.1378/chest.07-2743.

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29

Wilsher, M. L. "Exhaled nitric oxide in sarcoidosis." Thorax 60, no. 11 (November 1, 2005): 967–70. http://dx.doi.org/10.1136/thx.2004.033852.

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30

Bruce, C. "Caffeine decreases exhaled nitric oxide." Thorax 57, no. 4 (April 1, 2002): 361–63. http://dx.doi.org/10.1136/thorax.57.4.361.

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31

Warke, T. J. "Caffeine and exhaled nitric oxide." Thorax 58, no. 3 (March 1, 2003): 281—a—281. http://dx.doi.org/10.1136/thorax.58.3.281-a.

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32

Khan, Javaad, Mary Skowronski, Albert Coreno, and E. R. McFadden. "OBESITY AND EXHALED NITRIC OXIDE." Chest 130, no. 4 (October 2006): 249S. http://dx.doi.org/10.1378/chest.130.4_meetingabstracts.249s-a.

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33

MATSUMOTO, Akihiro, Yasunobu HIRATA, Masao KAKOKI, Daisuke NAGATA, Shin-ichi MOMOMURA, Tokuichiro SUGIMOTO, Hitoshi TAGAWA, and Masao OMATA. "Increased excretion of nitric oxide in exhaled air of patients with chronic renal failure." Clinical Science 96, no. 1 (January 1, 1999): 67–74. http://dx.doi.org/10.1042/cs0960067.

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Nitric oxide exerts multiple effects on renal function. It remains unclear whether endogenous nitric oxide production is increased or decreased in patients with chronic renal failure. To evaluate endogenous nitric oxide production in these patients we studied exhaled nitric oxide output by an ozone chemiluminescence method and plasma NO2-/NO3- levels by the Griess method in 40 patients with end-stage chronic renal failure who underwent regular continuous ambulatory peritoneal dialysis (n = 30) or haemodialysis (n = 10), and in 28 healthy subjects. Patients with chronic renal failure had a higher exhaled nitric oxide concentration [39±3 versus 19±1 parts per billion, (mean±S.E.M.), P< 0.0001], a greater nitric oxide output (177±11 versus 96±7 ;nl·min-1·m-2, P< 0.001) and a higher plasma NO2-/NO3- concentration (96±14 versus 33±4 ;μmol, P< 0.01) than controls. These values did not differ between patients on haemodialysis and those on continuous ambulatory peritoneal dialysis. Patients with chronic renal failure had significantly higher plasma concentrations of both interleukin-1β and interferon-γ than controls. The exhaled nitric oxide output did not correlate with plasma NO2-/NO3- or with peritoneal dialysate NO2-/NO3-, but plasma NO2-/NO3- correlated with dialysate NO2-/NO3- in patients who underwent continuous ambulatory peritoneal dialysis (r = 0.77, P< 0.01). Haemodialysis for 4 ;h acutely decreased plasma NO2-/NO3- (92±17 versus 50±8 ;μmol, P< 0.05) and cGMP concentration (16.5±4.3 versus 5.1±1.7 ;pmol/ml, P< 0.01), but did not decrease exhaled nitric oxide output. The increase in exhaled nitric oxide with the simultaneous increase in circulating cytokines suggests that nitric oxide synthase seems to be induced significantly in patients with chronic renal failure. Increased endogenous nitric oxide production may have a pathophysiological role in patients with uraemia.

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34

Sato, K., T. Sakamaki, H. Sumino, H. Sakamoto, J. Hoshino, H. Masuda, Y. Sawada, et al. "Rate of nitric oxide release in the lung and factors influencing the concentration of exhaled nitric oxide." American Journal of Physiology-Lung Cellular and Molecular Physiology 270, no. 6 (June 1, 1996): L914—L920. http://dx.doi.org/10.1152/ajplung.1996.270.6.l914.

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The level of nitric oxide (NO) in exhaled air fluctuates in normal individuals depending on the physiological conditions. We evaluated the effects of duration of exhalation and breath-holding on the exhaled concentrations of NO in 16 normal human volunteers. Exhaled gas corresponding to vital capacity was collected in 6-liter Tedlar bags and analyzed by chemiluminescence. The NO concentration in exhaled gas increased significantly in proportion to the duration of exhalation [P = 0.009 +/- 0.011 (SD)] and was increased after breath-holding. There was no significant difference in the exhaled NO concentration among 10-s phases of a 30-s exhalation, as determined from multiple breath collections. The NO released from the airways is presumably unaffected by fluctuation of exhalation speed. The NO release rate, calculated from a single regression analysis between the NO concentration and the duration of exhalation, was 39 +/- 29 pmol/s, a value which was about fourfold greater in nine patients with bronchial asthma.

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35

Kryvopustovа, Mariia. "Evaluation of fractional exhaled nitric oxide in school-age children with asthma and sensitization to cat allergens." Ukrainian Scientific Medical Youth Journal 132, no. 3 (September 28, 2022): 76–82. http://dx.doi.org/10.32345/usmyj.3(132).2022.76-82.

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bronchial asthma is a chronic condition that is considerably prevalent among children. According to scientific evidence, cat allergens are most frequently responsible for the onset of asthma manifestations in children. Children are more likely to develop atopic asthma with eosinophilic inflammation. Under these circumstances, specific biomarkers are used as indicators of this inflammation. Fractional exhaled nitric oxide has been identified as a marker of eosinophilic airway inflammation in asthma. The aim of the research was to determine the fractional exhaled nitric oxide concentrations in school-age children with bronchial asthma and sensitization to cat allergens in order to predict asthma control status and assess therapeutic response. A total of 430 children aged between 6 and 17 years with asthma and sensitization to cat allergens participated in the study. The sensitization profile was investigated using a multicomponent molecular allergy diagnostic test (ALEX², Austria). The fractional exhaled nitric oxide levels were evaluated (NIOX VERO, Sweden). A total of 302 patients were enrolled in a retrospective study to find out how likely they were to gain bronchial asthma control over the course of therapy. As a result, a one-factor logistic regression analysis was conducted. A total of 128 children were included in the 12-month prospective research. All patients had a rise in fractional exhaled nitric oxide of > 20 ppb, with children with severe asthma having levels of 35 ppb or higher. The study discovered that changes in the fractional exhaled nitric oxide concentrations at the end of a three-month therapy could be linked to the maintenance of bronchial asthma control after a 12-month treatment period (r = 0.619; p <0.001). After a year of therapy, increasing baseline fractional exhaled nitric oxide levels reduced the probability of establishing bronchial asthma control in children (OR <1; p <0.001). The dynamics of fractional exhaled nitric oxide reduction increased the probability of achieving bronchial asthma control after completion of a three-month therapy (OR> 1; p <0.001). The effect of allergen-specific immunotherapy on the specified indicator of eosinophilic inflammation was demonstrated by a statistically significant difference in the mean values of fractional exhaled nitric oxide after a 12-month treatment period in the group of patients who received allergen-specific immunotherapy in combination with controller therapy versus the group of patients who received only controller therapy (p = 0.012). Thus, among school-age children with asthma and sensitization to cat allergens, the levels of fractional exhaled nitric oxide increased, especially in severe asthma. Not only the baseline fractional exhaled nitric oxide levels but also their dynamics after a three-month therapy should be considered when predicting the probability of establishing asthma control in these children. The inclusion of allergen-specific immunotherapy in the complex treatment of bronchial asthma in school-age children with sensitization to cat allergens has been shown to have a favourable therapeutic effect on the fractional exhaled nitric oxide levels.

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36

Kharitonov, Sergei A., Gert Lubec, Barbara Lubec, Magnus Hjelm, and Peter J. Barnes. "l-Arginine Increases Exhaled Nitric Oxide in Normal Human Subjects." Clinical Science 88, no. 2 (February 1, 1995): 135–39. http://dx.doi.org/10.1042/cs0880135.

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1. Endogenous nitric oxide plays an important physiological role and is synthesized by several isoforms of nitric oxide synthase from the semiessential amino acid l-arginine. Nitric oxide is detectable in the exhaled air of normal individuals and may be used to monitor the formation of nitric oxide in the respiratory tract. 2. We have investigated the effect of orally administered l-arginine (0.05, 0.1, 0.2 g/kg) compared with matched placebo on the concentration of nitric oxide in the exhaled air in 23 normal individuals. 3. l-Arginine caused significant increases in the concentration of nitric oxide in exhaled air at doses of 0.1 and 0.2 mg/kg, which was maximal 2 h after administration. This was associated with an increase in the concentration of l-arginine and nitrate in plasma. There were no significant changes in heart rate, blood pressure or forced expiratory volume in 1 s. 4. These results suggest that an increase in the amount of substrate for nitric oxide synthase can increase the formation of endogenous nitric oxide. This may have therapeutic relevance in diseases in which there is defective production of nitric oxide.

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37

Vaughan, David J., Thomas V. Brogan, Mark E. Kerr, Steven Deem, Daniel L. Luchtel, and Erik R. Swenson. "Contributions of nitric oxide synthase isozymes to exhaled nitric oxide and hypoxic pulmonary vasoconstriction in rabbit lungs." American Journal of Physiology-Lung Cellular and Molecular Physiology 284, no. 5 (May 1, 2003): L834—L843. http://dx.doi.org/10.1152/ajplung.00341.2002.

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We investigated the source(s) for exhaled nitric oxide (NO) in isolated, perfused rabbits lungs by using isozyme-specific nitric oxide synthase (NOS) inhibitors and antibodies. Each inhibitor was studied under normoxia and hypoxia. Only nitro-l-arginine methyl ester (l-NAME, a nonselective NOS inhibitor) reduced exhaled NO and increased hypoxic pulmonary vasoconstriction (HPV), in contrast to 1400W, an inhibitor of inducible NOS (iNOS), and 7-nitroindazole, an inhibitor of neuronal NOS (nNOS). Acetylcholine-mediated stimulation of vascular endothelial NOS (eNOS) increased exhaled NO and could only be inhibited by l-NAME. Selective inhibition of airway and alveolar epithelial NO production by nebulized l-NAME decreased exhaled NO and increased hypoxic pulmonary artery pressure. Immunohistochemistry demonstrated extensive staining for eNOS in the epithelia, vasculature, and lymphatic tissue. There was no staining for iNOS but moderate staining for nNOS in the ciliated cells of the epithelia, lymphoid tissue, and cartilage cells. Our findings show virtually all exhaled NO in the rabbit lung is produced by eNOS, which is present throughout the airways, alveoli, and vessels. Both vascular and epithelial-derived NO modulate HPV.

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38

George, Steven C., Marieann Hogman, Solbert Permutt, and Philip E. Silkoff. "Modeling pulmonary nitric oxide exchange." Journal of Applied Physiology 96, no. 3 (March 2004): 831–39. http://dx.doi.org/10.1152/japplphysiol.00950.2003.

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Nitric oxide (NO) was first detected in the exhaled breath more than a decade ago and has since been investigated as a noninvasive means of assessing lung inflammation. Exhaled NO arises from the airway and alveolar compartments, and new analytical methods have been developed to characterize these sources. A simple two-compartment model can adequately represent many of the observed experimental observations of exhaled concentration, including the marked dependence on exhalation flow rate. The model characterizes NO exchange by using three flow-independent exchange parameters. Two of the parameters describe the airway compartment (airway NO diffusing capacity and either the maximum airway wall NO flux or the airway wall NO concentration), and the third parameter describes the alveolar region (steady-state alveolar NO concentration). A potential advantage of the two-compartment model is the ability to partition exhaled NO into an airway and alveolar source and thus improve the specificity of detecting altered NO exchange dynamics that differentially impact these regions of the lungs. Several analytical techniques have been developed to estimate the flow-independent parameters in both health and disease. Future studies will focus on improving our fundamental understanding of NO exchange dynamics, the analytical techniques used to characterize NO exchange dynamics, as well as the physiological interpretation and the clinical relevance of the flow-independent parameters.

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39

Karlsson, Lars L., Yannick Kerckx, Lars E. Gustafsson, Tryggve E. Hemmingsson, and Dag Linnarsson. "Microgravity decreases and hypergravity increases exhaled nitric oxide." Journal of Applied Physiology 107, no. 5 (November 2009): 1431–37. http://dx.doi.org/10.1152/japplphysiol.91081.2008.

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Inhalation of toxic dust during planetary space missions may cause airway inflammation, which can be monitored with exhaled nitric oxide (NO). Gravity will differ from earth, and we hypothesized that gravity changes would influence exhaled NO by altering lung diffusing capacity and alveolar uptake of NO. Five subjects were studied during microgravity aboard the International Space Station, and 10 subjects were studied during hypergravity in a human centrifuge. Exhaled NO concentrations were measured during flows of 50 (all gravity conditions), 100, 200, and 500 ml/s (hypergravity). During microgravity, exhaled NO fell from a ground control value of 12.3 ± 4.7 parts/billion (mean ± SD) to 6.6 ± 4.4 parts/billion ( P = 0.016). In the centrifuge experiments and at the same flow, exhaled NO values were 16.0 ± 4.3, 19.5 ± 5.1, and 18.6 ± 4.7 parts/billion at one, two, and three times normal gravity, where exhaled NO in hypergravity was significantly elevated compared with normal gravity ( P ≤ 0.011 for all flows). Estimated alveolar NO was 2.3 ± 1.1 parts/billion in normal gravity and increased significantly to 3.9 ± 1.4 and 3.8 ± 0.8 parts/billion at two and three times normal gravity ( P < 0.002). The findings of decreased exhaled NO in microgravity and increased exhaled and estimated alveolar NO values in hypergravity suggest that gravity-induced changes in alveolar-to-lung capillary gas transfer modify exhaled NO.

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40

Verbanck, Sylvia, Yannick Kerckx, Daniel Schuermans, Claire de Bisschop, Hervé Guénard, Robert Naeije, Walter Vincken, and Alain Van Muylem. "The effect of posture-induced changes in peripheral nitric oxide uptake on exhaled nitric oxide." Journal of Applied Physiology 106, no. 5 (May 2009): 1494–98. http://dx.doi.org/10.1152/japplphysiol.91641.2008.

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Airway and alveolar NO contributions to exhaled NO are being extracted from exhaled NO measurements performed at different flow rates. To test the robustness of this method and the validity of the underlying model, we deliberately induced a change in NO uptake in the peripheral lung compartment by changing body posture between supine and prone. In 10 normal subjects, we measured exhaled NO at target flows ranging from 50 to 350 ml/s in supine and prone postures. Using two common methods, bronchial NO production [Jaw(NO)] and alveolar NO concentration (FANO) were extracted from exhaled NO concentration vs. flow or flow−1 curves. There was no significant Jaw(NO) difference between prone and supine but a significant FANO decrease from prone to supine ranging from 23 to 33% depending on the method used. Total lung capacity was 7% smaller supine than prone ( P = 0.03). Besides this purely volumetric effect, which would tend to increase FANO from prone to supine, the observed degree of FANO decrease from prone to supine suggests a greater opposing effect that could be explained by the increased lung capillary blood volume (Vc) supine vs. prone ( P = 0.002) observed in another set of 11 normal subjects. Taken together with the relative changes of NO and CO transfer factors, this Vc change can be attributed mainly to pulmonary capillary recruitment from prone to supine. Realistic models for exhaled NO simulation should include the possibility that a portion of the pulmonary capillary bed is unavailable for NO uptake, with a maximum capacity of the pulmonary capillary bed in the supine posture.

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STEUDEL, WOLFGANG, MAX KIRMSE, JÖRG WEIMANN, ROMAN ULLRICH, JONATHAN HROMI, and WARREN M ZAPOL. "Exhaled Nitric Oxide Production by Nitric Oxide Synthase–deficient Mice." American Journal of Respiratory and Critical Care Medicine 162, no. 4 (October 2000): 1262–67. http://dx.doi.org/10.1164/ajrccm.162.4.9909037.

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Melo, Bruno, Patrício Costa, Ariana Afonso, Vânia Machado, Carla Moreira, Augusta Gonçaves, and Jean-Pierre Gonçalves. "Fração Exalada de Óxido Nítrico no Controlo e Abordagem Terapêutica da Asma." Acta Médica Portuguesa 27, no. 1 (January 8, 2014): 59. http://dx.doi.org/10.20344/amp.2371.

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<strong>Introduction:</strong> Asthma is a chronic respiratory disease characterized by hyper-responsiveness and bronchial inflammation. The bronchial inflammation in these patients can be monitored by measuring the fractional exhaled nitric oxide. This study aims to determine fractional exhaled nitric oxide association with peak expiratory flow and with asthma control inferred by the Global Initiative for Asthma.<br /><strong>Material and Methods:</strong> Observational, analytical and cross-sectional study of children with asthma, 6-12 years-old, followed in the Outpatient Respiratory Pathology of Braga Hospital. Sociodemographic and clinical information were collected through a questionnaire. fractional exhaled nitric oxide and peak expiratory flow were determined by portable analyzer Niox Mino® and flow meter, respectively.<br /><strong>Results:</strong> The sample is constituted by 101 asthmatic children, 63 (62.4%) of males and 38 (37.6%) females. The mean age of participants in the sample is 9.18 (1.99) years. The logistic regression performed with the cutoff value obtained by ROC curve, revealed that fractional exhaled nitric oxide (bFENO classes = 0.85; χ2 Wald (1) = 8.71; OR = 2.33; p = 0.003) has a statistical significant effect on the probability of changing level of asthma control. The odds ratio of going from “controlled” to “partly controlled/uncontrolled” is 2.33 per each level of fractional exhaled nitric oxide.<br /><strong>Discussion and Conclusion: </strong>The probability of an asthmatic children change their level of asthma control, from ‘controlled’ to ‘partly controlled/uncontrolled’, taking into account a change in their fractional exhaled nitric oxide level, increases 133%.

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Nesic, V. S., V. Z. Djordjevic, V. Tomic-Spiric, Z. R. Dudvarski, I. A. Soldatovic, and N. A. Arsovic. "Measuring nasal nitric oxide in allergic rhinitis patients." Journal of Laryngology & Otology 130, no. 11 (November 2016): 1064–71. http://dx.doi.org/10.1017/s0022215116009087.

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AbstractObjective:This study aimed to compare two sampling methods for nasal nitric oxide in healthy individuals and allergic rhinitis patients, and to examine the within-subject reliability of nasal nitric oxide measurement.Methods:The study included 23 allergic rhinitis patients without concomitant asthma and 10 healthy individuals. For all participants, nitric oxide levels were measured non-invasively from the lungs through the mouth (i.e. the oral fractional exhaled nitric oxide) and the nose. Nasal nitric oxide was measured by two different methods: (1) nasal aspiration via one nostril during breath holding and (2) single-breath quiet exhalation against resistance through a tight facemask (i.e. the nasal fractional exhaled nitric oxide).Results:Compared with healthy participants, allergic rhinitis patients had significantly higher average oral and nasal nitric oxide levels. All methods of nitric oxide measurement had excellent reliability.Conclusion:Nasal nitric oxide measurement is a useful and reliable clinical tool for diagnosing allergic rhinitis in patients without asthma in an out-patient setting.

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Kovesi, Thomas A., and Robert E. Dales. "Effects of the Indoor Environment on the Fraction of Exhaled Nitric Oxide in School-Aged Children." Canadian Respiratory Journal 16, no. 3 (2009): e18-e23. http://dx.doi.org/10.1155/2009/954382.

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BACKGROUND: The fractional concentration of exhaled nitric oxide (FeNO) appears to be a good marker for airway inflammation in children with asthma.OBJECTIVE: To evaluate the effect of environmental exposures on exhaled nitric oxide in a community sample of children.METHODS: The relationship among exhaled nitric oxide, underlying disease and home environmental exposures was examined using questionnaire data and measurement of exhaled nitric oxide in a cross-sectional study of 1135 children that included healthy children, and children with allergies and/or asthma who were attending grades 4 through 6 in Windsor, Ontario.RESULTS: Among healthy children, there was a positive association between FeNO and occupancy (P<0.02). Compared with forced air and hot water radiant heat, electric baseboard heating was associated with a significant increase of FeNO in healthy children (P=0.007) and children with allergies (P=0.043). FeNO was not associated with environmental tobacco smoke exposure or reported surface mold. The presence of pet dog(s), but not cats, was associated with a significantly lower FeNO in healthy children (P<0.001) and in children with reported allergies (P<0.001).CONCLUSIONS: The type of heating system, but not previously reported environmental tobacco smoke or mold exposure appears to affect exhaled nitric oxide in children. Exposure to different types of pets may have disparate effects on airway inflammation.

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Fike, Candice D., Mark R. Kaplowitz, Carol J. Thomas, and Leif D. Nelin. "Chronic hypoxia decreases nitric oxide production and endothelial nitric oxide synthase in newborn pig lungs." American Journal of Physiology-Lung Cellular and Molecular Physiology 274, no. 4 (April 1, 1998): L517—L526. http://dx.doi.org/10.1152/ajplung.1998.274.4.l517.

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To examine the effect of chronic hypoxia on nitric oxide (NO) production and the amount of the endothelial isoform of nitric oxide synthase (eNOS) in lungs of newborn piglets, studies were performed using 1- to 3-day-old piglets raised in room air (control) or 10% O2 (chronic hypoxia) for 10–12 days. Exhaled NO output and plasma nitrites and nitrates (collectively termed[Formula: see text]) were measured in anesthetized animals. [Formula: see text]concentrations were measured in the perfusate of isolated lungs. eNOS amounts were assessed in whole lung homogenates. In the intact piglets, exhaled NO outputs and plasma [Formula: see text]were lower in the chronically hypoxic (exhaled NO output = 0.2 ± 0.1 nmol/min; plasma [Formula: see text] = 10.3 ± 3.7 nmol/ml) than in control animals (exhaled NO output = 0.8 ± 0.2 nmol/min; plasma [Formula: see text] = 22.3 ± 4.3 nmol/ml). In perfused lungs, the perfusate accumulation of [Formula: see text] was lower in chronic hypoxia (1.0 ± 0.3 nmol/min) than in control (2.6 ± 0.6 nmol/min) piglets. The amount of whole lung homogenate eNOS from the chronic hypoxia piglets was 40 ± 8% less than that from the control piglets. The reduced NO production observed in anesthetized animals or perfused lungs of chronically hypoxic newborn piglets is consistent with the finding of reduced lung eNOS protein amounts. Decreased NO production might contribute to the development of chronic hypoxia-induced pulmonary hypertension in newborns.

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&NA;. "Montelukast reduces exhaled nitric oxide levels." Inpharma Weekly &NA;, no. 1414 (November 2003): 18. http://dx.doi.org/10.2165/00128413-200314140-00046.

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Horvath, Ildiko, Raed Dweik, and Peter J. Barnes. "Exhaled nitric oxide comes of age." Journal of Breath Research 6, no. 4 (November 27, 2012): 040201. http://dx.doi.org/10.1088/1752-7155/6/4/040201.

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Zetterquist, W., C. Pedroletti, J. O. n. Lundberg, and K. Alving. "Salivary contribution to exhaled nitric oxide." European Respiratory Journal 13, no. 2 (February 1999): 327–33. http://dx.doi.org/10.1034/j.1399-3003.1999.13b18.x.

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Maniscalco, Mauro, Alessandro Vatrella, and Mateo Sofia. "PASSIVE SMOKE AND EXHALED NITRIC OXIDE." American Journal of Respiratory and Critical Care Medicine 165, no. 8 (April 15, 2002): 1188. http://dx.doi.org/10.1164/ajrccm.165.8.correspondence_b.

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Beilman, Greg. "Exhaled Nitric Oxide in Pathophysiologic States." Chest 125, no. 1 (January 2004): 11–13. http://dx.doi.org/10.1378/chest.125.1.11.

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