Bronchial Allergen Challenge in Allergic Children: Continuous Increase of Nitric Oxide in Exhaled Air 72 Hours After Allergen Inhalation Independent of Bronchial Obstruction

Allergic airway inflammation (AI) is commonly associated with enhanced exhaled nitric oxide (ENO) in both humans and mice. Since mouse models are being used to understand various mechanisms of asthma, a noninvasive, simple, and reproducible method to determine ENO in mice is required for serial nonterminal assessment that can be used independent of environmental situations in which the ambient air contains substantial amounts of NO as a contaminant. The aim of this study was to noninvasively measure ENO in individual mice and to test its utility as a marker of AI in different models of allergic AI. We modified the existing ENO measuring methods by incorporating flushing and washout steps that allowed simple but reliable measurements under highly variable ambient NO conditions (1–100 ppb). This method was used to serially follow ENO in acute and chronic models of allergic AI in mice. ENO was reproducibly measured by this modified method and was positively correlated to AI in both acute and chronic models of asthma but was not independently related to airway remodeling. Resolution of AI and other related parameters in dexamethasone-treated mice resulted in reduction of ENO, further confirming this association. Restriction of allergen challenge to pulmonary but not nasal airways was associated with a smaller increase in ENO compared with allergen challenge to both. Hence, ENO can now be reliably measured in mice independent of ambient NO levels and is a valid biomarker for AI. However, nasal and pulmonary airways are likely to be independent sources of ENO, and any results must be interpreted as such.

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Increased Nitric Oxide in the Exhaled Air of Patients with Decompensated Liver Cirrhosis

Annals of Internal Medicine ◽

10.7326/0003-4819-123-2-199507150-00005 ◽

1995 ◽

Vol 123 (2) ◽

pp. 110 ◽

Cited By ~ 68

Author(s):

Akihiro Matsumoto

Keyword(s):

Nitric Oxide ◽

Liver Cirrhosis ◽

Decompensated Liver Cirrhosis ◽

Exhaled Air

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Abnormal Modulation of Cholinergic Neurotransmission by Endogenous Nitric Oxide in the Bronchus of Rats with Hyperresponsiveness Induced by Allergen Challenge

The Japanese Journal of Pharmacology ◽

10.1254/jjp.60.125 ◽

1997 ◽

Vol 73 (2) ◽

pp. 125-132

Author(s):

Miwa Misawa ◽

Junya Sato

Keyword(s):

Nitric Oxide ◽

Allergen Challenge ◽

Cholinergic Neurotransmission ◽

Endogenous Nitric Oxide

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Association of Indoor Air Pollution with Rhinitis Symptoms, Atopy and Nitric Oxide Levels in Exhaled Air

International Archives of Allergy and Immunology ◽

10.1159/000316352 ◽

2010 ◽

Vol 153 (4) ◽

pp. 403-412 ◽

Cited By ~ 17

Author(s):

Lars-Georg Hersoug ◽

Lise Lotte N. Husemoen ◽

Simon Francis Thomsen ◽

Torben Sigsgaard ◽

Betina H. Thuesen ◽

...

Keyword(s):

Nitric Oxide ◽

Air Pollution ◽

Indoor Air ◽

Indoor Air Pollution ◽

Exhaled Air

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Inhibition of nitric oxide synthesis attenuates thermally induced asthma

Journal of Applied Physiology ◽

10.1152/jappl.2001.91.2.703 ◽

2001 ◽

Vol 91 (2) ◽

pp. 703-708 ◽

Cited By ~ 10

Author(s):

C. Kotaru ◽

M. Skowronski ◽

A. Coreno ◽

E. R. McFadden

Keyword(s):

Nitric Oxide ◽

Minute Ventilation ◽

Isotonic Saline ◽

Forced Expiratory Volume ◽

Response Curves ◽

Thermally Induced ◽

Stimulus Response ◽

Fractional Concentration ◽

Exhaled Air ◽

The Right

To determine whether the inhibition of nitric oxide (NO) synthesis attenuates thermally induced obstruction, we had 10 asthmatic volunteers perform isocapnic hyperventilation with frigid air after inhaling 1 mg of N G-monomethyl-l-arginine (l-NMMA) or isotonic saline in a blinded fashion. The challenges were identical in all respects, and there were no differences in baseline lung function [1-s forced expiratory volume (FEV1); saline 2.8 ± 0.3 liters, l-NMMA 2.9 ± 0.3 liters; P = 0.41] or prechallenge fractional concentration of nitric oxide in the exhaled air (FeNO) [saline 23 ± 6 parts/billion (ppb),l-NMMA 18 ± 4 ppb; P = 0.51]. Neither treatment had any impact on the FEV1, pulse, or blood pressure. After l-NMMA, FeNO fell significantly ( P < 0.0001), the stimulus-response curves shifted to the right, and the minute ventilation required to reduce the FEV1 20% rose 53.5% over control ( P = 0.02). The results of this study demonstrate that NO generated from the airways of asthmatic individuals may play an important role in the pathogenesis of thermally induced asthma.

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