Endogenous nitric oxide is decreased in asthmatic patients by an inhibitor of inducible nitric oxide synthase.

Yates, D H; Kharitonov, Sergei A.; Thomas, Paul S.; Barnes, Peter J.

doi:10.1164/ajrccm.154.1.8680689

Cited by 143 publications

(89 citation statements)

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“…In the absence of airway inflammation, FeNO levels represent constitutive NO. 11,22 Subjects with depression also have low levels of plasma and platelet NO. 23,24 The low systemic levels of NO have been postulated to be responsible for the increased risk of cardiovascular events observed in subjects with depression, 24 as NO produces vasodilatation.…”

Section: Discussionmentioning

confidence: 99%

Depression Is Associated With High Levels of C-Reactive Protein and Low Levels of Fractional Exhaled Nitric Oxide

Cepeda¹,

Stang²,

Makadia³

2016

J. Clin. Psychiatry

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Section: Discussionmentioning

confidence: 99%

Depression Is Associated With High Levels of C-Reactive Protein and Low Levels of Fractional Exhaled Nitric Oxide

Cepeda¹,

Stang²,

Makadia³

2016

J. Clin. Psychiatry

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“…Techniques that permit separate measurement of the airway and alveolar components of FeNO would be useful in this context to address the hypothesis that smoking primarily alters airway respiratory epithelial production of FeNO [47]. Experiments using intravenous and inhaled inhibitors of the different isoforms of NOS would also be useful to delineate the relative contributions of neural NOS1, airway NOS2 and vascular NOS3 to the difference in FeNO between older smokers and nonsmokers [15,48].…”

Section: Discussionmentioning

confidence: 99%

“…FeNO levels increase after smoking cessation but not to normal levels [2,6,10], which suggests that smoking-related declines in FeNO may be associated with permanent lung damage. As respiratory epithelium is the likely source of most FeNO [11][12][13][14][15] and is damaged by chronic smoke exposure [16][17][18][19][20], smoking-related declines in FeNO may be a marker of airway epithelial damage.…”

mentioning

confidence: 99%

Smoking is associated with an age-related decline in exhaled nitric oxide

Sundy

Hauswirth²,

Mervin-Blake³

et al. 2007

Eur Respir J

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Age-related declines in forced expiratory volume in one second are accelerated in smokers. Smoking is associated with decreased exhaled nitric oxide fraction (FeNO). The aim of the present study was to determine the impact of age on FeNO in otherwise healthy smokers and nonsmokers.FeNO and serum cotinine levels were measured in 994 healthy subjects aged 18-40 yrs. American Thoracic Society questionnaire data on smoking habits was used to validate serum cotinine levels as a surrogate marker for categorisation of smokers and nonsmokers in the cohort.Serum cotinine levels were a good discriminator of smokers (n599) and nonsmokers (n5895). FeNO levels were significantly lower in otherwise healthy smokers compared with nonsmokers. There was an inverse correlation of serum cotinine levels with FeNO. No correlation of age with FeNO was found in nonsmokers but an inverse correlation of FeNO with age in smokers was found. FeNO was significantly lower in smokers aged 21-40 yrs compared with nonsmokers aged 21-40 yrs, but was not lower in smokers aged 18-20 yrs compared with nonsmokers of the same age.Smoking was associated with decreased exhaled nitric oxide. The greatest smoking-related declines in exhaled nitric oxide occurred in older subjects. This suggests that smoking is associated with age-related declines in exhaled nitric oxide and justifies future mechanistic studies that address the impact of exhaled nitric oxide decline on lung function.

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“…The increased presence of NOS II in the inflamed lung has been shown to contribute to complement-induced pulmonary injury, 40 lung transplant rejection, 41 and airway hyperresponsiveness in asthma. 42,43 Conversely, others 44 have shown that increased nitric oxide production by lung epithelial cells protects these cells from polymorphonuclear-cell-mediated injury. Increased nitric oxide Figure 6.…”

Section: Discussionmentioning

confidence: 99%

Collagen Deposition in a Non-Fibrotic Lung Granuloma Model after Nitric Oxide Inhibition

Hogaboam

Gallinat

Bone-Larson

et al. 1998

The American Journal of Pathology

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Recent studies support the concept that pulmonary granulomatous inflammation directed by interferon (IFN)-␥, interleukin (IL)-12, and nitric oxide usually resolves in the absence of fibrosis. To determine whether nitric oxide participates in modulating the fibrotic response during the development of pulmonary granulomas in response to purified protein derivative (PPD) , mice presensitized to PPD received daily intraperitoneal injections of N G -nitro-D-arginine-methyl ester (D-NAME) , N G -nitro-L-argininemethyl ester (L-NAME) , or aminoguanidine after delivery of PPD-coated beads to the lungs. Eight days later , morphometric analysis of lung granulomas revealed that L-NAME-treated mice when challenged with PPD in vitro for 36 hours had the largest pulmonary granulomas and the greatest collagen deposition among the treated groups. In addition , equivalent numbers of dispersed lung cells from L-NAME-and aminoguanidine-treated mice produced significantly higher levels of IL-4 , monocyte chemoattractant protein (MCP)-1 , and macrophage inflammatory protein (MIP)-1␣ and significantly lower levels of eotaxin compared with D-NAME-treated mice. Cultures of dispersed lung cells from L-NAME-treated mice also produced significantly more IL-10 and less IL-12 compared with similar numbers of dispersed lung cells from D-NAME-treated mice. Cultures of isolated lung fibroblasts from L-NAME-treated mice expressed higher levels of C-C chemokine receptor 2 (CCR2) and CCR3 mRNA and contained less MCP-1 and eotaxin protein than a similar number of fibroblasts from D-NAME-treated mice. Thus , nitric oxide appears to regulate the deposition of extracellular matrix in lung granulomas through the modulation of the cytokine and chemokine profile of these lesions. Alterations in the cytokine , chemokine , and procollagen profile of this lesion may be a direct effect of nitric oxide on the pulmonary fibroblast and provide an important signal for regulating fibroblast activity during the evolu- It is not uncommon for chronic pulmonary granulomatous inflammation to result in irreversible tissue injury and end-stage fibrosis. 1 For reasons that are presently unclear, the reparative process associated with interstitial pulmonary inflammation can progress uncontrollably, as evidenced by increased lung fibroblast proliferation and the deposition of collagenous material. 2 Clinical and laboratory evidence suggest that the progressive and unregulated reparative process in the lung is potentially related to the persistence of a variety of inflammatory signals. 3 Unfortunately, clinical strategies directed at preventing deleterious fibrotic responses through the nonselective inhibition of the inflammatory process with corticosteroid, cyclophosphamide, and azathioprine treatments have been both largely unsuccessful and often associated with severe side effects. 4 Previous studies of experimental, antigen-driven granulomatous pulmonary inflammatory responses has demonstrated that inflammatory cytokine profiles have a major role in the degree of extra...

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Endogenous nitric oxide is decreased in asthmatic patients by an inhibitor of inducible nitric oxide synthase.

Cited by 143 publications

References 0 publications

Depression Is Associated With High Levels of C-Reactive Protein and Low Levels of Fractional Exhaled Nitric Oxide

Depression Is Associated With High Levels of C-Reactive Protein and Low Levels of Fractional Exhaled Nitric Oxide

Smoking is associated with an age-related decline in exhaled nitric oxide

Collagen Deposition in a Non-Fibrotic Lung Granuloma Model after Nitric Oxide Inhibition

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