Effects of chronic <scp>l</scp>-NAME treatment lung tissue mechanics, eosinophilic and extracellular matrix responses induced by chronic pulmonary inflammation

Angeli, Patricia; Prado, Carla M.; Xisto, Débora G.; Silva, Pedro L.; Pássaro, Caroline P.; Nakazato, Hugo D.; Leick-Maldonado, Edna A.; Martins, Mílton A.; Rocco, Patrícia Rieken Macêdo; Tibério, Iolanda F.L.C.

doi:10.1152/ajplung.00199.2007

Cited by 54 publications

(91 citation statements)

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“…This was associated with an increase in lung tissue inflammation, mainly characterised by eosinophils, and a repair process due to a deposition of collagen fibres in alveolar septa [9,10] .…”

Section: Discussionmentioning

confidence: 99%

“…Adrenal glands were dissected, removed and weighted. After thoracotomy, the heart and lungs were excised en bloc, and the lungs were subjected to oscillatory mechanics evaluation as previously described [10,11] . Briefly, lungs were infused with Krebs solution (Sigma Chemical).…”

Section: Oscillatory Mechanics Evaluationmentioning

confidence: 99%

“…We analysed the percentage of increase in the resistance (%R), elastance (%E) and hysteresivity in relation to baseline [10,11] . After mechanical oscillation, the strips were fixed in 10% formalin for 48 h and embedded in paraffin for histological analysis.…”

Section: Oscillatory Mechanics Evaluationmentioning

confidence: 99%

“…NO derived from the constitutive isoforms (neuronal NOS and endothelial NOS) and other NO-adduct molecules (nitrosothiols) are capable of protecting the lung, reducing the constriction of airways and the distal lung [10,29,30] . However, Prado et al [31] showed that inducible NO synthase (iNOS)-derived NO contributes to bronchoconstriction, airway inflammation and remodelling.…”

mentioning

confidence: 99%

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Inducible Nitric Oxide Synthase Inhibition Attenuates Physical Stress-Induced Lung Hyper-Responsiveness and Oxidative Stress in Animals with Lung Inflammation

Marques

Reis²,

Starling³

et al. 2012

Neuroimmunomodulation

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Mechanisms involved in stress-induced asthmatic alterations have been poorly characterised. We assessed whether inducible nitric oxide synthase (iNOS) inhibition modulates the stress-amplified lung parenchyma responsiveness, oxidative stress and extracellular matrix remodelling that was previously increased by chronic lung inflammation. Guinea pigs were subjected to 7 exposures to ovalbumin (1–5 mg/ml) or saline (OVA and SAL groups) over 4 weeks. To induce behavioural stress, animals were subjected to a forced swimming protocol (5 times/week, over 2 weeks; SAL-Stress and OVA-Stress groups) 24 h after the 4th inhalation. 1400W (iNOS-specific inhibitor) was administered intraperitoneally in the last 4 days of the protocol (SAL-1400W, OVA-1400W, SAL-Stress+1400W and OVA-Stress+1400W groups). Seventy-two hours after the last inhalation, animals were anaesthetised and exsanguinated, and adrenal glands were removed. Lung tissue resistance and elastance were evaluated by oscillatory mechanics and submitted for histopathological evaluation. Stressed animals had higher adrenal weights compared to non-stressed groups, which were reduced by 1400W treatment. Behavioural stress in sensitised animals amplified the resistance and elastance responses after antigen challenge, numbers of eosinophils and iNOS+ cells, actin content and 8-iso-PGF2α density in the distal lung compared to the OVA group. 1400W treatment in ovalbumin-exposed and stressed animals reduced lung mechanics, iNOS+ cell numbers and 8-iso-PGF2α density compared to sensitised and stressed animals that received vehicle treatment. We concluded that stress amplifies the distal lung constriction, eosinophilic inflammation, iNOS expression, actin content and oxidative stress previously induced by chronic lung inflammation. iNOS-derived NO contributes to stress-augmented lung tissue functional alterations in this animal model and is at least partially due to activation of the oxidative stress pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Oscillatory Mechanics Evaluationmentioning

confidence: 99%

Section: Oscillatory Mechanics Evaluationmentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Inducible Nitric Oxide Synthase Inhibition Attenuates Physical Stress-Induced Lung Hyper-Responsiveness and Oxidative Stress in Animals with Lung Inflammation

Marques

Reis²,

Starling³

et al. 2012

Neuroimmunomodulation

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“…The importance of NO in regulating lung collagen content was supported in a guinea pig model of ongoing asthma. Thus, the allergen-induced collagen deposition around non-cartilaginous airways [156], but not in the alveolar septa [157] was further increased by chronic treatment with the NOS inhibitor L-NAME. Moreover, increased deposition of collagen in the lung has been observed in allergen-challenged NOS2 -/-mice compared to allergen-challenged wild types [158].…”

Section: Arginase In Chronic Airway Remodelingmentioning

confidence: 94%

Arginase in Asthma Recent Developments in Animal and Human Studies~!2009-11-12~!2010-03-23~!2010-05-04~!

North¹,

Zaagsma²,

Scott³

et al. 2010

TONOJ

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Abstract:The enzyme, arginase, converts L-arginine into L-ornithine and urea, and has been implicated in the pathogenesis of lung diseases, related to dysregulation of L-arginine metabolism and remodeling. Allergic asthma is a chronic condition characterized by inflammation, lung remodeling and airways hyperresponsiveness (AHR). Increased expression of arginase may contribute to AHR in asthma by reducing L-arginine bioavailability for the nitric oxide synthase (NOS) isozymes, thus, limiting the production of the endogenous bronchodilator, nitric oxide (NO). Reduction of intracellular L-arginine concentrations as a consequence of augmented arginase expression and activity may also promote NOS uncoupling, resulting in increased formation of peroxynitrite, a powerful oxidant that promotes bronchoconstriction and inflammation. In chronic asthma, increased arginase expression may also contribute to airways remodeling, through increased synthesis of L-ornithine, and hence the production of polyamines and L-proline, which are involved in cell proliferation and collagen deposition, respectively. New drugs targeting the arginase pathway could have therapeutic benefits in asthma. This review focuses on recent developments in our understanding of the role of arginase in AHR, inflammation and remodeling, highlighting studies that advance our knowledge of L-arginine dysregulation in human asthma and animal studies that explore the therapeutic potential of arginase inhibition.

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RETRACTED ARTICLE: The role of nitric oxide during healing of trauma to the skeletal muscle

et al. 2010

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Effects of chronic l-NAME treatment lung tissue mechanics, eosinophilic and extracellular matrix responses induced by chronic pulmonary inflammation

Abstract: Angeli P, Prado CM, Xisto DG, Silva PL, Pá ssaro CP, Nakazato HD, Leick-Maldonado EA, Martins MA, Rocco PR, Tibério IF. Effects of chronic L-NAME treatment lung tissue mechanics, eosinophilic and extracellular matrix responses induced by chronic pulmonary inflammation.

Cited by 54 publications

References 41 publications

Inducible Nitric Oxide Synthase Inhibition Attenuates Physical Stress-Induced Lung Hyper-Responsiveness and Oxidative Stress in Animals with Lung Inflammation

Inducible Nitric Oxide Synthase Inhibition Attenuates Physical Stress-Induced Lung Hyper-Responsiveness and Oxidative Stress in Animals with Lung Inflammation

Arginase in Asthma Recent Developments in Animal and Human Studies~!2009-11-12~!2010-03-23~!2010-05-04~!

RETRACTED ARTICLE: The role of nitric oxide during healing of trauma to the skeletal muscle

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Effects of chronic l-NAME treatment lung tissue mechanics, eosinophilic and extracellular matrix responses induced by chronic pulmonary inflammation

Abstract: Angeli P, Prado CM, Xisto DG, Silva PL, Pá ssaro CP, Nakazato HD, Leick-Maldonado EA, Martins MA, Rocco PR, Tibério IF. Effects of chronic L-NAME treatment lung tissue mechanics, eosinophilic and extracellular matrix responses induced by chronic pulmonary inflammation.

Cited by 54 publications

References 41 publications

Inducible Nitric Oxide Synthase Inhibition Attenuates Physical Stress-Induced Lung Hyper-Responsiveness and Oxidative Stress in Animals with Lung Inflammation

Inducible Nitric Oxide Synthase Inhibition Attenuates Physical Stress-Induced Lung Hyper-Responsiveness and Oxidative Stress in Animals with Lung Inflammation

Arginase in Asthma  Recent Developments in Animal and Human Studies~!2009-11-12~!2010-03-23~!2010-05-04~!

RETRACTED ARTICLE: The role of nitric oxide during healing of trauma to the skeletal muscle

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Arginase in Asthma Recent Developments in Animal and Human Studies~!2009-11-12~!2010-03-23~!2010-05-04~!