Dual action of nitric oxide on airway plasma leakage.

Bernareggi, Micaela; Mitchell, Jane A.; Barnes, Peter J.; Belvisi, Maria G.

doi:10.1164/ajrccm.155.3.9117019

Cited by 84 publications

(31 citation statements)

References 34 publications

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“…1b), the animals in both the L-NA and control situations showed a rapid increase in Raw. L-NA did not change the airway reactivity to histamine challenge, which is also indicated by the areas under the curves, 0±75 min, which were 1,150247 cmH 2 …”

Section: Bronchial Reactivitymentioning

confidence: 59%

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Nitric oxide synthase inhibition augments acute allergic reactions in the pig airways in vivo

Middelveld¹,

Zetterquist²,

Bergman³

et al. 2000

Eur Respir J

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The aim of this study was to examine the effects of nitric oxide synthase inhibition on antigen-and histamine-induced acute airway reactions, in order to clarify the possible modulating role of NO.Twelve specific-pathogen-free pigs (sensitized with Ascaris suum antigen) were challenged with an antigen aerosol during mechanical ventilation and anaesthesia. Six pigs were pretreated with), a NO synthase inhibitor, 30 min before challenge. In separate experiments, seven sensitized pigs received histamine (5 mg) aerosols before and after L-NA treatment.It was found that pretreatment with L-NA resulted in an enhanced airways resistance response to antigen (areas under the curve 0±90 min were (meanSEM) 1,119160 versus 55556 (cmH 2 O . L -1 . s -1 . min for controls, p<0.05 (Mann-Whitney Utest), whereas this response to histamine was not affected by L-NA. Moreover, L-NA pretreatment significantly enhanced total protein (1.850.43 versus 0.310.06 g . L -1 , p<0.01) and histamine levels (42.816.0 versus 2.60.8 nM, p<0.05) in bronchoalveolar lavage fluid 45 min after antigen challenge.In conclusion, this study showed that N G -nitro-L-arginine enhanced reactions occurring during the acute allergic reaction in pigs in vivo. This indicates a protective role of nitric oxide, which might occur through downregulation of histamine release from mast cells rather than a direct bronchodilating effect of nitric oxide. Eur Respir J 2000; 16: 836±844.

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Section: Bronchial Reactivitymentioning

confidence: 59%

“…There is increasing evidence that endogenously produced NO has effects on the airways that can be either favourable or deleterious depending on the type of NOS that is activated [2].…”

mentioning

confidence: 99%

Nitric oxide synthase inhibition augments acute allergic reactions in the pig airways in vivo

Middelveld¹,

Zetterquist²,

Bergman³

et al. 2000

Eur Respir J

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“…Furthermore, NOS inhibitors such as L-NAME increase vascular resistance, and despite any increase in blood pressure, this could in some vascular beds lead to a reduced perfusion pressure, which in turn would mitigate edema formation. In fact, we have previously demonstrated that L-NAME increases plasma leakage under normal conditions (Bernareggi et al, 1997).…”

Section: Role Of No In Airway Inflammation In Rats 1289mentioning

confidence: 93%

Pharmacological Assessment of the Nitric-Oxide Synthase Isoform Involved in Eosinophilic Inflammation in a Rat Model of Sephadex-Induced Airway Inflammation

Birrell

McCluskie²,

Haddad³

et al. 2003

The Journal of Pharmacology and Experimental Therapeutics

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Excessive local production of nitric oxide (NO) has been suggested to play a role in rodent models of airway inflammation and in pulmonary diseases such as asthma. However, even given the plethora of data available including gene expression data, pharmacological data, and gene deletion studies in animal models, it is still not clear which nitric-oxide synthase (NOS) isoform is involved in eosinophilic airway inflammation. In this rat study, the nonselective NOS inhibitor L-NAME (N G -nitro-L-arginine methyl ester), but not a selective inducible NOS (iNOS) inhibitor 1400W (N-3-(aminomethyl)benzyl)acetamidine), impacted on Sephadex-induced inflammation by significantly inhibiting lung edema, eosinophil infiltration, tumor necrosis factor ␣, interleukin-13, and eotaxin levels in the lung tissue. Furthermore, iNOS gene expression was not induced following Sephadex administration, which confirms that iNOS does not play a role in this model. To demonstrate that this phenomenon was not restricted to this model of asthma, L-NAME, but not 1400W, was shown to reduce eosinophilia in an antigen-induced model. However, in contrast to the Sephadex model, there was an induction of iNOS gene expression after antigen challenge. In a model of aerosolized lipopolysaccharide-induced inflammation, where iNOS gene expression is increased, 1400W inhibited the increased neutrophilia. These data suggest that the compound has been administered using an appropriate dosing regimen for iNOS inhibition in the rat lung. In conclusion, it appears that constitutive, not inducible, NOS isoforms are important in NO production in models of allergic inflammation, which questions whether there is a role for iNOS inhibitors as therapy for the treatment of asthma.

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“…Airway plasma extravasation was assessed using Evans blue dye, as employed in many previous studies [13][14][15][16].…”

Section: Effect Of Pacap On Airway Plasma Extravasationmentioning

confidence: 99%

Pituitary adenylate cyclase activating peptide regulates neurally mediated airway responses

Shigyo¹,

Aizawa²,

Inoue³

et al. 1998

Eur Respir J

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Pituitary adenylate cyclase activating peptide (PACAP) is a vasoactive intestinal peptide (VIP)-like peptide that has been purified from the ovine hypothalami [1]. PACAP has the same potency as VIP in relaxing airway and vascular smooth muscle [2][3][4][5]. Recently, it has been demonstrated that PACAP induced bronchodilatation in animals treated with histamine or allergen [6]. However, the pathophysiological roles of PACAP in mammalian airways have not been fully elucidated. The structural and functional homology between PACAP and VIP makes it likely that PACAP may participate in the modulation of airway responses in a similar manner to VIP.VIP immunoreactivity is localized to the vagus nerve in the smooth muscle of mammalian airways [7][8][9]. It has been reported that VIP inhibits cholinergic neuroeffector transmission by suppressing acetylcholine (ACh) release from vagal nerve termini [10]. PACAP may have the same effects on cholinergic nerves. It has also been reported that VIP suppresses the smooth muscle contraction evoked by substance P (SP) [11]. SP belongs to the tachykinin family and is released from bronchial C-fibres, causing smooth muscle contraction and plasma extravasation [12].Increased plasma extravasation and smooth muscle contraction mediated by the vagus nerve may contribute to the airway hyperresponsiveness and inflammation observed in asthma. However, it is not known whether SP and PACAP interact.For these reasons, in the present study, we examined the roles of PACAP involved in airway smooth muscle response and plasma extravasation induced by cholinergic and excitatory nonadrenergic noncholinergic (eNANC) nerves in guinea-pigs. Methods Immunohistochemical examinationLungs were dissected out from three guinea-pigs after sacrifice. The specimens were immersed for 12 h in an ice-cold fixative solution composed of 2% formaldehyde buffered to pH 7.2 with 0.1 M phosphate buffer and 0.2% picric acid. They were then rinsed in a Tyrode solution containing 10% sucrose for 48 h, frozen on dry ice, and sectioned by a cryostat at a thickness of 10 µm. Then, they were immersed in sucrose-enriched Tyrode solution for 24-48 h, briefly rinsed in 0.1 M phosphate buffer (pH 7.4), and stretched on chrome-alum subbed glass slides as whole mounts. Cryostat sections and whole mounts were processed for immunohistochemical demonstration of PACAP using an avidin-biotin complex method. The PACAP antiserum (Yanaihara Institute Inc., Shizuoka, Japan) was raised in a rabbit against human PACAP 27 or PACAP 38 and used at a dilution of 1:12,000. The sections were exposed to the peptide antiserum for 4 h at room temperature. The antigen-antibody reaction was demonstrated by application of biotin-labelled anti-rabbit immunoglobulin G (IgG) Smooth muscle contraction evoked by electrical field stimulation (EFS) or exogenously applied acetylcholine (ACh) or substance P (SP) was measured before and after PACAP in vitro. The effect of PACAP on airway plasma extravasation was also measured in vivo.In trachea, PACAP (10 -9 -10 -...

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Dual action of nitric oxide on airway plasma leakage.

Cited by 84 publications

References 34 publications

Nitric oxide synthase inhibition augments acute allergic reactions in the pig airways in vivo

Nitric oxide synthase inhibition augments acute allergic reactions in the pig airways in vivo

Pharmacological Assessment of the Nitric-Oxide Synthase Isoform Involved in Eosinophilic Inflammation in a Rat Model of Sephadex-Induced Airway Inflammation

Pituitary adenylate cyclase activating peptide regulates neurally mediated airway responses

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