Strain dependence of the airway response  to dry-gas hyperpnea challenge in the rat

Yang, Xiaofeng; Powell, William S.; Xu, Lijing; Martin, James G.

doi:10.1152/jappl.1999.86.1.152

Cited by 4 publications

(3 citation statements)

References 36 publications

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“…It has been previously demonstrated that pulmonary resistance in response to dry-gas hyperpnea challenge is increased in BN rats compared with ACI, L, and Fischer 344 rats and is associated with the release of tachykinins and cysteinyl leukotrienes (32). Although levels of these proteins were not measured in the present study, we have observed significantly elevated levels of cysteinyl leukotrienes in HDM-allergic BN rats exposed to diesel exhaust particles (unpublished observation).…”

Section: Discussioncontrasting

confidence: 48%

Phenotypic comparison of allergic airway responses to house dust mite in three rat strains

Singh

Daniels

Winsett

et al. 2003

American Journal of Physiology-Lung Cellular and Molecular Phys

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Brown Norway (BN) rats develop a robust response to antigens in the lung, characterized by a large increase in allergen-specific immune function and pulmonary eosinophilia. The objective of this study was to investigate alternative models by determining whether other rat strains could be sensitized to house dust mite (HDM) antigen and whether the allergic disease process could be worsened with repeated allergen exposure. In general, BN rats sensitized by either subcutaneous or intratracheal routes exhibited increased pulmonary allergy compared with Sprague-Dawley (SD) and Lewis (L) rats. Multiple intratracheal allergen exposures incrementally increased HDM-specific immune function in BN rats but progressively decreased eosinophil recruitment and markers of lung injury. SD rats had more moderate responses, whereas L rats were relatively unresponsive. Because BN rats developed stronger clinical hallmarks of allergic asthma under various immunization regimes compared with SD and L rats, we conclude that the BN is the most appropriate strain for studying allergic asthma-like responses in rats. Phenotypic differences in response to HDM were associated with differences in the Th1/Th2 cytokine balance and antioxidant capacity.

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Section: Discussioncontrasting

confidence: 48%

Phenotypic comparison of allergic airway responses to house dust mite in three rat strains

Singh

Daniels

Winsett

et al. 2003

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…The same doses of SR-48968 and L-732138 almost completely prevented the increase in RL evoked by bolus intravenous injection of neurokinin A (NKA; 0.2 M, 0.15 ml) and substance P (SP; 0.2-0.5 M, 0.15 ml) in anesthetized rats: the peak ⌬RL values (above the baseline) after NKA injection were 137 Ϯ 31% before and 24 Ϯ 4% (P Ͻ 0.01, n ϭ 5) after the pretreatment with SR-48968 and L-732138, and the peak ⌬RL values after SP injection were 29 Ϯ 3% before and 16 Ϯ 2% (P Ͻ 0.05, n ϭ 5) after the pretreatment with SR-48968 and L-732138. These results are in agreement with the effective blocking doses of these NK receptor antagonists reported in the literature (25,45).…”

Section: Seriessupporting

confidence: 92%

Bronchoconstriction induced by increasing airway temperature in ovalbumin-sensitized rats: role of tachykinins

Hsu

Lin

et al. 2013

Journal of Applied Physiology

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Hsu CC, Lin RL, Lin YS, Lee LY. Bronchoconstriction induced by increasing airway temperature in ovalbumin-sensitized rats: role of tachykinins. J Appl Physiol 115: 688 -696, 2013. First published July 11, 2013 doi:10.1152/japplphysiol.00491.2013.-This study was carried out to determine the effect of allergic inflammation on the airway response to increasing airway temperature. Our results showed the following: 1) In Brown-Norway rats actively sensitized by ovalbumin (Ova), isocapnic hyperventilation with humidified warm air (HWA) for 2 min raised tracheal temperature (Ttr) from 33.4 Ϯ 0.6°C to 40.6 Ϯ 0.1°C, which induced an immediate and sustained (Ͼ10 min) increase in total pulmonary resistance (RL) from 0.128 Ϯ 0.004 to 0.212 Ϯ 0.013 cmH2O·ml Ϫ1 ·s (n ϭ 6, P Ͻ 0.01). In sharp contrast, the HWA challenge caused the same increase in Ttr but did not generate any increase in RL in control rats.2) The increase in RL in sensitized rats was reproducible when the same HWA challenge was repeated 60 -90 min later. 3) This bronchoconstrictive effect was temperature dependent: a slightly smaller increase in peak T tr (39.6 Ϯ 0.2°C) generated a significant but smaller increase in RL in sensitized rats. 4) The HWA-induced bronchoconstriction was not generated by the humidity delivered by the HWA challenge alone, because the same water content delivered by saline aerosol at room temperature had no effect. 5) The HWA-evoked increase in RL in sensitized rats was not blocked by atropine but was completely prevented by pretreatment either with a combination of neurokinin (NK)-1 and NK-2 antagonists or with formoterol, a ␤ 2 agonist, before the HWA challenge. This study showed that increasing airway temperature evoked a pronounced and reversible increase in airway resistance in sensitized rats and that tachykinins released from the vagal bronchopulmonary C-fiber endings were primarily responsible. vagus; reflex; hyperthermia; extravasation; asthma BODY TEMPERATURE INCREASES as a result of elevated metabolic rate or hindered heat dissipation. Although the lungs are enclosed in the thoracic chamber and constantly exposed to body temperature, an increase in lung temperature can occur under both normal and pathophysiological conditions. For example, body core temperature exceeding 41°C has been reported in healthy humans and animals during exertional exercise (7, 30). Body temperature higher than 40.5°C occurs frequently in patients suffering from severe fever or heatstroke (5). In addition, tissue inflammation can lead to an increase in local temperature in the inflamed area (16,38). Indeed, a recent report showed that the end-expiratory temperature plateau was 2.7°C higher in mild allergic asthmatic children than in healthy children, and the difference was closely correlated with the exhaled nitric oxide concentration as well as the sputum eosinophil percentage, suggesting an involvement of local tissue inflammation (37).A recent study in our lab reported that an increase in intrathoracic temperature to above a threshold of ϳ39.2°...

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“…The mediation of HIB by leukotrienes has been demonstrated pharmacologically using leukotriene-receptor antagonists (8,25,27,29,30,43,44) and biosynthesis inhibitors (28,31,55). Similar results have been reported for several animal models, including rats (61), guinea pigs (22,24,60), and dogs (39). In contrast to leukotrienes, the mediation of HIB by prostanoids has received little attention.…”

mentioning

confidence: 72%

Eicosanoid and muscarinic receptor blockade abolishes hyperventilation-induced bronchoconstriction

Freed

McCulloch

Wang

2000

Journal of Applied Physiology

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This study was designed to test the hypothesis that hyperventilation-induced bronchoconstriction (HIB) results from the combined effects of prostanoid and leukotriene metabolism. A bronchoscope was used in anesthetized dogs to record peripheral airway resistance and HIB before and after combined treatment with inhibitors of cyclooxygenase (indomethacin) and 5-lipoxygenase (MK-0591). Bronchoalveolar lavage fluid (BALF) cells and mediators from hyperventilated and control airways were also measured. Pretreatment with MK-0591 and indomethacin significantly attenuated, but did not abolish, HIB. However, addition of atropine nearly eliminated the residual response. Blockade of eicosanoid metabolism markedly reduced the concentrations of eicosanoids recovered in BALF after hyperventilation. Positive correlations between posthyperventilation BALF prostanoid and epithelial cell concentrations are suggestive of mucosal injury-induced mediator production and release. We conclude that HIB is prevented in the presence of eicosanoid and muscarinic-receptor blockade and that both classes of eicosanoids contribute similarly to the development of HIB.

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Strain dependence of the airway response to dry-gas hyperpnea challenge in the rat

Cited by 4 publications

References 36 publications

Phenotypic comparison of allergic airway responses to house dust mite in three rat strains

Phenotypic comparison of allergic airway responses to house dust mite in three rat strains

Bronchoconstriction induced by increasing airway temperature in ovalbumin-sensitized rats: role of tachykinins

Eicosanoid and muscarinic receptor blockade abolishes hyperventilation-induced bronchoconstriction

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