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Báo cáo y học: " Detrimental effects of albuterol on airway responsiveness requires airway inflammation and is independent of b-receptor affinity in murine models of asthma"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài:" Detrimental effects of albuterol on airway responsiveness requires airway inflammation and is independent of b-receptor affinity in murine models of asthma. | Lundblad et al. Respiratory Research 2011 12 27 http respiratory-research.eom content 12 1 27 RESPIRATORY RESEARCH RESEARCH Open Access Detrimental effects of albuterol on airway responsiveness requires airway inflammation and is independent of b-receptor affinity in murine models of asthma Lennart KA Lundblad Lisa M Rinaldi Matthew E Poynter Erik P Riesenfeld Min Wu Steven Aimi Leesa M Barone2 Jason HT Bates Charles G Irvin Abstract Background Inhaled short acting b2-agonists SABA e.g. albuterol are used for quick reversal of bronchoconstriction in asthmatics. While SABA are not recommended for maintenance therapy it is not uncommon to find patients who frequently use SABA over a long period of time and there is a suspicion that long term exposure to SABA could be detrimental to lung function. To test this hypothesis we studied the effect of long-term inhaled albuterol stereoisomers on immediate allergic response IAR and airway hyperresponsiveness AHR in mouse models of asthma. Methods Balb C mice were sensitized and challenged with ovalbumin OVA and then we studied the IAR to inhaled allergen and the AHR to inhaled methacholine. The mice were pretreated with nebulizations of either racemic RS -albuterol or the single isomers S - and R -albuterol twice daily over 7 days prior to harvest. Results We found that all forms of albuterol produced a significant increase of IAR measured as respiratory elastance. Similarly we found that AHR was elevated by albuterol. At the same time a mouse strain that is intrinsically hyperresponsive A J mouse was not affected by the albuterol isomers nor was AHR induced by epithelial disruption with Poly-L-lysine affected by albuterol. Conclusions We conclude that long term inhalation treatment with either isomer of albuterol is capable of precipitating IAR and AHR in allergically inflamed airways but not in intrinsically hyperresponsive mice or immunologically naive mice. Because S -albuterol which lacks affinity for the b2-receptor .