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Target Concepts:
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Query: UMLS:C0242706 (
hyperoxia
)
5,219
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Premature infants are at increased risk of developing airway hyper-reactivity (AHR) after oxidative stress and inflammation. Mast cells contribute to AHR partly by mediator release, so we sought to determine whether blocking mast cell degranulation or recruitment prevents
hyperoxia
-induced AHR, mast cell accumulation, and airway smooth muscle (ASM) changes. Rats were exposed at birth to air or 60% O2 for 14 d, inducing significantly increased AHR in the latter group, induced by nebulized methacholine challenge and measured by forced oscillometry. Daily treatment (postnatal d 1-14) with intraperitoneal cromolyn prevented
hyperoxia
-induced AHR, as did treatment with imatinib on postnatal d 5-14, compared with vehicle treated controls.
Cromolyn
prevented mast cell degranulation in the trachea but not hilar airways and blocked mast cell accumulation in the hilar airways. Imatinib treatment completely blocked mast cell accumulation in tracheal/hilar airway tissues.
Hyperoxia
-induced AHR in neonatal rats is mediated, at least in part, via the mast cell.
...
PMID:Mast cells mediate hyperoxia-induced airway hyper-reactivity in newborn rats. 2578 Aug 66