ABSTRACT
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.
Subject(s)
Bronchial Hyperreactivity/physiopathology , Hyperoxia/metabolism , Mast Cells/physiology , Animals , Animals, Newborn , Anti-Asthmatic Agents/pharmacology , Benzamides , Bronchoconstrictor Agents/pharmacology , Cromolyn Sodium/pharmacology , Female , Imatinib Mesylate , Lung/cytology , Lung/drug effects , Lung/physiology , Mast Cells/drug effects , Methacholine Chloride/pharmacology , Piperazines/pharmacology , Pregnancy , Protein Kinase Inhibitors/pharmacology , Pyrimidines/pharmacology , Random Allocation , Rats , Rats, Sprague-Dawley , RespirationABSTRACT
The rate of methicillin-resistant Staphylococcus aureus (MRSA) infection is increasing in neonatal intensive care units. We determined the economic impact of isolating and cohorting MRSA-colonized neonates on total hospital cost at a 49-bed, level III-IV neonatal intensive care unit.
