Despite changes in the epidemiology of bronchopulmonary dysplasia (BPD), longer-term morbidity, particularly in the form of airway dysfunction, remains a substantial problem in former preterm infants. The stage for this respiratory morbidity may begin as early as the transition from fetal to neonatal life. Newer therapeutic approaches for BPD should be directed toward minimizing this longer-term respiratory morbidity. Neonatal animal models focused primarily on hyperoxic exposure may provide important insights into the pathogenesis of longer-term airway hyperreactivity in this population.
Copyright © 2012 S. Karger AG, Basel.