ABSTRACT
Bronchopulmonary dysplasia (BPD) results from acute and chronic interactions between lung developmental, injury, and repair pathways that interfere with airspace septation and microvascular development. The major postnatal associations with BPD in very low birth weight infants are supplemental oxygen, mechanical ventilation, sepsis, and patent ductus arteriosis (1). Other variables that are less defined clinically, but that cause BPD-type changes in animal models, are corticosteroids and nutritional deficiency (2,3). Our thesis is that prenatal exposures can inform us about postnatal associations with BPD. Postnatal associations such as oxygen and mechanical ventilation are complex and interdependent, and similarities with and differences from prenatal exposures can provide some insights into the pathophysiology of BPD. Preterm infants are not born with BPD, but clinical information supports prenatal events as promoting progression to BPD after very preterm birth, suggesting a sequential hit pathophysiology. Studies of prenatal exposures in animal models that may promote BPD are in their infancy compared with postnatal lung injury studies of the pathogenesis of BPD. Our goal is to link prenatal exposures with airway septation abnormalities and abnormal microvascular development.
