ABSTRACT
The search for the appropriate experimental model for bronchopulmonary dysplasia (BPD) is ongoing owing to the complex multifactorial etiology and pathogenesis of the disease. In this era of prenatal glucocorticoid treatment and postnatal surfactant therapy, disruption of normal intrauterine lung growth yields an increasingly immature lung to which injury is augmented by exposure to oxygen levels above that of the uterine environment; tissue stress, induced by excessive pressure or stretch; and inflammation or infection. Clinicians readily recognize the difference in treating a 24-week-gestation human infant of borderline viability when compared with that of a 30-week-gestation infant. Considerable lung growth and differentiation normally occurs during this gestational period. At 24 weeks, lungs are still in a canalicular stage (1-3); for example, vascular development at the capillary level has been ongoing for only about 6 weeks (3), no alveolar macrophages are present (4), and surfactant secretion is negligible (5). Immaturity of nonpulmonary organ systems, such as the kidney, heart, and gastrointestinal tract, further complicate the pulmonary status of these immature infants. Finally, factors known to initiate preterm deliveries in the human, such as chorioamnionitis and premature rupture of membranes (6-8), probably influence the
*Deceased.
