Bronchopulmonary dysplasia (BPD) results from arrested lung development in premature infants exposed to supplemental oxygen and mechanical ventilation during the critical period of alveolarization (24-36 weeks gestation). Oxygen-derived free radicals and barotrauma/volutrauma damage the immature alveolar epithelium and inhibit secondary septation, resulting in fewer, larger alveoli with decreased surface area for gas exchange. Pulmonary vascular remodeling causes thickened vessel walls, reduced vascular bed density, and pulmonary hypertension. Chronic inflammation with fibrosis further impairs lung compliance and gas exchange.