ABSTRACT
Despite the array of recent improvements in neonatal intensive care, chronic lung disease (CLD) of early infancy, which is often referred to as bronchopulmonary dysplasia (BPD), is still a significant cause of long-term morbidity and mortality in extremely low-birth-weight infants, many of whom have had early respiratory distress syndrome (RDS), sometimes despite prenatal steroid and postnatal surfactant treatments. CLD has a multifactorial etiology. The principal risk factors that have been identified are lung immaturity, barotrauma, and overdistended airspaces from positive-pressure ventilation, and oxygen administration. Nevertheless, the exact mechanisms that lead to lung injury and hinder healing are incompletely understood. There is growing evidence, however, that repetitive positive-pressure inflation and oxygen toxicity induce a complex inflammatory reaction in the airways and the interstitium of the immature lungs of infants with RDS and CLD (reviewed in Refs. 1-5). This pulmonary inflammation is characterized by an accumulation of various cells and associated release of inflammatory mediators that contribute to increased lung microvascular permeability and tissue injury, with resultant chronic respiratory failure.
