Bronchopulmonary Dysplasia: The Role of Oxidative Stress

Prior to the era of mechanical ventilation, few infants of very low birth weight (less than 1500 g) survived, and neonatal mortality for extremely low birth weight infants (less than 1000 g) exceeded 90% Most survivors required little or no oxygen supplementation initially but later deteriorated to requirements of up to 40% in order to prevent cyanosis. On radiography, findings included microcystic changes as well as varying degrees of hyperinflation and flattening of the diaphragm. Some infants recovered spontaneously over weeks to months but others died, with postmortem examination revealing hyperaeration and reduced alveolar septa. Wilson and Mikity in 1960 were the first to describe this chronic pulmonary syndrome, in a case report of five very small preterm survivors At that time, assisted ventilation was not used in preterm infants. An additional 29 babies with Wilson-Mikity syndrome (WMS) were identified at the same medical institution in 1969 After the introduction of mechanical ventilation to manage respiratory distress syndrome in the mid-1960s, reports began to appear of radiographic and pathological abnormalities that www.intechopen.com Lung Diseases -Selected State of the Art Reviews 486 seemed to result from exposure to high concentrations of oxygen and mechanical ventilation. In 1967, Northway et al. coined the term "bronchopulmonary dysplasia" to describe findings of pulmonary complications following respiratory therapy for hyaline membrane disease Northway et al. believed the critical factor to be exposure to an inspired oxygen concentration > 80% for longer than 150 hours. The 1990s saw major changes in both obstetric and neonatal care for preterm labour, with surfactant administration and assisted ventilation. The outcome of most preterm infants improved in the first half of the decade, particularly for infants with very low birth weight, who benefitted from decreased mortality and morbidity Following these changes, classical BPD, which occurred as a result of injury to the immature lung, became less common. Chronic lung disease in preterm infants became increasingly attributable to the response of the immature lung to early air breathing rather than to damage from barotrauma or oxygen toxicity. In 1999, Jobe described the "new" BPD as occurring in immature infants who did not have extensive lung disease soon after birth Jobe attributed the "new" BPD to pulmonary anomalies resulting from an inhibition of alveolar and vascular development

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