Mechanisms initiating lung injury in the preterm

Bronchopulmonary dysplasia (BPD)/chronic lung disease occurs primarily in v ery low birth weight infants (VLBW) often without antecedent severe respira tory distress syndrome. The BPD in these VLBW infants results in less fibro sis than the traditional BPD but the normal process of alveolarization seem s to be disrupted. This review develops the thesis that BPD in VLBW infants results from inflammatory mediators interfering with the singaling require d for normal late gestational lung development. Proinflammatory mediators m ay be elevated because of fetal exposure, postnatal infection or by release form preterm lungs ventilated at either low or high lung volumes. The pret erm lung is highly susceptible to injury resuscitation or more chronic mech anical ventilation because the gas volumes/kg body weight of the lungs are small. An understanding of what causes cytokine release and how cytokines i nfluence lung development is necessary to develop targeted therapies to min imize BPD. However, care strategies that minimize inflammation and ventilat or-induced lung injury should Help decrease BPD. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.