ASSOCIATION OF PULMONARY INFLAMMATION AND INCREASED MICROVASCULAR PERMEABILITY DURING THE DEVELOPMENT OF BRONCHOPULMONARY DYSPLASIA - A SEQUENTIAL-ANALYSIS OF INFLAMMATORY MEDIATORS IN RESPIRATORY FLUIDS OF HIGH-RISK PRETERM NEONATES

Objectives. Bronchopulmonary dysplasia (BPD) of preterm neonates is as sociated with an increased recruitment of inflammatory cells into the airways. To evaluate further the role of inflammation in the pathogene sis of BPD, tracheobronchial aspirate fluid of neonates with birth wei ght < 1200 g (n = 59) was sequentially analyzed in a prospective study . Methods. Tracheobronchial aspirate fluid was assessed for chemotacti c activity, neutrophil cell count, concentrations of elastase-alpha(1) -proteinase inhibitor and activity of free elastase, concentrations of chemoattractants (complement component C5-derived anaphylatoxin, leuk otrien B-4, interleukin-8), and albumin concentrations as well as alph a(1)-proteinase inhibitor activity. The secretory component for immuno globulin A was used as reference protein. Only specimens without evide nce of microbiological colonization were studied. Results. In neonates with prolonged respiratory disease (BPD-risk neonates, n = 24, fracti on of inspired oxygen greater than or equal to 0.3 and/or peak inspira tory pressure greater than or equal to 16 cm H2O at day 10 postnatal a ge, birth weight 892 +/- 36 g, gestational age 27.2 +/- 0.3 weeks) che motactic activity, cell count, concentrations of the chemoattractants complement component C5-derived anaphylatoxin, leukotriene B-4, interl eukin-8, as well as levels of elastase-alpha(1)-proteinase inhibitor w ere significantly higher at day 10 and/or day 15 of postnatal age comp ared with neonates without chronic pulmonary disease (total n = 35; da y 10, n = 11; day 15, n = 8). There was no difference in free elastoly tic activity. Concentrations of albumin as well as alpha(1)-proteinase inhibitor activity were higher in BPD-risk patients on day 15, indica ting an increased pulmonary leak. Conclusion. We conclude that preterm neonates at risk for the development of BPD show an enhanced inflamma tory reaction in the lungs and an associated increase in pulmonary mic rovascular permeability. We speculate that inflammation may play an im portant role in the pathogenesis of BPD.