Regional Neonatal Associates for cooperative study of platelet-activating factor (PAF). Summary report

Lipid inflammatory mediators are thought to play an important role in the pathogenesis of the respiratory distress syndrome, including neonatal lung injury and bronchopulmonary dysplasia (BPD). One such mediator is platelet-activating factor (PAF), a potent bioactive phospholipid that induces adverse airway, vascular, and microcirculatory responses. To study the role of PAF in neonatal lung disease, we used an {sup 125}I-radioimmunoassay to measure PAF in whole blood and tracheal lavage in very low birthweight infants at 1, 3, 5, 9, 21 and 28 days after birth. PAF was found in the pulmonary lavagate and blood of ventilated infants as early as one day after birth. Lavagate levels of PAF increased with acute injury (pneumothorax, pneumonia) but were not associated with BPD. Our results indicate PAF could be associated with the pathogenesis of BPD. We suggest that as a consequence of the pathophysiologic processes associated with BPD, PAF is released by pulmonary cells. Our preliminary data indicate that low birthweight infants also have lower PAF acetylhydrolase levels in cord blood and tracheal lavagate as compared to adults. Therefore, it is possible the increased levels of PAF in the blood of low birthweight infants might be due to persistent transient increases in PAF alveolar levels coupled with lower blood acetylhydrolase activities and could be important in the development of symptoms associated with BPD. Future plans for this project call for completing the enzymatic study of acetylhydrolase activity in pulmonary lavage of the BPD infants