MECONIUM INDUCED INJURY IN THE RAT ALTERS SURFACTANT DISTRIBUTION AND COMPOSITION. † 1197

Abstract

Meconium aspiration syndrome (MAS) remains a common cause of respiratory failure in neonates resulting from lung injury with surfactant inhibition. In this study we examined the effect of meconium injury on alveolar surfactant phospholipids (PL) and proteins over 72 hours in spontaneously breathing animals. Twenty two adult rats were given 4.5 mg dry weight human meconium as a 20% slurry after endotracheal intubation. Rats were mechanically ventilated in room air briefly (5-10 minutes) and extubated to spontaneously breathe room air. They were sacrificed at 16 (n=5), 24 (n=6), 48 (n=7) and 72 hrs (n=4). Healthy control animals (n=7) received no meconium. Lavages (BAL) were obtained from excised lungs and sequentially centrifuged for isolation of cells (Cell Ct × 106), then large (Lag) and small (Sag) surfactant aggregates. The mean ± SE for BAL total protein (mg), total PL (mg), and Dipalmitoylphosphatidylcholine (DPPC, mg) in Lag and Sag were:Table Western blot and immunoblot analysis demonstrated semi-quantitative increases in surfactant proteins A and B compared to controls at 16 and 24 hours. This suggests that meconium injury may have differential effects on surfactant PL and proteins. In this model, meconium instillation resulted in reversible injury with exudative changes preceding alterations in surfactant composition. We speculate that surfactant inhibition in MAS may be partially attributed to exudative lung injury resulting in accelerated surfactant PL metabolism.