Abstract 1371 Poster Session IV, Tuesday, 5/4 (poster 292)

Preterm infants born to women with clinical amnionitis may have a decreased incidence of Respiratory Distress Syndrome (RDS). We recently found that exposure to an inflammatory stimulus (endotoxin) prior to delivery leads to significantly improved lung function in preterm sheep. We wished to examine whether this functional improvement could be attributed to morphologic changes in the lung parenchyma. Methods: Date-bred Merino ewes received 4ml (5mg/ml) of E. Coli endotoxin (n=10) or saline (n=5) by ultrasound guided intra-amniotic injection at 119 days gestation. Comparison ewes received 0.5 mg/kg betamethasone (n=10) or saline (n=9) by maternal IM injection at 118 days. Lambs were delivered by cesarean section at 125 days (term = 150 days). The right cranial lobe was inflation fixed at 30 cmH2O for morphometric assessments. Volume fraction of parenchyma (PF), non-parenchyma (NPF; conducting airways and blood vessels), pleura (PLF) and interlobular septa (ISF) were estimated from photographic enlargements of 5µm sections. Mean alveolar wall thickness (TD), and mean linear intercept (MLI), which provides an indication of alveolar size, were estimated by point and intercept counting. Results: Intraamniotic endotoxin led to maturational changes in lung structure, characterized by an increase in PF and a loss of interstitium as indicated by a decrease in TD, ISF and PLF. Maternal betamethasone treatment led to changes which were qualitatively similar, although generally more pronounced. Conclusions: Fetal exposure to intraamniotic significant maturational changes in lung structure which may partly account for the improvement in lung function. The structural changes induced by intraamniotic endotoxin resemble those induced by maternal betamethasone treatment. (Table)

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