Introduction. The premature baboon is a good model for human neonatal RDS and developing BPD. Studies are conflicting on the stimulatory effect of steroids on surfactant synthesis. We used our new method with stable isotopes to study surfactant metabolism in premature baboons as we did in human preterm infants. Methods. Nine preterm baboons (birth weight 390±40 g) were randomised to receive either 2 doses of prenatal betamethasone or saline, 48 and 24 hours before caesarian section at 125 days gestational age. At birth, 1 dose of surfactant (100 mg/kg) was administered and conventional ventilation initiated. The baboons received a 24 hour[U-13C]glucose infusion (start,t=0) as precursor for synthesis of palmitic acid in surfactant phosphatidylcholine (palm-PC). Blood and tracheal aspirates were obtained to measure 13C-enrichment of plasma glucose and palm-PC, by GC-IRMS. After killing at day 6, alveolar washes and lung homogenates were obtained. From the enrichment-vs-time curve kinetic parameters were calculated. Secretion time is the time to first enrichment in palm-PC, fractional synthetic rate is the percentage of the total surfactant PC pool newly synthesized from glucose per day.Results. See table. The enrichment (in atom percent excess, APE) of palm-PC from the tracheal aspirates, alveolar washes, and lung homogenates was identical in all fractions at killing(0.05±0.02 APE). These enrichments were similar in the control and betamethasone groups. Conclusion. The enrichments of palm-PC in tracheal aspirates reflect surfactant metabolism in the alveolus and lung tissue. The data show that the metabolism of surfactant is a slow process in very premature baboons. We did not find a significant increase in surfactant synthesis and turnover after prenatal betamethasone. Early effects after birth cannot be excluded as suggested by a significant decrease in secretion time in the betamethasone treated group.

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