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The present investigation examines the biochemical and physiologic changes produced in fetal rabbit lungs by adding a prostaglandin synthetase inhibitor, sodium indomethacin trihydrate, to the pulmonary perfusate. A control group was similarly perfused without adding indomethacin. The ductus arteriosus was ligated and perfusion was then continued for 2 h while pulmonary artery pressures were monitored. At the end of this period, with perfusion continuing, the lungs were inflated with air at 5 cm H2O increments. Volume changes were recorded. After deflation, the lungs were lavaged with normal saline. Phospholipids were extracted from lung homogenates and lavage. Total lipid phosphorus was determined. Pulmonary vascular resistances in both groups manifested a sharp increase in pressure with ligation of the ductus. After 2 h of perfusion, pulmonary pressures in the control groups had returned very nearly to preligation levels, while in the indomethacin-treated group, pulmonary pressures remained significantly elevated. The first full inflation produced a slight fall in pulmonary vascular resistance in all control animals and a slight rise in all the treated rabbits. Perfused but untreated lungs had higher volumes during inflation as compared to both indomethacin-perfused lungs and unperfused untreated lungs. In this model, prostaglandins appear to have a significant role at two key points in transition: 1) the gradual accommodation to mechanically or hemodynamically mediated increases in pulmonary vascular resistance and 2) the drop in pulmonary vascular resistance which occurs with the first inflation of the lungs. No direct effect of prostaglandin inhibition on surfactant production was documented.

Indomethacin and the Cardiopulmonary Adaptations of Transition