Effect of Hydrocortisone on the Metabolism of Phosphatidylcholine in Maternal and Fetal Rabbit Lungs and Livers

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It has been observed that glucocorticoids stimulate fetal lung maturation. This study examined the effects of glucocorticoids on the phosphatidylcholine (PC) metabolism in maternal and fetal lungs and livers. At 24 days of gestation, pregnant does were injected im with either hydrocortisone or an equal volume of saline. At 27 days of gestation, the maternal and fetal lungs and livers were removed for study. Maternal hydrocortisone treatment significantly decreased the fetal body weight and lung weight, but had no effect on the weights of fetal liver or the ratios of maternal lung/body or liver/body weights. Concentrations of protein, total phospholipids, or PC of fetal lung and liver and of maternal liver were not affected by hydrocortisone. However, the amounts of maternal lung protein, total phospholipids, and PC were significantly increased. No stimulation by hydrocortisone was seen in the specific activities of the enzymes: choline kinase, phosphocholine cytidyltransferase, and choline phosphotransferase of cytidine 5'-diphosphocholine (CDP-choline) pathway and lysoPC-lysoPC acyltransferase, lysophospholipase, and acyl-CoA lysoPC acyl-transferase of PC-lysoPC cycle pathway.

Maternal administration of hydrocortisone stimulated the incorporation of [methyl-14C] choline into fetal lung PC. Additionally, hydrocortisone also accelerated the secretion of PC from maternal lung tissue. The acceleration of the secretion of PC was not observed in the fetal lung tissue, possibly because of a low basal secretory rate. The acceleration of PC secretion by hydrocortisone in maternal lung may suggest a relation of this mechanism to the fetal lung maturation affected by steroids.

One biochemical effect of antenatal maternal hydrocortisone is the acceleration of choline incorporation into fetal lung PC. Maternally administered glucocorticoids, in addition to affecting fetal lung, might also affect maternal lung and liver PC metabolism by alteration of enzyme activity or changing turnover or transfer rates. Though studied indirectly, hydrocortisone might stimulate the secretion of lung PC onto the alveolar surface.

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