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Beta-sympathomimetic drugs and glucocorticoid agents are given in preterm labor to prevent severe consequences of prematurity. It is unclear whether beta-sympathomimetics accelerate lung maturation, or whether they only tend to delay preterm delivery. We have evaluated the effects of betamethasone and ritodrine in rabbits on alveolar lavage phospholipids in premature rabbits, a mean of 28.7 days from conception. Betamethasone given to 26-day-old fetuses increased the surfactant phospholipids, phosphatidylinositol and disaturated phosphatidylcholine; increased disaturated phosphatidylcholine/sphingomyelin ratio, and phosphatidylinositol (percent of phospholipids), as compared to untreated littermates, or to saline treated controls. A low dose of ritodrine given to the pregnant doe, and a high dose given at premature birth had no detectable effects on alveolar lavage phospholipids. However, a high dose of ritodrine given one day before the delivery to the fetus and at premature birth decreased the disaturated phosphatidylcholine/sphingomyelin ratio and phosphatidylinositol in alveolar lavage. While glucocorticoid administration increases the synthesis and secretion of surfactant phospholipids, a high dose of a betasympathomimetic drug may decrease the surfactant. However, spontaneous premature labor is associated with accelerated lung maturation, and accordingly the present results do not contradict the use of a low dosage of betasympathomimetic drug to delay preterm delivery.

Effects of betamethasone and ritodrine on the fetal secretion of lung surfactant