Direct fetal glucocorticoid treatment alters postnatal adaptation in premature newborn baboons.

Abnormalities of premature newborn adaptation after preterm birth result in significant perinatal mortality and morbidity. We assessed the effects of short-term (24 h) fetal betamethasone exposure on preterm newborn baboon pulmonary and cardiovascular regulation and renal sodium handling during the first 24 h after birth. Male fetal baboons ( Papio) (124-day gestation, term 185 days) received ultrasound-guided intramuscular injections of saline ( n = 5) or betamethasone (0.5 mg/kg; n = 5). Fetuses were cesarean delivered 24 h later, treated with 100 mg/kg surfactant, and ventilated by adjusting peak inspiratory pressures to maintain[Formula: see text] values of 35-50 mmHg for 24 h. Betamethasone- vs. saline-treated mean ± SE newborn body weights (0.45 ± 0.02 vs. 0.41 ± 0.01 kg) were similar. Although prenatal betamethasone did not affect postnatal lung function ([Formula: see text], arterial/alveolar O2 gradient, or dynamic compliance), plasma hormone (cortisol or thyroxine), or catecholamine levels, mean arterial pressure (25 ± 1 vs. 32 ± 1 mmHg), plasma sodium concentration (132 ± 2 vs. 138 ± 1 meq/l), glomerular filtration rate (0.07 ± 0.02 vs. 0.16 ± 0.02 ml ⋅ min-1 ⋅ kg-1), and renal total sodium reabsorption (1.5 ± 0.5 vs. 16.0 ± 3.0 μeq ⋅ min-1 ⋅ kg-1) values were significantly lower in saline-treated than in betamethasone-treated newborns at 24 h. We conclude that despite the fact that there are no pulmonary and endocrine effects, antenatal glucocorticoid exposure alters premature newborn baboon vascular and renal glomerular function and improves sodium reabsorption after preterm delivery.