DIRECT FETAL GLUCOCORTICOID TREATMENT ALTERS POSTNATAL ADAPTATION IN PREMATURE NEWBORN BABOONS

Abnormalities of premature newborn adaptation after preterm birth resu lt in significant perinatal mortality and morbidity. We assessed the e ffects of short-term (24 h) fetal betamethasone exposure on preterm ne wborn 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 intramu scular 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 Pco(2) values of 35-50 mmHg for 24 h. Betamethasone-vs. salin e-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 (Pco(2), arterial/ alveolar O-2 gradient, or dynamic compliance), plasma hormone (cortisol or thyroxine), or catech olamine levels, mean arterial pressure (25 +/- 1 vs. 32 +/- 1 mmHg), p lasma 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 mu eq . min(-1) . kg(-1) values were significantly lower in saline-tre ated than in betamethasone-treated newborns at 24 h. We conclude that despite the fact that there are no pulmonary and endocrine effects, an tenatal glucocorticoid exposure alters premature newborn baboon vascul ar and renal glomerular function and improves sodium reabsorption afte r preterm delivery.