Low doses of dexamethasone suppress pituitary-adrenal function but augmentthe glycemic response to acute hypoxemia in fetal sheep during late gestation

Despite the widespread use of antenatal glucocorticoid therapy in obstetric practice, little is known about the effects of synthetic glucocorticoids o n the fetal capacity to respond to episodes of acute hypoxemia, such as may occur during labor and delivery. This study investigated the effects of pr olonged fetal exposure to low concentrations of dexamethasone on the fetal ACTH, cortisol, and glycemic responses to an episode of acute hypoxemia dur ing the period of dexamethasone treatment in sheep. Ar 118 d of gestation ( term is approximately 145 d), 11 fetal sheep had catheters implanted under halothane anesthesia. From 124 d, five fetuses were infused i.v. continuous ly with dexamethasone (1.80 +/- 0.15 mu g.kg(-1).h(-1) in 0.9% saline at 0. 5 mL/h) for 48 h, and the other six fetuses received saline solution i.v, a t the same rate. At 45 h of infusion, acute hypoxemia was induced in all fe tuses for 1 h by reducing the maternal inspired fraction of oxygen. During glucocorticoid treatment, fetal plasma dexamethasone concentrations increas ed to 3.9 +/- 0.2 nM by 24 h and remained elevated for the rest of the infu sion period. During hypoxemia, a similar fall in fetal arterial Po-2 occurr ed in both saline-infused and dexamethasone-treated fetuses. In control fet uses, significant increases in plasma ACTH and cortisol concentrations and in blood glucose concentrations occurred during hypoxemia. Dexamethasone tr eatment prevented the increases in fetal plasma ACTH and cortisol, and augm ented the blood glucose response, induced by hypoxemia, These data indicate that prolonged fetal exposure to low concentrations of dexamethasone suppr esses pituitary-adrenal function. but augments the glycemic response, to ac ute hypoxemia in fetal sheep during late gestation.