Abstract

29 ewes and their chronically catheterized fetuses(0.46-0.99 gestation)were allowed 48 hr to recover from surgery prior to study. We measured plasma ACTH and Corticosteroid(C)concentration by radioimmunoassay. Maternal plasma ACTH(54±4 pg.ml−1)and C(3.0 ± 0.2 μg.dl−1)did not change. Fetal ACTH(44±4 pg.ml−1)was low. Fetal C increased progressively from 1.5±0.1 μg.dl−1 before 0.85 gestation to maximal concentrations of 9.4±1.2 μg.dl−1 after 0.95 gestation. Lack of parallel increase in fetal ACTH and C suggested increasing fetal adrenal responsiveness to apparently constant fetal ACTH. In 7 of 8 fetuses(0.72-0.89 gestation)hemorrhage of 15% estimated fetal blood volume at 1.5% min−1 caused a decrease(P<0.05) in fetal mean arterial pressure(FMAP)from 43±3 Torr to 26±4 Torr, and increase(P<0.05)in ACTH(Δ ACTH=140±45pgml−1) and a small increase(P<0.05)in C(ΔC=0.9±0.2 μg.dl−1). A much larger increase in plasma C levels(ΔC=7 μg.dl−1)despite comparable FMAP and ACTH responses to hemorrhage occurred in 2 fetuses >0.95 gestation. These findings also suggest increased fetal adrenal responsiveness to endogenous ACTH towards term. Hemorrhage of 15% in 6 younger fetuses(0.55-0.67 gestation)produced no increase in plasma ACTH or C despite a drop in FMAP from 37±1 Torr to 29±2 Torr(P<0.01). This suggests system(s) subserving the plasma ACTH response to mild hemorrhage are either not yet developed or are inactive in fetuses <0.67 gestation. Fetal hemorrhage caused no change in maternal blood pressure, ACTH or C.

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