To ascertain whether repeated hypoxic stress would alter the response of the adrenal cortex to adrenocorticotropic hormone (ACTH), by premature activation of the hypothalamic–pituitary–adrenal axis, we studied fetal sheep subjected to daily reduction of arterial oxygen content by embolization of the fetal placental circulation with 15 μm microspheres for 8 days from about day 124 of gestation (term ∼147 days) and sham-embolized controls. Starting before the final embolization (or shamembolization) on day 8, and continuing for 24 h, the fetus was given an intravenous infusion of ACTH1–24 (0·5 μg/h) or vehicle. Fetal and maternal blood samples were taken for determination of immunoreactive cortisol, and regional adrenal and fetal placental blood flows were measured by the microsphere technique at three time points: 1 h before infusion, 3 h after the start of the infusion (1 h after embolization), and after 24 h of infusion. Prior to infusion of ACTH or vehicle, fetal placental blood flow was lower in microsphere-embolized fetuses than in sham-embolized controls (199 ± 15 vs 292 ± 25 ml/min per 100 g tissue; mean ± s.e.; P<0·01). However, plasma cortisol and adrenal cortical blood flow did not differ between embolized fetuses and controls. Adrenal vascular responses to the 24-h infusion of ACTH were similar in embolized and shamembolized fetuses. Adrenal cortical blood flow increased 3-fold (P<0·05) due to decreased vascular resistance (P<0·01), with no change in adrenal medullary blood flow. Thus, while daily embolization of the fetal placental circulation caused a sustained decrease in cotyledonary blood flow, no evidence of altered responsiveness of the adrenal cortex to ACTH was found in these experiments.
Journal of Endocrinology (1996) 148, 517–522
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