Our goal was to develop a model for the study of maternal adrenal glan
d regulation and the effects of maternal cortisol secretion on fetal h
omeostasis, At about 108 days of gestation, before the time of rapid f
etal growth or fetal adrenocortical maturation, ewes, under halothane
anesthesia with controlled ventilation and positioned in sternal recum
bency, were adrenalectomized. Ewes were treated with aldosterone by in
travenous infusion (3 mu g/kg of body weight per day) to induce normal
late-gestation aldosterone concentration. Ewes were also treated with
cortisol; for 2 postoperative days, this infusion (1 to 2 mu g/kg per
min) induced plasma concentration similar to that associated with str
ess. Thereafter, the dosage of cortisol was reduced to induce plasma v
alues similar to normal late-gestation cortisol concentration in ewes
(1 mg/kg per day), or to values in nonpregnant ewes (0.6 mg/kg per day
), Administration of cortisol and aldosterone was required to prevent
electrolyte imbalance and signs of hypoadrenocorticism. With steroid r
eplacement, plasma protein, electrolyte, and glucose concentrations in
adrenalectomized ewes were not different from those in sham-operated
pregnant ewes, Of 11 adrenalectomized ewes, one died as a result of fa
ilure of the infusion pump, and one died as a result of inappropriate
treatment for hypoglycemia, Of the remaining ewes, two aborted fetuses
, three ewes each delivered one live and one dead fetus, two delivered
live singleton fetuses, and two delivered twins, Therefore, this mode
l of relative hypoadrenocorticism in pregnancy is feasible and practic
al for studying the influence of maternal cortisol concentration on ma
ternal and fetal homeostasis.