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Reproductive Endocrinology Center, Department of Obstetrics, Gynecology, and Reproductive Sciences, and the Cardiovascular Research Institute, University of California San Francisco, San Francisco, California 94143
Address requests for reprints to: Dr. Robert B. Jaffe, University of California, School of Medicine, Department of Obstetrics, Gynecology, and Reproductive Sciences, San Francisco, California 94143.
Abstract
Fetal adrenal function in utero was studied in chronically catheterized rhesus monkey fetuses (129–154 days gestational age). Measurements of fetal pH, pCO2, pO2, heart rate, and fetal and maternal blood pressure were normal by 24 h after surgery. Maternal cortisol levels were 484.6 ± 60.7 ng/ml (mean ± SE) after surgery, decreasing to 300 ± 26.9 and 227.8 ± 30.6 ng/ml by the second and third day after surgery and stabilizing thereafter. No consistent pattern in fetal cortisol was seen after surgery. A significant increase in fetal concentration was observed between 145 and 149 and 150 and 154 days' gestation (87.9 ± 9.3 and 123.8 ± 20.0 ng/ml, respectively). A significant diurnal variation of cortisol levels was found in the fetal, but not maternal, circulation (fetal levels: AM, 167 ± 13.4 ng/ml, PM, 115 ± 8.9 ng/ml; maternal levels: AM, 326 ± 18.8 ng/ml, PM, 319 ± 38.5 ng/ml). Seven fetuses were challenged with bolus injections of 0.5 IU ACTH. An increase in circulating cortisol levels in response to ACTH was seen in only two of the fetuses. Dexamethasone (8 mg/day) was administered in four pregnancies. Fetal ACTH decreased from a baseline of 55.8 ± 14.5 to 30.5 ±4.1 and 17.9 ± 4.5 pg/ml 24 and 48 h after starting the dexamethasone infusion. Basal cortisol levels were 78.5 ± 8.7 ng/ml and decreased to 16.4 ± 2.8 and 12.3 ±1.6 ng/ml at 24 and 48 h, respectively, after dexamethasone. Both ACTH and cortisol values returned to pretreatment levels after cessation of treatment. These data are interpreted as indicating that fetal adrenal function is regulated by the fetal pituitary. However, the limited response of the fetal adrenal in situ to exogenous ACTH suggests a decreased responsiveness of the gland in utero.
Footnotes
* These studies were supported in part by NIH Grants HD-08478 and HD-09980 and by a grant from the Rockefeller Foundation.
Received September 9, 1977.
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