Fetal and maternal endocrine responses to reduced uteroplacental blood flow

Robert W. Shepherd, Frank Z. Stanczyk, Cynthia Bethea, Miles J. Novy

    Research output: Contribution to journalArticle

    21 Citations (Scopus)

    Abstract

    In clinical practice, falling or reduced maternal estrogen levels are commonly regarded as indicators of fetal distress. However, experimental studies in primate animal models demonstrate that changes in maternal estradiol concentrations vary in response to reduced uteroplacental blood flow and are elevated during fetal hypoxemic stress, suggesting an increase in fetal adrenal precursor steroids. We studied the effects of graded reductions in maternal distal aortic blood flow (Qda) on the fetal MCR of dehydroepiandrosterone (D; MCR-D), the fetal production rate of D (PR-D), and changes in maternal and fetal plasma concentrations of D, D sulfate, cortisol, androstenedione, estrone (E1), and estradiol (E2) and in fetal plasma ACTH, PRL, and LH. A continuous iv infusion of [7-3H]D was administered to fetuses in five pregnant baboons (Papio anubis) at 155-165 days gestation (term, 184 days) for 270 min. A 50% reduction in mean distal aortic blood flow was imposed after 60 min by means of partial occlusion of the aorta with a snare device, which was released at 180 min. Maternal and fetal blood samples were collected at 10-min intervals from 30-60, 120-180, and 240-270 min. Equilibrium concentrations of [3H]D in fetal plasma were determined, and the MCR-D and PR-D were calculated for each of the three levels of Qda, corresponding to the control, occlusion, and release intervals. Concentrations of steroid and peptide hormones in maternal and fetal plasma were determined by RIA, and arterial blood pH, pO2, and pCO2 were measured. Control fetal PR-D (mean ± SE, 4.4 ± 2.0 mg/day) rose significantly during aortic occlusion accompanied by fetal hypoxemia (11.8 ± 3.1 mg/day; P <0.05) and remained elevated with release of the aortic constriction (13.8 ± 2.9 mg/day). Changes in fetal MCR-D were variable and not statistically significant. Among the maternal plasma steroids, only E1 and E2 increased significantly, doubling from control values during aortic occlusion and increasing by another 50% after release (P <0.05). There was a significant correlation between fetal PR-D and maternal plasma E2 and E1 concentrations (r2 = 0.76 and 0.71, respectively; P <0.01). Fetal hypoxemia was associated with dramatic increases in fetal plasma D, D sulfate, androstenedione, E1, and E2. No significant change occurred in fetal plasma cortisol, which tended to decline throughout the study. We observed a dramatic and sustained increase in fetal plasma ACTH during the period of reduced Qda and for 90 min thereafter, but no change in PRL or LH. We conclude that placental hypoperfusion with fetal hypoxemic stress results in elevated maternal and fetal E1 and E2 levels, which represent increased production of fetal androgen. Fetal adrenal activation during hypoxemic stress is probably mediated by ACTH, but not by PRL or LH.

    Original languageEnglish (US)
    Pages (from-to)301-307
    Number of pages7
    JournalJournal of Clinical Endocrinology and Metabolism
    Volume75
    Issue number1
    StatePublished - Jul 1992

    Fingerprint

    Blood
    Mothers
    Plasmas
    Adrenocorticotropic Hormone
    Androstenedione
    Steroids
    Estradiol
    Papio anubis
    Steroid hormones
    Fetal Distress
    Dehydroepiandrosterone
    Peptide Hormones
    Papio
    Estrone
    Fetal Blood
    Constriction
    Primates
    Androgens
    Sulfates
    Aorta

    ASJC Scopus subject areas

    • Biochemistry
    • Endocrinology, Diabetes and Metabolism

    Cite this

    Fetal and maternal endocrine responses to reduced uteroplacental blood flow. / Shepherd, Robert W.; Stanczyk, Frank Z.; Bethea, Cynthia; Novy, Miles J.

    In: Journal of Clinical Endocrinology and Metabolism, Vol. 75, No. 1, 07.1992, p. 301-307.

    Research output: Contribution to journalArticle

    Shepherd, Robert W. ; Stanczyk, Frank Z. ; Bethea, Cynthia ; Novy, Miles J. / Fetal and maternal endocrine responses to reduced uteroplacental blood flow. In: Journal of Clinical Endocrinology and Metabolism. 1992 ; Vol. 75, No. 1. pp. 301-307.
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    abstract = "In clinical practice, falling or reduced maternal estrogen levels are commonly regarded as indicators of fetal distress. However, experimental studies in primate animal models demonstrate that changes in maternal estradiol concentrations vary in response to reduced uteroplacental blood flow and are elevated during fetal hypoxemic stress, suggesting an increase in fetal adrenal precursor steroids. We studied the effects of graded reductions in maternal distal aortic blood flow (Qda) on the fetal MCR of dehydroepiandrosterone (D; MCR-D), the fetal production rate of D (PR-D), and changes in maternal and fetal plasma concentrations of D, D sulfate, cortisol, androstenedione, estrone (E1), and estradiol (E2) and in fetal plasma ACTH, PRL, and LH. A continuous iv infusion of [7-3H]D was administered to fetuses in five pregnant baboons (Papio anubis) at 155-165 days gestation (term, 184 days) for 270 min. A 50{\%} reduction in mean distal aortic blood flow was imposed after 60 min by means of partial occlusion of the aorta with a snare device, which was released at 180 min. Maternal and fetal blood samples were collected at 10-min intervals from 30-60, 120-180, and 240-270 min. Equilibrium concentrations of [3H]D in fetal plasma were determined, and the MCR-D and PR-D were calculated for each of the three levels of Qda, corresponding to the control, occlusion, and release intervals. Concentrations of steroid and peptide hormones in maternal and fetal plasma were determined by RIA, and arterial blood pH, pO2, and pCO2 were measured. Control fetal PR-D (mean ± SE, 4.4 ± 2.0 mg/day) rose significantly during aortic occlusion accompanied by fetal hypoxemia (11.8 ± 3.1 mg/day; P <0.05) and remained elevated with release of the aortic constriction (13.8 ± 2.9 mg/day). Changes in fetal MCR-D were variable and not statistically significant. Among the maternal plasma steroids, only E1 and E2 increased significantly, doubling from control values during aortic occlusion and increasing by another 50{\%} after release (P <0.05). There was a significant correlation between fetal PR-D and maternal plasma E2 and E1 concentrations (r2 = 0.76 and 0.71, respectively; P <0.01). Fetal hypoxemia was associated with dramatic increases in fetal plasma D, D sulfate, androstenedione, E1, and E2. No significant change occurred in fetal plasma cortisol, which tended to decline throughout the study. We observed a dramatic and sustained increase in fetal plasma ACTH during the period of reduced Qda and for 90 min thereafter, but no change in PRL or LH. We conclude that placental hypoperfusion with fetal hypoxemic stress results in elevated maternal and fetal E1 and E2 levels, which represent increased production of fetal androgen. Fetal adrenal activation during hypoxemic stress is probably mediated by ACTH, but not by PRL or LH.",
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    N2 - In clinical practice, falling or reduced maternal estrogen levels are commonly regarded as indicators of fetal distress. However, experimental studies in primate animal models demonstrate that changes in maternal estradiol concentrations vary in response to reduced uteroplacental blood flow and are elevated during fetal hypoxemic stress, suggesting an increase in fetal adrenal precursor steroids. We studied the effects of graded reductions in maternal distal aortic blood flow (Qda) on the fetal MCR of dehydroepiandrosterone (D; MCR-D), the fetal production rate of D (PR-D), and changes in maternal and fetal plasma concentrations of D, D sulfate, cortisol, androstenedione, estrone (E1), and estradiol (E2) and in fetal plasma ACTH, PRL, and LH. A continuous iv infusion of [7-3H]D was administered to fetuses in five pregnant baboons (Papio anubis) at 155-165 days gestation (term, 184 days) for 270 min. A 50% reduction in mean distal aortic blood flow was imposed after 60 min by means of partial occlusion of the aorta with a snare device, which was released at 180 min. Maternal and fetal blood samples were collected at 10-min intervals from 30-60, 120-180, and 240-270 min. Equilibrium concentrations of [3H]D in fetal plasma were determined, and the MCR-D and PR-D were calculated for each of the three levels of Qda, corresponding to the control, occlusion, and release intervals. Concentrations of steroid and peptide hormones in maternal and fetal plasma were determined by RIA, and arterial blood pH, pO2, and pCO2 were measured. Control fetal PR-D (mean ± SE, 4.4 ± 2.0 mg/day) rose significantly during aortic occlusion accompanied by fetal hypoxemia (11.8 ± 3.1 mg/day; P <0.05) and remained elevated with release of the aortic constriction (13.8 ± 2.9 mg/day). Changes in fetal MCR-D were variable and not statistically significant. Among the maternal plasma steroids, only E1 and E2 increased significantly, doubling from control values during aortic occlusion and increasing by another 50% after release (P <0.05). There was a significant correlation between fetal PR-D and maternal plasma E2 and E1 concentrations (r2 = 0.76 and 0.71, respectively; P <0.01). Fetal hypoxemia was associated with dramatic increases in fetal plasma D, D sulfate, androstenedione, E1, and E2. No significant change occurred in fetal plasma cortisol, which tended to decline throughout the study. We observed a dramatic and sustained increase in fetal plasma ACTH during the period of reduced Qda and for 90 min thereafter, but no change in PRL or LH. We conclude that placental hypoperfusion with fetal hypoxemic stress results in elevated maternal and fetal E1 and E2 levels, which represent increased production of fetal androgen. Fetal adrenal activation during hypoxemic stress is probably mediated by ACTH, but not by PRL or LH.

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