Fetal response to thyrotropin-releasing hormone after thyroid hormone administration to the rhesus monkey: Lack of pituitary suppression

Shlomo Melmed, Akira Harada, Yuji Murata, Michael Socol, Allan Reed, Harold E. Carlson, Mizuo Azukizawa, Chester Martin, Eugene Jorgensen, Jerome M. Hershman*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

32 Scopus citations

Abstract

Chronically catheterized maternal fetal monkey preparations were used to study pituitary suppression by thyroid hormones in the fetus. Baseline maternal T3, T4, and PRL were all significantly higher than fetal levels of these hormones. TRH was given iv (10 μg/kg) to the mother 3, 6, 12, 20, or 44 h after giving varying doses of T3to the fetus. Amniotic fluid and fetal tracheal aspirate did not contain detectable TSH. Nonpregnant females and pregnant mothers showed complete suppression of the TSH response to TRH after receiving 20 μg T3iv 24 h before TRH. Two micrograms of T3iv to the fetus 3 h before TRH failed to suppress the TSH response (fetal ΔTSH, 26 μU/ml; ΔT4, 3.6 μg/dl). Six micrograms of T3iv (three doses of 2 μg) to the fetus over 36 h achieved a basal T3level of 2500 ng/dl and lowered fetal ΔTSH to 9.1 μU/ml. Six micrograms of T3infused iv to the fetus over 24 h achieved fetal T3blood levels of 5000 ng/dl, which suppressed ΔTSH to 2.7 μU/ml. 3, 5, -Dimethyl-3’-isopropyl-L-thyronine (DIMIT; 300 μg iv to mother 24 h before TRH) completely suppressed maternal TSH response and delayed and mildly blunted fetal TSH responses. DIMIT given iv to the fetus suppressed both maternal and fetal TSH responses to TRH. The data show that moderate doses of T3do not suppress the exaggerated fetal monkey pituitary TSH response to TRH. DIMIT crosses the primate placenta in both directions and can suppress the fetal ituitary-thyroid axis.

Original languageEnglish (US)
Pages (from-to)334-341
Number of pages8
JournalEndocrinology
Volume105
Issue number2
DOIs
StatePublished - Aug 1979

ASJC Scopus subject areas

  • Endocrinology

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