Role of thyroid hormone in postnatal circulatory and metabolic adjustments.

Abstract

At bstract. To assess the role of the early postnatal surge in plasma thyroid hormone concentrations on cardiovascular and metabolic adaptations, we measured cardiac output, total oxygen consumption, and plasma triiodothyronine (T3) concentrations in three groups of lambs in the first 6 h after delivery. 15 fetal lambs were prepared at gestational ages of 128-129 d by placing catheters in the brachiocephalic artery, descending aorta, distal inferior vena cava, left atrium, and pulmonary artery so that measurements could be made soon after delivery. They were divided into three groups: Group I comprised five control animals; Group II consisted of five fetuses in which thyroidectomy was performed at surgery at 129 d gestation; and Group III consisted of five animals in which thyroidectomy was performed at term gestation during delivery by caesarian section, prior to severing the umbilical cord. The lambs in Group I exhibited a rapid postnatal rise in T3 concentrations, similar to that described previously, reaching a peak value of about 5 ng/ml. Although the postnatal surge in T3 concentration was arrested in Group II and III animals, Group II had no detectable plasma T3, while the Group III animals had T3 concentrations of about 0.8 ng/ml, which were within the range previously reported for term lamb fetuses. The lambs in group II showed 40-50% lower left ventricular outputs (190 vs. 297 lambs in Group II also had significantly lower heart rates (131 vs. 192 beats/min) and mean systemic arterial pressures (56 vs. 72 torr). However, there were no significant differences for any of these measurements between the Group III and Group I lambs. The reduction in cardiac output in the Group II animals were reflected in a significantly lower blood flow to the peripheral circulation, but there were no significant differences in blood flow to other organs in the three groups. These studies indicate that plasma thyroid concentrations in the 2-3 wk prior to delivery and not the increase in thyroid hormone concentrations which occur after birth are important for postnatal cardiovascular and metabolic adjustments. We speculate that lack of circulating triiodothyronine in late gestation may affect postnatal cardiovascular adaptation by modifying normal beta adrenergic receptor development.

Thyroid hormone inhibits proliferation of fetal cardiac myocytes in vitro

“…7-0 . 8 ng/ml at w142 dGA (Breall et al 1984, Forhead et al 1998, 2002 and there is a further surge in T 3 in the first 6 h after birth. If the normal increase in T 3 is prevented, the resulting hypothyroidism suppresses growth and leads to low circulating insulin-like growth factor (IGF) concentrations in the fetus (Latimer et al 1993, Forhead et al 1998 and suppressed maturation of a number of fetal tissues (Fowden 1995, Fowden & Silver 1995.…”

Endocrine And Metabolic Adaptations Of Calves To Extra-Uterine Life

“…This maturation includes increased thyroid stimulating hormone (TSH), T 3 and T 4 levels, and decreased reverse triodothironine (rT 3 ) levels as birth approaches [50]. The thyroid function prior to birth strongly interferes with cardiovascular and lung adaptation, as well as with thermogenesis in the newborn lamb [51]. At birth T 3 and T 4 levels are high [23,43] and increase during the fi rst hours of life due to both cortisol surge which supports the maturation of the thyroid axis and increased TSH secretion [52].…”

Reversible Umbilical Cord Occlusion: Effects on Thermogenesis In Utero

“…Thyroidectomy at 133 d gestation in fetal sheep was associated with reduced neonatal serum FFA levels and rectal temperatures (29). In contrast, acute thyroidectomy during delivery abolished the postnatal surge in plasma Ti concentration, but there was no significant difference in oxygen consumption compared with controls (30). This may be due to the long half-life of thyroxine, which would allow intracellular conversion of thyroxine to Ti to continue in the brown adipocyte.…”