Role of thyroid hormone in postnatal circulatory and metabolic adjustments

Insights

The early postnatal surge in thyroid hormone (T3) is not crucial for cardiovascular and metabolic adaptations. Instead, thyroid hormone levels in late gestation are vital for these adjustments in newborns.

Area of Science:

  • Physiology
  • Endocrinology
  • Neonatal Adaptation

Background:

  • Thyroid hormones play a critical role in mammalian development.
  • The early postnatal period is characterized by a surge in plasma thyroid hormone concentrations.
  • The specific contribution of this postnatal surge to cardiovascular and metabolic adaptations remains unclear.

Purpose of the Study:

  • To investigate the role of the early postnatal surge in plasma thyroid hormone concentrations on cardiovascular and metabolic adaptations in newborn lambs.
  • To determine whether thyroid hormone levels prior to birth or the postnatal surge are more critical for these adaptations.

Main Methods:

  • Fetal lambs underwent surgical preparation with vascular catheters.
  • Three groups were studied: controls, lambs thyroidectomized before umbilical cord clamping, and lambs thyroidectomized during fetal surgery.
  • Measurements included cardiac output, oxygen consumption, heart rate, blood pressure, and plasma triiodothyronine (T3) concentrations post-delivery.

Main Results:

  • Lambs thyroidectomized before cord clamping (Group II) showed significantly reduced cardiac output, systemic blood flow, oxygen consumption, heart rate, and blood pressure compared to controls.
  • Lambs thyroidectomized during fetal surgery (Group III) did not exhibit these deficits, maintaining levels similar to controls.
  • Group II lambs had undetectable plasma T3, while Group III had low levels similar to fetal ranges.

Conclusions:

  • Plasma thyroid hormone concentrations in the weeks prior to delivery, not the postnatal surge, are critical for postnatal cardiovascular and metabolic adjustments.
  • Lack of circulating triiodothyronine in late gestation may impair postnatal cardiovascular adaptation, potentially by affecting beta-adrenergic receptor development.

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