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19 June 2013 Uterine Infusion of Melatonin or Melatonin Receptor Antagonist Alters Ovine Feto-Placental Hemodynamics During Midgestation
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Abstract

Dietary melatonin supplementation from mid- to late gestation increases umbilical artery blood flow and causes disproportionate fetal growth. Melatonin receptors have been described throughout the cardiovascular system; however, there is a paucity of data on the function of placental melatonin receptors. The objectives of the current experiment were to determine fetal descending aorta blood flow, umbilical artery blood flow, and placental and fetal development following a 4-wk uterine infusion of melatonin (MEL), melatonin receptor 1 and 2 antagonist (luzindole; LUZ), or vehicle (CON) from Day 62 to Day 90 of gestation. After 4 wk of infusion, umbilical artery blood flow and umbilical artery blood flow relative to placentome weight were increased (P < 0.05) in MEL- versus CON- and LUZ-infused dams. Fetal descending aorta blood flow was increased (P < 0.05) in MEL- versus CON- and LUZ-infused dams, while fetal descending aorta blood flow relative to fetal weight was increased in MEL- versus CON-infused dams and decreased in LUZ- versus CON-infused dams. Following the 4-wk infusion, we observed an increase in placental efficiency (fetal-placentome weight ratio) in MEL- versus LUZ-infused dams. The increase in umbilical artery blood flow due to chronic uterine melatonin infusion is potentiated by an increased fetal cardiac output through the descending aorta. Moreover, melatonin receptor antagonism decreased fetal descending aorta blood flow relative to fetal weight. Therefore, melatonin receptor activation may partially mediate the observed increase in fetal blood flow following dietary melatonin supplementation.

Caleb O. Lemley, Leticia E. Camacho, and Kimberly A. Vonnahme "Uterine Infusion of Melatonin or Melatonin Receptor Antagonist Alters Ovine Feto-Placental Hemodynamics During Midgestation," Biology of Reproduction 89(2), (19 June 2013). https://doi.org/10.1095/biolreprod.113.109074
Received: 1 March 2013; Accepted: 1 June 2013; Published: 19 June 2013
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