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Fetal vascular responses to prostacyclin
1Department of Obstetrics, Gynecology and Reproductive Sciences, University of Texas Medical School, Houston 77030.
American Journal of Obstetrics and Gynecology
|April 1, 1989
Summary
Prostacyclin infusion in fetal sheep did not dilate placental blood vessels in vivo, contrary to in vitro findings. This treatment led to fetal acidemia, suggesting blood may be shunted away from the placenta.
Area of Science:
- Perinatal physiology
- Fetal circulation
- Vascular pharmacology
Background:
- Prostacyclin is a known vasodilator in maternal and fetal tissues.
- In vitro studies suggest prostacyclin dilates umbilical placental vasculature.
Purpose of the Study:
- To investigate the in vivo effects of prostacyclin on fetal placental circulation.
- To test if prostacyclin causes vasodilation in the fetal placental circulation.
Main Methods:
- Radioactive microsphere technique used to measure blood flow.
- Infusion of prostacyclin in unanesthetized near-term ovine fetuses.
- Monitoring of fetal arterial pressure, heart rate, and blood gas parameters.
Main Results:
- Prostacyclin infusion did not significantly alter placental blood flow (p=0.07) or vascular resistance.
- Fetal mean arterial pressure decreased by 15% and heart rate increased significantly.
- Fetal arterial pH decreased, indicating significant fetal acidemia and a trend toward hypercarbia.
Conclusions:
- In vivo administration of prostacyclin to the ovine fetus does not induce fetal placental vasodilation.
- Prostacyclin infusion causes significant fetal acidemia.
- Potential mechanism involves blood flow shunting away from the placenta due to systemic vasodilation.