Abstract
Objective: The aim of this prospective study was to establish whether or not there is any relationship between activation of the prostaglandin system and changes in systemic and uteroplacental hemodynamics in pregnancy.
Methods: Urinary excretion of prostaglandin E2 (PGE2) and the main metabolites of prostacyclin (PGI2) and thromboxane A2 (TXA2) was determined, and indices of the vascular resistance of the uteroplacental bed were measured in 10 normotensive women studied in each trimester of pregnancy and in 15 women with pregnancy-induced hypertension in the third trimester. None of these subjects presented renal insufficiency or coagulation disorders, and all were monitored up to delivery to assess the outcome of pregnancy. Urinary excretion of prostanoids was measured by radioimmunoassay after purification of samples with high-pressure liquid chromatography. Blood pressure was measured and vascular resistance indices were calculated, using ultrasonography to measure the amplitude of systolic and diastolic blood flow at the arcuate artery level.
Results: Inverse correlations were observed between increased systemic PGI2 synthesis and reductions in blood pressure and uteroplacental vascular resistance in normotensive pregnancy. Positive correlations were found between increased uteroplacental vascular resistance, increased blood pressure, and indices related to the outcome of pregnancy; but no relationship with reduced PGI2 synthesis was detected in women with pregnancy-induced hypertension.
Conclusions: We conclude that PGI2 appears to play a role in the regulation of systemic and uteroplacental hemodynamics, particularly in the course of normal pregnancy, and seems to be related to the development of pregnancy-induced hypertension. No evidence emerged to suggest that TXA2 plays a role in inducing hemodynamic changes in either normotensive or hypertensive pregnancy.