G. Covi et al., SYSTEMIC AND UTEROPLACENTAL HEMODYNAMICS AND THE PROSTAGLANDIN SYSTEMIN PREGNANCY-INDUCED HYPERTENSION AND NORMAL-PREGNANCY, Hypertension in pregnancy, 13(3), 1994, pp. 273-283
Objective: The aim of this prospective study was to establish whether
or not there is any relationship between activation of the prostagland
in system and changes in systemic and uteroplacental hemodynamics in p
regnancy. Methods: Urinary excretion of prostaglandin E(2) (PGE(2)) an
d the main metabolites of prostacyclin (PGI(2)) and thromboxane A(2) (
TXA(2)) was determined, and indices of the vascular resistance of the
uteroplacental bed were measured in 10 normotensive women studied in e
ach trimester of pregnancy and in 15 women with pregnancy-induced hype
rtension in the third trimester. None of these subjects presented rena
l insufficiency or coagulation disorders, and all were monitored up to
delivery to assess the outcome of pregnancy. Urinary excretion of pro
stanoids was measured by radioimmunoassay after purification of sample
s with high-pressure liquid chromatography. Blood pressure was measure
d and vascular resistance indices were calculated, using ultrasonograp
hy to measure the amplitude of systolic and diastolic blood flow at th
e arcuate artery level. Results: Inverse correlations were observed be
tween increased systemic PGI(2) synthesis and reductions in blood pres
sure and uteroplacental vascular resistance in normotensive pregnancy.
Positive correlations were found between increased uteroplacental vas
cular resistance, increased blood pressure, and indices related to the
outcome of pregnancy; but no relationship with reduced PGI(2) synthes
is was detected in women with pregnancy-induced hypertension. Conclusi
ons: We conclude that PGI(2) appears to play a role in the regulation
of systemic and uteroplacental hemodynamics, particularly in the cours
e of normal pregnancy, and seems to be related to the development of p
regnancy-induced hypertension. No evidence emerged to suggest that TXA
(2) plays a role in inducing hemodynamic changes in either normotensiv
e or hypertensive pregnancy.