Evidence that prostacyclin deficiency is a specific feature in preeclampsia.
Much evidence has implied a deficient production of the antiaggregatory and vasodilator agent prostacyclin (PGI2) in preeclampsia and some other chronic fetoplacental insufficiency syndromes. So that we could study whether this might be due to the possible effects of the mode of delivery and maternal epidural or general anesthesia, specimens of the umbilical arteries of infants born after normal (n = 46) or complicated (n = 25) pregnancies were superfused in vitro and their production of PGI2 was determined by measuring 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha, the hydrolysis product of PGI2) by radioimmunoassay. The amounts of umbilical 6-keto-PGF1 alpha released in normal pregnancies after induced vaginal delivery (20.9 +/- 2.4 ng/gm/min dry weight of tissue, mean +/- SEM) and elective cesarean section (21.8 +/- 2.2 ng/gm/min) were smaller (p less than 0.025) than the amounts released after spontaneous onset of labor (35.0 +/- 6.2 ng/gm/min). Epidural or general anesthesia had no effect on this production. When the types of deliveries were matched, the production of 6-keto-PGF1 alpha was even less (p less than 0.05) in cases of preeclampsia (14.2 +/- 3.7 ng/gm/min; n = 9) than in the control subjects (21.3 +/- 1.6 ng/gm/min) and in cases of essential hypertension (21.6 +/- 5.2 ng/gm/min). Our data suggest that umbilical PGI2 deficiency is a specific feature of preeclampsia.
D015121:6-Ketoprostaglandin F1 alpha / Q000378:metabolism; D000773:Anesthesia, Obstetrical; D036861:Delivery, Obstetric / Q000379:methods; D011464:Epoprostenol / Q000172:deficiency*; D005260:Female; D005317:Fetal Growth Retardation / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000378:metabolism; D011225:Pre-Eclampsia / Q000378:metabolism*; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000378:metabolism; D014469:Umbilical Arteries / Q000378:metabolism
D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol