Decrease prostacyclin production: a characteristic of chronic placental insufficiency syndromes.
Prostacyclin production in neonates born at various gestational ages (28 weeks to term) was compared with that in neonates born of pregnancies complicated by various acute and chronic placental insufficiency states. Prostacyclin levels were reflected by the amount of conversion of 14C arachidonic acid to 6-keto-PGF1 alpha (the stable end-product of prostacyclin) by umbilical arteries. The uptake of 14C arachidonic acid by the umbilical arteries was also determined, and since this was similar for all groups it was not the cause of the differences noted in prostacyclin production. Neonates born of normal pregnancies had similar levels of prostacyclin production regardless of gestational age. Prostacyclin production was very low in neonates born of pregnancies complicated by chronic placental insufficiency (intrauterine growth retardation, essential hypertension, and pre-eclampsia), but normal with acute placental insufficiency (abruptio placentae). Hence the decrease in fetal prostacyclin production in pre-eclampsia is not related to gestational age; furthermore, it is also seen in other chronic placental insufficiency states.
D015121:6-Ketoprostaglandin F1 alpha; D000037:Abruptio Placentae / Q000378:metabolism; D002908:Chronic Disease; D011464:Epoprostenol / Q000096:biosynthesis*; D005260:Female; D005865:Gestational Age; D006801:Humans; D006973:Hypertension / Q000378:metabolism; D010922:Placenta Diseases / Q000378:metabolism*; D010927:Placental Insufficiency / Q000378:metabolism*; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000378:metabolism; D011453:Prostaglandins / Q000096:biosynthesis*; D011460:Prostaglandins F / Q000096:biosynthesis; D013577:Syndrome; D014469:Umbilical Arteries / Q000378:metabolism
D011453:Prostaglandins; D011460:Prostaglandins F; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol