6-ketoprostaglandin-f1-alpha and Fetal-Death

Intra-uterine growth retardation, intra-uterine fetal death and pre-eclampsia have common abnormalities: A reduction of uteroplacental perfusion, lack of vasodilation of spiral arteries and subsequent thrombosis. These physiological processes have been explained by an imbalance between prostacyclin and thromboxane A2 production. Many studies have suggested that treatment with low-dose aspirin and steroids is effective in preventing pregnancy loss or pre-eclampsia, but the mechanism has not been established. We evaluated the effectiveness of these therapies in patients at risk for pregnancy loss with the aspect of intracellular ionized calcium mobilization. Low-dose aspirin directs the prostacyclin/thromboxane A2 balance to the dominance of prostacyclin and steroids suppress the activities of lupus anticoagulant or antiphospholipid antibodies. The intracellular ionized calcium concentration in platelets is decreased significantly after these therapies. Concerning the pathological examination of placenta, there were deposits of fibrin in only 2 out of 8 cases and there were no abnormal findings in the other 6 cases. These data show that the aggregation of platelets is suppressed in microvascular circulations. These therapies do not cause any adverse effect on the mother or fetus. It is concluded that low-dose aspirin therapy with steroids is useful for patients with a poor obstetrical history.

Topics: 6-Ketoprostaglandin F1 alpha; Aspirin; Calcium; Female; Fetal Death; Fetal Growth Retardation; Humans; Lupus Coagulation Inhibitor; Placenta; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Thromboxane B2; Treatment Outcome

A number of compounds in pregnancy blood reach a maximum or minimum concentration at around 20-24 weeks of pregnancy, a period of conspicuous clinical tranquility. The compounds mostly derive from either fetal tissue or decidua and it is suggested that they may be part of an elaborate mechanism which controls invasion of the uterine wall by trophoblast.

Topics: 6-Ketoprostaglandin F1 alpha; Amine Oxidase (Copper-Containing); Amniotic Fluid; Amylases; Chorionic Gonadotropin; Female; Fetal Death; Humans; Oxidoreductases Acting on CH-NH Group Donors; Polyamine Oxidase; Pregnancy; Pregnancy Trimester, Second

Topics: 6-Ketoprostaglandin F1 alpha; Adaptation, Physiological; Animals; Blood Coagulation Factors; Epoprostenol; Female; Fetal Death; Hemodynamics; Humans; Hypertension; Imidazoles; Lupus Coagulation Inhibitor; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Cardiovascular; Rats; Thrombosis; Thromboxane-A Synthase; Vitamin E Deficiency

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Female; Fetal Death; Gestational Age; Pregnancy; Prostaglandins E; Prostaglandins F; Sheep; Tissue Distribution; Uterine Contraction; Uterus

To study the involvement of antiaggregatory and vasodilatory prostacyclin (PGI2) in various pregnancy complications, we measured the concentrations of 6-ketoprostaglandin F1 alpha, a stable hydration product of PGI2, using a specific radioimmunoassay, in plasma samples from 123 women between 22 and 41 weeks of complicated or normal pregnancy. The levels of 6-keto-PGF1 alpha (mean +/- SE) in pre-eclampsia (267.0 +/- 26.6 pg/ml, n = 22), diabetic pregnancy (266.6 +/- 19.2 pg/ml, n =21), twin pregnancy (310.7 +/- 28.2 pg/ml, n = 10), threatened premature labour (285.9 +/- 23.2 pg/ml, n = 26), placenta praevia or placental abruption (248.9 +/- 24.5 pg/ml, n = 6), hepatosis gravidarum (249.3 +/- 15.0 pg/ml, n = 3) or in pregnancies complicated by intrauterine fetal growth retardation (296.9 +/- 34.2 pg/ml, n = 14) or fetal death (267.5 +/- 20.9 pg/ml, n = 6) did not differ from each other or from the 6-keto-PGF1 alpha levels in normal pregnancy (266.4 +/- 15.0 pg/ml, n = 22). Furthermore, the 6-keto-PGF1 alpha levels bore no relation to the gestational age, maternal drug use (insulin, glucocorticoids, antihypertensive drugs) or to the sex, birth weight or condition of the newborn infant, or to the placenta weight.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Epoprostenol; Female; Fetal Death; Fetal Growth Retardation; Humans; Obstetric Labor, Premature; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Pregnancy in Diabetics; Pregnancy, Multiple; Prostaglandins