Preeclampsia: An imbalance in placental prostacyclin and thromboxane Production

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Preeclampsia is characterized by increased vasoconstriction frequently associated with increased platelet aggregation, reduced uteroplacental blood flow, and premature delivery. Because prostacyclin antagonizes the vasoconstrictor, platelet-aggregating, and uterine-activating actions of thromboxane, we considered the hypothesis that placental production of thromboxane was increased coincident with decreased production of prostacyclin in preeclampsia. Fresh human term placentas were obtained immediately after delivery from 11 normal and 10 preeclamptic pregnancies (blood pressure 140190 mm Hg, urinary protein >0.3 gm/24 hr). Tissues (350 mg) were incubated sterilely in 6 ml of Dulbecco's Modified Eagle's Medium for 48 hours at 37° C with 95% oxygen and 5% carbon dioxide in a metabolic shaker. Samples were collected at 8, 20, 32, and 48 hours and analyzed for thromboxane by radiommunoassay of its stable metabolite, thromboxane B2, and for prostacyclin by radioimmunoassay of its stable metabolite, 6-keto prostaglandin F. The production of thromboxane was significantly increased in preeclamptic versus normal placental tissue (22.9 ± 4.7 versus 6.3 ± 1.5 pglmglhr, mean ± SE, p < 0.01), whereas the production of prostacyclin was significantly decreased (3.0 ± 0.3 versus 6.7 ± 0.5 pglmglhr, p < 0.001). In both normal and preeclamptic placentas, the production rates of thromboxane and prostacyclin were inhibited by indomethacin (5 [,mol/L) and not affected (p > 0.50) by arachidonic acid (100 µmol/L). Therefore, during normal pregnancy, the placenta produces equivalent amounts of thromboxane and prostacyclin, so that their biologic actions on vascular tone, platelet aggregation, and uterine activity will be balanced. In preeclamptic pregnancy, however, the placenta produces seven times more thromboxane than prostacyclin.

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  • M Linton et al.
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    Supported in part by Grants HD 16991 from the National Institute of Child Health and Human Development, BRSG S07 RR0562315 awarded by the Biomedical Research Support Grant Program, Division of Research Resources, National Institutes of Health, and a gift from The Upjohn Company, Kalamazoo, Michigan. Presented in preliminary form at the Thirty first Annual Meeting of the Society for Gynecologic Investigation, San Francisco, California, March 21-24, 1984 (Abstract No. 414); the Fourth World Congress of the International Society for the Study of Hypertension in Pregnancy, Amsterdam, The Netherlands, June 18-21, 1984 (Abstract, p. 44); and the International Symposium for Physiological Development of Fetus and Newborn, Oxford, England, July 24-28,1984 (Abstract No. C59).

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