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Renal Prostacyclin and Thromboxane in Normotensive and Preeclamptic Pregnant Women and Their Infants^*

First Department of Obstetrics and Gynecology University of Helsinki, Helsinki,Finland
Children's Hospital University of Helsinki, Helsinki,Finland

Address all correspondence and requests for reprints to: Dr. Olavi Ylikorkala, M.D., First Department of Obstetrics and Gynecology, University of Helsinki, Haartmaninkatu 2, SF-00290 Helsinki, Finland.

Renal synthesis of the antiaggregatory and vasodilatory prostacyclin and its endogenous antagonist thromboxane A₂ may be disturbed in patients with preeclampsia. We tested this hypothesis by measuring 6-keto-prostaglandin Fio (6- keto-PGF₁; a hydration product of prostacyclin), 2,3-dinor-6- keto-PGF₁ (generated from 6-keto-PGF1; through β-oxidation) and thromboxane B₂ (a hydration product of thromboxane A₂) in the urine of healthy pregnant and preeclamptic women.Urinary excretion of 6-keto-PGF₁ [19.8 ± 10.5 pmol/mmol creatinine, (mean ± SD)] and 2,3-dinor-6-keto-PGF_l (19.2 ± 7.5 pmol/mmol creatinine) increased during normal pregnancy, reaching a maximum (about 5-fold rise) during the last month of pregnancy. No significant changes occurred in the urinary excretion of thromboxane B₂. In women with severe preeclampsia(n = 17), the excretion of both 6-keto-PGF_l (37.7 ± 29.5 pmol/mmol creatinine) and 2,3-dinor-6-keto-PGF₁ (54-5 ± 56.2 pmol/mmol creatinine) was lower (P < 0.001) than in the normotensive women during the last trimester of pregnancy (80.6 ± 43.7 and 98.7 ± 42.9 pmol/mmol creatinine, respectively). The neonates excreted 6-25 times more 6-keto-PGF₁, 2,3-dinor-6-keto-PGF₁, and thromboxane B₂ than did the nonpregnantwomen. In contrast to the adults, neonatal 6-keto-PGF₁ excretion was 2-3 times greater than that of 2,3-dinor-6-keto-PGF₁, suggesting reduced β-oxidation in the newborns. Infants born to preeclamptic women had reduced output of 6-keto-PGF₁ and 2,3-dinor-6-keto-PGF₁ on the first day of life. Thus, renal prostacyclin synthesis is diminished in women with severe preeclampsia and their infants.

^* The work was supported by grants from the Finnish Academy of Science, the Finnish Cancer Research Foundation, and the Sigrid Juselius Foundation.

Received February 4, 1986.

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