Increased placental progesterone may cause decreased placental prostacyclin production in preeclampsia

Article Abstract:

Preeclampsia is a complication of pregnancy marked by high blood pressure, swelling and protein in the urine. Placentas obtained from preeclamptic patients produce abnormal amounts of thromboxane, a substance produced by platelets (which are necessary for the formation of blood clots). Thromboxane constricts blood vessels. Blood vessel constriction may contribute to the development of major symptoms related to preeclampsia. Additionally, the placentas of preeclamptic patients produce less prostacyclin, a substance known to dilate blood vessels and inhibit platelet cells from aggregating during the clotting process. Thromboxane prevents prostacyclin from exerting its effect on platelets. When cells derived from placental tissue of preeclamptic patients were cultured in the laboratory, progesterone concentrations were found to be higher than normal placental tissue while estrogen production remained the same. Cells derived from normal placentas were grown in the laboratory and exposed to a progesterone concentration similar to that produced by preeclamptic placental cells in culture. The level of thromboxane and prostacyclin were then measured to see if progesterone or estrogen can cause an imbalance in normal placental tissue similar to that produced by preeclamptic placental cells. Progesterone levels similar to those produced by preeclamptic placental cells inhibited the production of prostacyclin. Thromboxane was not affected by progesterone or estrogen. The increased thromboxane production in preeclamptic patients appears to be independent of progesterone. (Consumer Summary produced by Reliance Medical Information, Inc.)

Research, Abnormalities, Thromboxanes, Progesterone, Placental hormones

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Preeclampsia: the effects of serum on endothelial cell prostacyclin, endothelin, and cell membrane integrity

Article Abstract:

Preeclampsia may inhibit production of endothelin in the blood without changing prostacyclin levels or killing endothelial cells. Preeclampsia is a serious complication of pregnancy involving high blood pressure and protein in the urine. Endothelin is a blood vessel constricting hormone while prostacyclin is a vasodilating hormone, and endothelial cells line blood vessels. Researchers compared the effect on endothelial cells of prostacyclin and endothelin in blood from 12 women with preeclampsia, 23 normal pregnant women, 11 pregnant women with high blood pressure alone, and 23 nonpregnant women. Blood from women with preeclampsia produced less endothelin than did blood from nonpregnant women or from normal pregnant women. Preeclamptic blood produced similar levels of prostacyclin as did normal pregnant women's blood.

Endothelium

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Elevated endothelin levels are associated with increased placental resistance

Article Abstract:

Increased levels of endothelin-1,2 may be found in fetuses with abnormal flow velocity in the umbilical artery or a reduced amniotic fluid volume. Researchers obtained endothelin-1,2 measurements before and at delivery from 16 growth-restricted infants with abnormal umbilical artery flow velocity Doppler waveforms and from 16 growth-restricted infants with normal flow velocity Doppler waveforms, and at delivery from 44 infants of normal size. Endothelin-1,2 levels were much higher in cord blood from growth-restricted infants with abnormal flow velocity waveforms than in growth-restricted infants with normal flow velocity waveforms or in normal-sized infants. Endothelin-1,2 may foster the development of abnormal vascular resistance between the fetus and placenta, leading to intrauterine growth restriction.

Diagnosis, Fetus, Fetal growth retardation, Oligohydramnios

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