Plasma and Amniotic Fluid Prostacyclin and Thromboxane in Mild Pregnancy-Induced Hypertension

Brown, Haywood L.; Klein, Luella; Waitzman, Morton B.

doi:10.1055/s-2007-999761

Cited by 2 publications

(1 citation statement)

References 7 publications

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“…Thus, prostacyclin seem to be involved as a direct cause of hypertension in pregnancy too. Other studies showed elevated as well as reduced prostacyclin and thromboxane concentrations in pregnancy [3,5,14,15,25,26,28,29]. Perhaps, pregnancy induced hypertension may have more than a single homogenous etiology.…”

Section: Discussionmentioning

confidence: 95%

Plasma prostacyclin and thromboxane concentrations in 160 normotensive, hypotensive, and preeclamptic patients during pregnancy, delivery, and the post partum period

Goeschen¹,

Henkel²,

Behrens³

1993

Jpme

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Plasma concentrations of 6-keto-prostaglandin F1 alpha, a stable metabolite of prostacyclin, and TxB2 were measured in 160 women during pregnancy (n = 106), delivery (n = 40), and in the postpartum period (n = 14). Fifty nine patients had normal blood pressure, 10 had mild and 9 severe preeclampsia while 38 patients were hypotensive. Normotensive patients were grouped according to their gestational age: 22-26 weeks (n = 22), 27-31 weeks (n = 22), and 32-38 weeks (n = 15). 20 patients were in early first stage of delivery (cervical dilatation < or = 5 cm), 20 patients in late first stage (cervical dilatation > or = 6 cm). The concentration (mean value +/- SEM) of the PGI2 metabolite tended to increase during pregnancy without reaching significance (218 +/- 11; 225 +/- 10; 250 +/- 15 pg/ml). At the same time, TxB2 showed a decrease, which was most pronounced at 27-31 weeks (65 +/- 15; 40 +/- 2; 48 +/- 4 pg/ml; p < 0.001). The ratio of PGI2/TxA2 increased in parallel (4.9 +/- 0.4; 6 +/- 0.4; 4 +/- 0.5). There was no difference in plasma concentrations of PGI2 (figure 4) and TxA2 in patients with normal blood pressure, mild preeclampsia and hypotension, whereas in severe preeclampsia, the plasma concentration of PGI2 was significantly lower (p < 0.001) and of TxA2 significantly higher (p < 0.001). The ratio of PGI2/TxA2 shifted significantly to vasoconstriction in patients with severe preeclampsia (p < 0.0001) and to vasodilatation in those with hypotension (p < 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 95%

Plasma prostacyclin and thromboxane concentrations in 160 normotensive, hypotensive, and preeclamptic patients during pregnancy, delivery, and the post partum period

Goeschen¹,

Henkel²,

Behrens³

1993

Jpme

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Pregnancy-Induced Hypertension

Rogers

Thorp²

1997

Obstetrical & Gynecological Survey

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This paper discusses the spectrum of pregnancy-induced hypertension and presents a theory for its etiology. Endothelial injury is the purported precursor to pregnancy-induced hypertensive disorders, and this discussion expands on a possible mechanism by which injury could occur as a result of incomplete trophoblastic invasion. We review endothelin physiology and compare and contrast the evidence surrounding endothelin 1 as a putative mediator of PIH. An approach to treatment utilizing antagonists to the endothelin 1 receptor is introduced.

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Plasma and Amniotic Fluid Prostacyclin and Thromboxane in Mild Pregnancy-Induced Hypertension

Cited by 2 publications

References 7 publications

Plasma prostacyclin and thromboxane concentrations in 160 normotensive, hypotensive, and preeclamptic patients during pregnancy, delivery, and the post partum period

Plasma prostacyclin and thromboxane concentrations in 160 normotensive, hypotensive, and preeclamptic patients during pregnancy, delivery, and the post partum period

Pregnancy-Induced Hypertension

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