Prostacyclin Activity in Amniotic Fluid in Pre-Eclampsia

Bodzenta, A; Thomson, Jean M.; Poller, L.

doi:10.1016/s0140-6736(80)90324-4

Cited by 56 publications

(7 citation statements)

References 10 publications

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“…Potentially PGI2 could be synthesised by the uterus, the placenta or by the foetus. Both foetal blood vessels (Remuzzi et al, 1980) and the uterus (Bodzenta et al, 1980) appear to produce less prostacyclin in PET than in normal pregnancies. This argues for a general defect in prostacyclin production which is supported by results from angiotensin infusion tests (Everett et al, 1978).…”

Section: Discussionmentioning

confidence: 91%

Kinetics of prostacyclin synthetase in umbilical artery microsomes from normal and pre‐eclamptic pregnancies.

Downing¹,

Shepherd²,

Pd³

1982

Brit J Clinical Pharma

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1 Prostacyclin synthetase in umbilical artery microsomes obeys Michaelis-Menten kinetics. 2 The maximum velocity (Vmax) of prostacyclin synthetase prepared from normal umbilical arteries was significantly higher than the Vmax of prostacyclin synthetase in umbilical arteries taken from pre-eclamptic pregnancies.3 The Michaelis-Menten constant (K1() of the two prostacyclin synthetase preparations was significantly different with the synthetase from pre-eclamptic arteries having a higher affinity for substrate. 4 The limiting factor for prostacyclin synthesis is Vmax at high substrate concentrations which appears to be the case in umbilical arteries. However, at low substrate concentration there would be no difference in prostacyclin synthesis by the two forms of prostacyclin synthetase.

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Section: Discussionmentioning

confidence: 91%

Kinetics of prostacyclin synthetase in umbilical artery microsomes from normal and pre‐eclamptic pregnancies.

Downing¹,

Shepherd²,

Pd³

1982

Brit J Clinical Pharma

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“…25 However, in preeclampsia PGI, production was reduced in umbilical and placental vascular tissue, 6 l7 26~M and in maternal subcutaneous and uterine vessels, 29 and a lower PGI 2 -like activity was found in amniotic fluid. 30 Surprisingly the plasmatic activity of prostacyclin-stimulating factor was not low in patients with severe preeclampsia 1 ' in contrast to late normotensive pregnancy; this has been seen as a compensatory phenomenon due to a decreased vascular prostacyclin synthesis in preeclampsia. 11 Furthermore, in the present study the lower urinary excretion of PGE, in preeclampsia most probably reflects a defect in renal prostaglandin synthesis, because PGE 2 is rapidly destroyed in the systemic circulation and thus is not carried to the kidneys by arterial blood.…”

Section: Discussionmentioning

confidence: 97%

“…The group consisted of 16 patients with a mean age of 28 years (range [18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35] and with a mean blood pressure of 153/ 103 mm Hg (range 173-142/117-90). All had proteinuria detected using a routine method, minimal 1.2 g/ day (range 0.2-5.5) and maximal 3.9 g/day (range 0.4-15.4).…”

Section: Patientsmentioning

confidence: 99%

“…Exclusion criteria were blood pressure elevation or proteinuria before, during or after delivery; symptoms of kidney, cardiovascular, liver, endocrine, or cerebrovascular disorders; or medical therapy. The group consisted of 18 patients with a mean age of 26 years (range [17][18][19][20][21][22][23][24][25][26][27][28][29][30], and a mean blood pressure of 108/64 mm Hg (range 125-93/80-50). Mean gestational age was 40 weeks (range 37-42) at delivery and 36 weeks at last examination in pregnancy.…”

Section: Patientsmentioning

confidence: 99%

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Preeclampsia -- a state of prostaglandin deficiency? Urinary prostaglandin excretion, the renin-aldosterone system, and circulating catecholamines in preeclampsia.

Pedersen¹,

Christensen²,

Christensen³

et al. 1983

Hypertension

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SUMMARY Urinary excretion of prostaglandin E 2 (PGE 2 ) and F^ (PGF^), plasma concentrations of renin, aldosterone, norepinephrine (NE) and epinephrine (E) were determined during pregnancy, 5 days, 3, and 6 months after delivery in preeciampsia, normotensive pregnant, and nonpregnant control subjects. The PGE 2 was higher in normotensive pregnant control subjects than in nonpregnant subjects. In preeciampsia, PGE, was reduced to nonpregnant level. PGF^ was the same in preeciampsia and in normotensive pregnancy, but elevated when compared to the normotensive nonpregnant control group. Plasma concentrations of renin and aldosterone were increased during pregnancy, but considerably less in preeciampsia than during normotensive pregnancy. NE and E were the same as in nonpregnant subjects during both hypertensive and normotensive pregnancy. All parameters were normal 3 months after delivery. There were no correlations between PGE 2 , PGF^, plasma concentrations of renin, aldosterone, NE, or E and blood pressure level in third trimester either in preeciampsia or in normotensive pregnancy. PGE, was positively correlated to plasma concentrations of renin. It is suggested that the lack of renal PGE 2 in preeciampsia might be responsible for the decrease in renal blood flow and sodium excretion. It is hypothesized that preeciampsia is a state of prostaglandin deficiency. The changes in the renin-aldosterone system may be secondary to changes in prostaglandin concentration both in preeciampsia and normotensive pregnancy. Received March 16, 1982, revision accepted August 12, 1982 with simultaneous evaluation of urinary prostaglandin excretion, the renin-aldosterone system, and sympathetic adrenergic activity in preeciampsia and normotensive pregnancy both before and after delivery.In the present study we measured urinary excretion of prostaglandin E 2 (PGE 2 ), prostaglandin F 2a (PGF 2 J, plasma renin concentration, plasma aldosterone concentration, plasma norepinephrine (NE) and plasma epinephrine (E) in patients with preeciampsia and in normotensive pregnant and nonpregnant control subjects. The pregnant groups were studied during pregnancy and 5 days, 3, and 6 months after delivery. To reveal possible pressor or depressor mechanisms in preeciampsia, it was our purpose to study changes in these parameters, correlations between these parameters and blood pressure, and relationships between urinary prostaglandins, the renin-aldosterone system, and the sympathetic nervous activity.

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“…Levels of prostacyclin (prostaglandin 12, PGI2), a potent inhibitor of platelet aggregation and a vasodilator (5), are decreased in the urine (6), amniotic fluid (7), and trophoblastic tissue (8) in preeclamptic pregnancies compared to levels in fluid and tissue samples obtained from normal pregnancies. Furthermore, umbilical vessels from preeclamptic patients synthesize less PGI2-like activity and convert arachidonic acid to PGI2 at a slower rate than those in normal pregnancy (9).…”

mentioning

confidence: 99%

Magnesium sulfate: rationale for its use in preeclampsia.

Watson

Moldow

Ogburn

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

125

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Preeclampsia is a disorder of pregnancy characterized clinically by hypertension, proteinuria, and edema and characterized pathologically in its late stages by widespread microvascular thrombi. There is evidence from a number of studies that production of prostacyclin (prostaglandin 12, PGI2), a potent vasodilator and inhibitor of platelet aggregation, is deficient in preeclamptic compared to normal pregnancy. Traditional therapy utilizes infusions of large amounts of MgSO4, but the physiologic basis for this is not clear. We studied the effect of MgSO4 on PGI2 release by cultured human umbilical vein endothelial cells (HUVEC) by several methods. By platelet aggregometry, the known antiaggregatory effect of intact HUVEC was enhanced by MgSO4. By radioimmunoassay for 6-keto-PGFia, the stable metabolite of PGI2, it was shown that MgSO4 amplifies release of PGI2 by HUVEC in a dose-dependent manner, with a peak occurring between 2 and 3 mM. In separate experiments, MgSO4 overcame the enhanced adherence of platelets to HUVEC exhausted by repeated exposure to thrombin. Finally, PGI2 production was 2-to 5-fold greater by HUVEC incubated with plasma obtained from preeclamptic patients undergoing MgSO4 therapy than by HUVEC incubated with pretherapy plasma. We conclude that MgSO4 mediates enhanced production of PGI2 by vascular endothelium, thereby potentially enhancing its thromboresistant properties.

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Prostacyclin Activity in Amniotic Fluid in Pre-Eclampsia

Cited by 56 publications

References 10 publications

Kinetics of prostacyclin synthetase in umbilical artery microsomes from normal and pre‐eclamptic pregnancies.

Kinetics of prostacyclin synthetase in umbilical artery microsomes from normal and pre‐eclamptic pregnancies.

Preeclampsia -- a state of prostaglandin deficiency? Urinary prostaglandin excretion, the renin-aldosterone system, and circulating catecholamines in preeclampsia.

Magnesium sulfate: rationale for its use in preeclampsia.

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