Effect of magnesium sulfate on eicosanoid levels in women with pregnancy-induced hypertension

William W. Andrews, Norman F. Gant, Ronald R. Magness

Research output: Contribution to journalArticle

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Abstract

Objective: The mechanism(s) by which magnesium sulfate (MgSO4) functions clinically to prevent eclamptic seizures in severe pregnancy-induced hypertension (PIH) is unknown; however, it has been reported to both enhance and inhibit prostacyclin (PGI2) production by umbilical vein endothelial cells. Because PGI2 is decreased in patients with PIH, we tested the hypothesis that MgSO4 increases vasodilatory prostaglandins [PGI2 and prostaglandin (PG)E2] relative to vasoconstrictor eicosanoids [thromboxane (Tx)A2 and PGF2aL] in patients with PIH. Methods: In 11 women with PIH (28-40 weeks' gestation), MgSO4 was administered i.v. as a 4-g loading dose, followed by 2 g/h continuous infusion. Plasma samples were obtained before and at 2 and 4 h of MgSO4 treatment. Main Outcome Measures: We measured the effects of i.v. MgSO4 on plasma 6-keto-PGF1aL, TxB2 (metabolites of PGI2 and TxA2, respectively), PGE2, and PGF2aL. Results: The control plasma 6-keto-PGF1aL levels and 6-keto-PGF1aL/TxB2 ratios averaged 22038 pg/mL and 1.410.35, respectively (SEM); they were decreased (P==0.03) after 2 h i.v. MgSO4 therapy to 7717 pg/mL and 0.470.13, respectively, and then rebounded by 4 h to 316122 pg/mL and 1.930.74, respectively. Although plasma TxB2 and PGE2 levels were unchanged by MgSO4 therapy (P>0.05), this treatment decreased (P==0.05) plasma PGF2aL concentrations from 13125 pg/mL to 9021 pg/mL at 2 h and to 8716 pg/mL at 4 h. Conclusion: These in vivo data obtained from women with PIH are consistent with in vitro observations that MgSO4 may either inhibit or stimulate PGI2 production by endothelial cells. Additionally, MgSO4 infusion resulted in a modest but statically significant reduction in circulating levels of PGF2aL.

Original languageEnglish (US)
Pages (from-to)71-82
Number of pages12
JournalHypertension in Pregnancy
Volume13
Issue number1
DOIs
StatePublished - 1994

Fingerprint

Magnesium Sulfate
Pregnancy Induced Hypertension
Eicosanoids
Epoprostenol
Dinoprostone
Endothelial Cells
Umbilical Veins
Thromboxane A2
Vasoconstrictor Agents
Therapeutics
Prostaglandins
Seizures
Outcome Assessment (Health Care)
Pregnancy

Keywords

  • Eicosanoids
  • Hypertension
  • Magnesium sulfate
  • Preeclampsia
  • Pregnancy

ASJC Scopus subject areas

  • Obstetrics and Gynecology
  • Internal Medicine

Cite this

Effect of magnesium sulfate on eicosanoid levels in women with pregnancy-induced hypertension. / Andrews, William W.; Gant, Norman F.; Magness, Ronald R.

In: Hypertension in Pregnancy, Vol. 13, No. 1, 1994, p. 71-82.

Research output: Contribution to journalArticle

Andrews, William W. ; Gant, Norman F. ; Magness, Ronald R. / Effect of magnesium sulfate on eicosanoid levels in women with pregnancy-induced hypertension. In: Hypertension in Pregnancy. 1994 ; Vol. 13, No. 1. pp. 71-82.
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N2 - Objective: The mechanism(s) by which magnesium sulfate (MgSO4) functions clinically to prevent eclamptic seizures in severe pregnancy-induced hypertension (PIH) is unknown; however, it has been reported to both enhance and inhibit prostacyclin (PGI2) production by umbilical vein endothelial cells. Because PGI2 is decreased in patients with PIH, we tested the hypothesis that MgSO4 increases vasodilatory prostaglandins [PGI2 and prostaglandin (PG)E2] relative to vasoconstrictor eicosanoids [thromboxane (Tx)A2 and PGF2aL] in patients with PIH. Methods: In 11 women with PIH (28-40 weeks' gestation), MgSO4 was administered i.v. as a 4-g loading dose, followed by 2 g/h continuous infusion. Plasma samples were obtained before and at 2 and 4 h of MgSO4 treatment. Main Outcome Measures: We measured the effects of i.v. MgSO4 on plasma 6-keto-PGF1aL, TxB2 (metabolites of PGI2 and TxA2, respectively), PGE2, and PGF2aL. Results: The control plasma 6-keto-PGF1aL levels and 6-keto-PGF1aL/TxB2 ratios averaged 22038 pg/mL and 1.410.35, respectively (SEM); they were decreased (P==0.03) after 2 h i.v. MgSO4 therapy to 7717 pg/mL and 0.470.13, respectively, and then rebounded by 4 h to 316122 pg/mL and 1.930.74, respectively. Although plasma TxB2 and PGE2 levels were unchanged by MgSO4 therapy (P>0.05), this treatment decreased (P==0.05) plasma PGF2aL concentrations from 13125 pg/mL to 9021 pg/mL at 2 h and to 8716 pg/mL at 4 h. Conclusion: These in vivo data obtained from women with PIH are consistent with in vitro observations that MgSO4 may either inhibit or stimulate PGI2 production by endothelial cells. Additionally, MgSO4 infusion resulted in a modest but statically significant reduction in circulating levels of PGF2aL.

AB - Objective: The mechanism(s) by which magnesium sulfate (MgSO4) functions clinically to prevent eclamptic seizures in severe pregnancy-induced hypertension (PIH) is unknown; however, it has been reported to both enhance and inhibit prostacyclin (PGI2) production by umbilical vein endothelial cells. Because PGI2 is decreased in patients with PIH, we tested the hypothesis that MgSO4 increases vasodilatory prostaglandins [PGI2 and prostaglandin (PG)E2] relative to vasoconstrictor eicosanoids [thromboxane (Tx)A2 and PGF2aL] in patients with PIH. Methods: In 11 women with PIH (28-40 weeks' gestation), MgSO4 was administered i.v. as a 4-g loading dose, followed by 2 g/h continuous infusion. Plasma samples were obtained before and at 2 and 4 h of MgSO4 treatment. Main Outcome Measures: We measured the effects of i.v. MgSO4 on plasma 6-keto-PGF1aL, TxB2 (metabolites of PGI2 and TxA2, respectively), PGE2, and PGF2aL. Results: The control plasma 6-keto-PGF1aL levels and 6-keto-PGF1aL/TxB2 ratios averaged 22038 pg/mL and 1.410.35, respectively (SEM); they were decreased (P==0.03) after 2 h i.v. MgSO4 therapy to 7717 pg/mL and 0.470.13, respectively, and then rebounded by 4 h to 316122 pg/mL and 1.930.74, respectively. Although plasma TxB2 and PGE2 levels were unchanged by MgSO4 therapy (P>0.05), this treatment decreased (P==0.05) plasma PGF2aL concentrations from 13125 pg/mL to 9021 pg/mL at 2 h and to 8716 pg/mL at 4 h. Conclusion: These in vivo data obtained from women with PIH are consistent with in vitro observations that MgSO4 may either inhibit or stimulate PGI2 production by endothelial cells. Additionally, MgSO4 infusion resulted in a modest but statically significant reduction in circulating levels of PGF2aL.

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