Massachusetts Medical Society

Evans, Stephen; Fd, Frigoletto; Jf, Jewett

doi:10.1056/nejm198312293092612

Cited by 18 publications

(1 citation statement)

References 11 publications

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“…Treatment of preeclampsia has not changed significantly in decades: rest, antihypertensive agents, timely delivery, and parenteral MgSO4 (13 (15). Cells were cultured under 95% air/5% CO2 at 37°C in medium 199 containing 20% fetal bovine serum (GIBCO).…”

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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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confidence: 99%