Vitamin E Attenuates Peroxideinduced Vasoconstriction in the Human Placenta

Abstract

Objective: Placental lipid peroxides and thromboxane are abnormally increased in preeclampsia. Peroxides stimulate thromboxane to increase placental vasoconstriction. Vitamin E is an antioxidant that inhibits lipid peroxidation. We, therefore, evaluated whether vitamin E would attenuate peroxideinduced vasoconstriction in the human placenta.Methods: Isolated human placental cotyledons (n = 6) were perfused for 20-min periods with control Krebs-Ringer-bicarbonate (KRB) buffer, 200 μM t-butyl hydroperoxide, control KRB buffer, 50 μM vitamin E, t-butyl hydroperoxide plus vitamin E, control KRB buffer, and t-butyl hydroperoxide alone.Main Outcome Measures: Fetal perfusion pressure was continually recorded and maternal (M) and fetal (F) effluent samples were collected for each treatment. Samples were analyzed for thromboxane and prostacyclin by RIA of their stable metabolites TXB2 and 6-keto PGF1α, respectively.Results: Compared to control KRB buffer, peroxide perfusion significantly increased perfusion pressure, vascular resistance, TXB2 secretion and 6-keto-PGF1α. After 20 min of perfusion with vitamin E, the ability of peroxide to increase perfusion pressure, vascular resistance, and TXB2, secretion was significantly attenuated and there was even further attenuation after 40 min of perfusion with vitamin E. Vitamin E did not affect the ability of peroxide to increase the secretion of 6-keto-PGF1α.Conclusions: (i) Vitamin E attenuates the ability of peroxide to increase placental vasoconstriction and thromboxane secretion, but not its ability to increase prostacyclin secretion, (ii) The attenuating effects of vitamin E increase with increased duration of exposure and its effects persist after it is discontinued, most likely because it is incorporated into the cell membranes.