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Short-Term Effects of Glucocorticoids in the Human Fetal-Placental Circulation in Vitro

Mothers and Babies Research Centre (V.L.C., R.S.), Department of Endocrinology, John Hunter Hospital, University of Newcastle and Hunter Medical Research Institute, Newcastle, New South Wales 2310, Australia; and Department of Obstetrics and Gynaecology (E.M.W.), Monash Medical Centre, Monash University, Clayton, Victoria, 3168 Australia

Address all correspondence and requests for reprints to: Dr. V. L. Clifton, Department of Endocrinology, John Hunter Hospital, Locked Bag 1, Hunter Region Mail Center, Newcastle, New South Wales 2310, Australia.

Abstract

A number of studies demonstrate that both long-term and short-term exposure to glucocorticoids alters vascular function. We have examined whether the short-term administration of glucocorticoids into the human fetal-placental circulation affects placental arterial pressure and alters vascular responses to vasoconstrictive and vasodilator agents. Single lobules of term human placentae were bilaterally perfused in vitro with Krebs’ solution (maternal and fetal, 5 ml/min Krebs, 95% O2, 5% CO2, 37 C, pH 7.3), and changes in fetal-placental arterial perfusion pressure were measured. Dexamethasone (100 nM) infusion for 1 h into the fetal-placental circulation caused a significant decrease in basal arterial pressure (n = 19, t test, P < 0.05). Continuous dexamethasone infusion (100 nM) did not alter vasoconstrictive responses to PGF₂ (0.5–120 pM, n = 12, ANOVA, P > 0.05) or potassium chloride (5–600 mM, n = 12, ANOVA, P > 0.05) or vasodilator responses to CRH (53–7400 pM, n = 13, ANOVA, P > 0.05). However when fetal-placental vessels were submaximally preconstricted and then infused with dexamethasone alone (40 nM–10 µM), there was a dose-dependent decrease in arterial pressure (n = 8). Dexamethasone-induced dilation was not inhibited by blocking nitric oxide synthase or cyclo-oxygenase activity. These data suggest that dexamethasone can cause dilation in the fetal-placental circulation, possibly via an endothelium-independent pathway.

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