Res Commun Chem Pathol Pharmacol
December 1993
The teratogenicity of 13-cis-retinoic acid (RA) either administered alone or following pretreatment with phenobarbital sodium (PB), was assessed. Groups of gravid CF-1 mice were administered dosages of either 10, 100, 200, or 400 mg/kg of RA orally on either days 11, 12 or 13 of gestation, in order to determine structural alterations. In addition, separate groups of mice were orally pretreated with 80 mg/kg/day of PB on days 7 through 10 of gestation prior to the administration of RA.
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August 1992
Because a balance between the vasodilator effect of Prostacyclin and the vasoconstrictor effect of Prostaglandin F2 alpha (PGF2 alpha) may be necessary for the regulation of utero-placental-fetal blood flow, a study was designed to assess the influence of a stable prostacyclin analogue, Cicaprost, on the response to Prostaglandin F2 alpha in the perfused human placenta. Cicaprost produced a dose-dependent inhibition of the pressor response of 50 mcg of PGF2 alpha. The decrease in PGF2 alpha-induced pressor response by 0.
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January 1992
Studies were undertaken to evaluate the efficacy of the beta 2-adrenergic agonist ritodrine and the calcium channel blocker nifedipine, alone and in combination, for inhibition of contraction in isolated rat uterine strips. Both compounds produced a dose-dependent reduction of area under the curve. When contractions were produced by oxytocin, a 26% reduction was observed with 0.
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October 1989
Studies were undertaken on perfused human placentas to examine the effect of a stable prostacyclin analogue (iloprost) on the angiotensin-II (A-II) response in the placental vessels, and to examine how this response is influenced by cyclooxygenase inhibition. Iloprost, in doses of 1, 5, and 10 micrograms significantly reduced the response of 50 micrograms of A-II. The vasoconstriction produced by the autacoid was attenuated by the three doses of iloprost by 43.
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August 1988
Studies on full-term human placentas were conducted to determine whether the vasogenic actions of certain agents on perfused placental vasculature are due to histamine release. Compound 48/80 and morphine were selected because they liberate the autacoid via different mechanisms. Initially, a control effluent was collected prior to each drug challenge and again collected throughout the rise and fall in perfusion pressure.
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