Abstract

The administration of a relatively high dose of delta-1 hydrocortisone to pregnant rats results in severe morphologic changes in virtually all of the placental tissues. As early as the fifteenth day of pregnancy, there is a marked inhibition of decidua formation and a severe decrease in decidual and “junctional zone” glycogen. In addition, delta-1 hydrocortisone inhibits trophoblastic proliferation and induces morphologic changes in the syncytial trophoblast which resemble “premature aging.” The over-all effect of these changes leads to a failure in placental growth during the eighteenth day of gestation and thereafter. The yolk sac epithelium becomes depleted of glycogen as early as the fifteenth day whereas the apical P.A.S.-positive granulations continue to increase in number until term, a process which leads to marked “clubbing” of the individual epithelial cells. These processes undoubtedly alter placental function severely and are reflected by a significant increase in intrauterine fetal death. The administration of a relatively high dose of delta-1 hydrocortisone to pregnant rats results in severe morphologic changes in virtually all of the placental tissues. As early as the fifteenth day of pregnancy, there is a marked inhibition of decidua formation and a severe decrease in decidual and “junctional zone” glycogen. In addition, delta-1 hydrocortisone inhibits trophoblastic proliferation and induces morphologic changes in the syncytial trophoblast which resemble “premature aging.” The over-all effect of these changes leads to a failure in placental growth during the eighteenth day of gestation and thereafter. The yolk sac epithelium becomes depleted of glycogen as early as the fifteenth day whereas the apical P.A.S.-positive granulations continue to increase in number until term, a process which leads to marked “clubbing” of the individual epithelial cells. These processes undoubtedly alter placental function severely and are reflected by a significant increase in intrauterine fetal death.

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