妊娠初期ラットにおけるprostaglandin F2αおよびE2による黄体退縮に及ぼすluteotropic factorの効果

DOI

書誌事項

タイトル別名
  • The effect of luteotropic factors on luteolysis by prostaglandin F2.ALPHA. and E2 in early pregnant rats.

抄録

There are various causes of abortion in the first trimester. Of all of these, endocrine dysfunction is least understood, and no definite treatment has been established.<BR>Therefore, the effect of luteotropic factors (prolactin, luteinizing hormone-releasing hormone, human chorionic gonadotropin, progesterone, and estradiol) on the breakdown of the endocrine system by the luteolytic factors (prostaglandin F2α and E2), was examined in early pregnant rats.<BR>1. Prolactin and luteinizing hormone-releasing hormone showed no luteotropic action for the corpus luteum of normal early pregnant rats. Human chorionic gonadotropin showed no luteotropic action, but follicle stimulating action was observed. Progesterone showed slight luteotropic action. Estradiol showed luteolytic action to induce abortion and can therefore be thought of as a luteolytic factor.<BR>2. It was ascertained that prostaglandin F2α and E2 caused luteolysis in early pregnant rats. This resulted in the breakdown of the endocrine system leading to an abortion in early pregnant rats. It was suggested that the prostaglandins acted directly against the corpus luteum. The luteolytic effect of prostaglandin F2α was higher than that of prostaglandin E2.<BR>3. Prolactin and luteinizing hormone-releasing hormone could not prevent the breakdown of the endocrine system by prostaglandin F2α and E2 in early pregant rats.<BR>Human chorionic gonadotropin showed luteotropic action, and prevented the breakdown of the endocrine system by prostaglandins. Its action was thought to be via its receptor in the corpus luteum graviditatis.<BR>Progesterone has a slight luteotropic action, as it maintained the endocrine system, which maintains pregnancy through secondary action against the luteolysis by prostaglandins. [Adv Obster Gynecol 47(1) : 61-76, 1995 (H7.1)]

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詳細情報 詳細情報について

  • CRID
    1390282679924221952
  • NII論文ID
    130004069577
  • DOI
    10.11437/sanpunosinpo1949.47.61
  • ISSN
    13476742
    03708446
  • 本文言語コード
    ja
  • データソース種別
    • JaLC
    • CiNii Articles
  • 抄録ライセンスフラグ
    使用不可

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