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Studies for Mechanisms of Fetal Placental Insufficiency Using Dually Perfused Human Placenta

Research Project

Project/Area Number 12671638
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Obstetrics and gynecology
Research InstitutionAichi Medical University

Principal Investigator

ASAI Mitsuoki (2001-2002)  Aichi Medical University, Department of Obstetrics and Gynecology, Associate Professor, 医学部, 助教授 (50151014)

鈴木 正利 (2000)  愛知医科大学, 医学部, 助教授 (90093426)

Co-Investigator(Kenkyū-buntansha) HOJO Keiko  Aichi Medical University, Department of Obstetrics and Gynecology, Assistant Professor, 医学部, 助手 (30288534)
浅井 光興  愛知医科大学, 医学部, 助教授 (50151014)
Project Period (FY) 2000 – 2002
Project Status Completed (Fiscal Year 2002)
Budget Amount *help
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2002: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2001: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2000: ¥1,600,000 (Direct Cost: ¥1,600,000)
KeywordsHuman Placenta / Chorionic Plate Vessel / Placental perfusion / ADMA / Serotonin / Ethanol / NO / L-NAME / 胎盤胎児側循環 / 胎盤灌流 / indomethacin / prostacyclin / tetrahydrobiopterin / asymmetrical dimethylarginine / endothelin-1 / serotonin / 血管リング
Research Abstract

The aim of this study was to investigate the effects of various vasoactive factors on the human fetal placental vessels and to elucidate their mechanisms of actions using dually perfused placenta in vitro.
At first, we studied the effect of ethanol on placental circulation, and the acting mechanisms for this using a ring model of human fetal-placental vessels. This study demonstrates that ethanol acts to constrict vessels and raise the perfusion pressure on the fetal side of human placental circulation. These results show that the mechanism for this vessel-constricting action is related to a Ca^<2+> channel agonist-like activity, and the release of Ca^<2+> from the endoplasmic reticulum. In experiments using placental perfusion, the pre-administration of NG-nitro-L-arginine metyl ester-2HCl (L-NAME) intensified the vasopressor response to ethanol, while indomethacin (INDO) weakened it. However, in the experiment using isolated placental vessel rings, the pre-administration of L-NAME or … More INDO had no effect on the ethanol induced constriction. These results show that the NO produced by placental tissue suppresses the vessel-constricting response brought about by ethanol, whereas PGs intensify it. In conclusion, it appears that in the mechanism for fetal alcohol syndrome, which represents developmental delays in the intrauterine fetus, the impaired placental circulation due to the vessel-constricting action of ethanol is clearly involved.
Nitric oxide has a very important role in pre-eclampsia. We elucidated that; 1) Preincubation with indomethacin or L-NAME potentiated the contraction response to ET-1 and 5-HT, and both maximum tension and sensitivity were significantly increased under the conditions in 5-HT, and with L-NAME. That sensitivity was almost equal as ET-1, which is a potent vasoconstrictor. 2) The blood concentration of 5-HT was significantly higher than ET-1. These results suggested that 5-HT under the condition of NO synthase insufficiency (pre-eclampsia) was most potent vasoconstrictor. 3) Asymmetric dimethylarginine (ADMA) is well known as a natural inhibitor for NO synthase, and the blood concentration of ADMA was significantly higher in pre-eclamptic patients, and remarkably high in fetal circulation than in maternal circulation. These results hypothesize that the most potent factor for the elevation of blood pressure and intra-uterine growth retardation (IUGR) may be ADMA.
We need more effort to elucidate the mechanisms of actions of other vasoactive factors in human fetal placental vessels and the interaction of these factors. If these mechanisms were elucidated, we could show the mechanisms of IUGR because of the impairment of fetal placental circulation, and also show the therapeutical way for IUGR. Less

Report

(4 results)
  • 2002 Annual Research Report   Final Research Report Summary
  • 2001 Annual Research Report
  • 2000 Annual Research Report

Research Products

(6 results)

All Other

All Publications (6 results)

  • [Publications] 酒向 香: "Ethanolのヒト胎盤循環に及ぼす影響"愛知医科大学医学会雑誌. 28(2). 105-114 (2000)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] K.Sako: "Effect of ethanol on human placental vessels"Placenta. 21(8). A.29 (2000)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Kaori Sako: "Effects of ethanol on human placental circulation"Journal of the Aichi Medical University Association. 28 (2). 105-114 (2000)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Mitsuoki Asai, Kaori Sako, Mayumi Matsushita, Masatoshi Suzuki, Masayoshi Noguchi and Masami Nakanishi: "Effects of ethanol on human placental vessels"Placenta. 21. A.29 (2000)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] 酒向香: "Ethanolのヒト胎盤循環に及ぼす影響"愛知医科大学医学会雑誌. 28・2. 105-114 (2000)

    • Related Report
      2000 Annual Research Report
  • [Publications] Mitsuoki ASAI: "Effect of ethanol on human placental vessels"Placenta. 21・7. A.29 (2000)

    • Related Report
      2000 Annual Research Report

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Published: 2000-03-31   Modified: 2016-04-21  

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