| Project/Area Number |
07671833
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Aichi Medical University |
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Principal Investigator |
SUZUKI Masatoshi Aichi Medical University, Department of Obstetrics and Gynecology, Associate Professor, 医学部, 助教授 (90093426)
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| Co-Investigator(Kenkyū-buntansha) |
MASAHASHI Tetsuo Aichi Medical University, Department of Obstetrics and Gynecology, Assistant Pro, 医学部, 講師 (60159142)
ASAI Mitsuoki Aichi Medical University, Department of Obstetrics and Gynecology, Associate Pro, 医学部, 助教授 (50151014)
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| Project Period (FY) |
1995 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1997: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1996: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1995: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | Human Placenta / Chorionic Plate Vessel / Nitric Oxide / Endothelin / Serotonin / Ethanol / Estrogen / L-NAME / ニトロプルシッド / ベラパミル / イオンチャンネル / カフェイン / EDHF / U-46619 / L-Arginine |
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| Research Abstract |
The aim of this study was to investigate the effects of various vasoactive factors on the human placental vessels and to elucidate their mechanisms of actions.
We could show that ; 1) endothelin-1 (ET-1), U-46619 and serotonin (5-HT) produced concentration-dependent contractions in placental vessels, but angiotensin II and phenylephrine demonstrated no constrictor activity, 2) a subthreshold concentration of ET-1 potentiated significantly the contractile response and sensitivity of 5-HT,3) preincubation in indomethacin and L-NAME potentiated the contraction response to ET-1 and 5-HT,and especially in 5-HT both maximum tension and sensitivity were significantly increased, 4) estradiol (E2) revealed a vasodilated activity antagonized to tamoxifen in fetal placental circulation, 5) the mechanisms of vasodilated activity of E2 were stimulation of cyclooxygenase activity, rapid antagonism of calcium channel, and agonistic function to potassium channel, 6) vasoconstrictor effect of ethanol was revealed in both placental perfusion study and vessel ring study, and 7) vasoconstricted activities of ethanol were induced by the influx of extracellular calcium and the release of calcium from the intracellular calcium store.
We need more effort to elucidate the mechanisms of actions of other vasoactive factors in human placental vessels and the interaction of these factors. If these studies were completed, we could show the mechanisms of intra-uterine growth retardation (IUGR) because of the impairment of placental circulation, and also show the therapeutical way for IUGR.
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