| Project/Area Number |
04454418
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Osaka University |
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Principal Investigator |
MIYAKE Akira Osaka Univ.Med.School Lecturer, 医学部, 講師 (90093468)
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| Co-Investigator(Kenkyū-buntansha) |
NISHIZAKI Takamichi Osaka Univ.Med.School Assistant Professor, 医学部, 助手 (20237689)
KURACHI Hirohisa Osaka Univ.Med.School Assistant Professor, 医学部, 助手 (40153366)
TASAKA Keiichi Osaka Univ.Med.School Assistant Professor, 医学部, 助手 (50155058)
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| Project Period (FY) |
1992 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥6,300,000 (Direct Cost: ¥6,300,000)
Fiscal Year 1994: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1993: ¥4,100,000 (Direct Cost: ¥4,100,000)
Fiscal Year 1992: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | superoxide / prostaglandin / SOD / calcium / magnesium / EGF / TGF-alpha / スーパーオキシド / 羊膜 / 脱落膜 / 子宮筋 / プロスタグランヂン / 細胞内カルシウム / スーパーオキシト / カルシウム / マグネシウム / pH |
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| Research Abstract |
Intrauterine infection is thought to be one of the major causes of the threatened premature delivery. However the mechanisms of uterine contraction caused by the intrauterine infection is still unknown. When a local infection occured, then some components of micro-organims induces the activation of immmune system, then the granulocytres gatherd to th local erea. Granulocytes produces superoxide, corticostatin'or some basic products which accerelates tissue damages. The aminion cells are supposed to have some roles in the infection-induced uterine contraction. We, first, determined the action of superoxide anion on the amnion cells. The results are as follows. Superoxide anion incresases intracellular free calcium concentrations and stimulates the production of prostaglandins which induces uterine contraction. The decrease in the intracellular magnesiun are also involved in the action of superoxide anion. Superoxide anion also has direct effects on the contarctility of uterine muscles v
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ia the increase of intracelluar free calcium concentrations. These effects are inhibited by the presense of a scavenger enzyme, SOD,or calcium channel blockers. Therefore aveilability of these substances as drugs for premature delivery induced by the intrauterine infection are also suggested. The administration of magnesium has long been tried for premature labor, but the mechanisms of this therapy has not been completely clarified. We clarified that the high concentartion of extracellular magnesium will raise the intracelluar magnesium concentartions, which resulted in irresponsiveness of the intracellular free calcium concentartions in the uterine muscles as a calcium channel blocker. We also clarified that amnion cells have high potency of proloferation. We clarified that the autocrine mechanisms of epideramal growth factor and TGF-alpha are involved in the proriferation. Tis results have an important meaning fron the view point of the repair of amniotic membrane.
The results of our study will have some contribution in the controle of of infection-induced premature labor. Less
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