| Project/Area Number |
05671906
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
応用薬理学・医療系薬学
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| Research Institution | Showa University |
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Principal Investigator |
YAMAMOTO Toshinori School of Pharmaceutical Sciences, Showa University, Associate Professor, 薬学部, 助教授 (30112741)
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| Co-Investigator(Kenkyū-buntansha) |
YASUDA Masako School of Pharmaceutical Sciences, Showa University, Assistant Researcher, 薬学部, 助手 (30260079)
FUNAYAMA Norio School of Pharmaceutical Sciences, Showa University, Assistant Researcher, 薬学部, 助手 (50245875)
SHIMIZU Shunichi School of Pharmaceutical Sciences, Showa University, Assistant Researcher, 薬学部, 助手 (60196516)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1994: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1993: ¥500,000 (Direct Cost: ¥500,000)
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| Keywords | ENDOTHELIAL CELL / REACTIVE OXYGEN SPECIES / NITRIC OXIDE / POLYMORPHONUCLEAR / ISCHEMIA-REPERFUSION / HYDROGEN PEROXIDE / MUSCLE RELAXATION / CELL INJURY / 細胞障害 / 多形核白血球 / カルシウムイオン |
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| Research Abstract |
Early step of mechanisms on endothelial cells injury caused by an activated polymorphonuclear (PMN) are not well understood. Especially, the interactions of nitric oxide and active oxygen species (ROS) are not known. In this study, we focused on the endothelial function (muscle relaxing action) to clarify the contribution of extra-and intracellular nitric oxide and ROS to cell injury.
1) By the addition of activated PMN to blood vessel, at first the relaxation of blood muscle was a little reduced and then recovered gradually. This phenomena could be caused by the interaction of nitric oxide and ROS formed from PMN.
2) Hydrogen peroxide (1 mM) stimulated a formation of nitric oxide in endothelial cells. Enhacement of NO formation lasted until cell death.
3) During ischemia-reperfusion, the relaxing ability of blood vessel reduced at the moment and then return to the basal level following the reperfusion.
From these results, the tonus of blood vessel could be regulated by the interaction of NO and ROS.In endothelial cells, the NO formation increased by exposing to ROS.Reperfusion after short term ischemia caused a temporal inhibition of relaxing action. Finally, the early step of ROS injury are static and reversible.
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