1993 Fiscal Year Final Research Report Summary
Role of Endothellial Cells in Reperfusion Injury : Studies on Mechanisms and Prohibition of Reperfusion Injury :
| Project/Area Number |
04454342
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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 |
Thoracic surgery
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| Research Institution | MIE UNIVERSITY |
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Principal Investigator |
YADA Isao MIE UNIV.FACULTY of MEDICINE, 医学部, 教授 (80093152)
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| Co-Investigator(Kenkyū-buntansha) |
SHINPO Hideto MIE UNIV.UNIVERSITY HOSPITAL, 医学部・附属病院, 助手 (70179076)
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| Project Period (FY) |
1992 – 1993
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| Keywords | Reperfusion injury / Endothelial cell / EDRF / Activated leucocyte / Ca^<++> influx / Calmodulin inhibitor |
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| Research Abstract |
Endothelial cells control the vessel tension with the production of EDRF, endothelin-1(ET-1) and so on. We studied about changes of EDRF and ET-1 between before and after the reperfusion. We used Ca^<++>blockers for studying their protecting effects of endothelial cells from reperfusion injury.
Our experimental model was perfectly separated endothelial cells and vessel smooth muscles, and only endothlial cells were added the ischemic and reperfusion damage. When activated leucocytes by PMA were added to ischemic edothelial cells, the production of EDRF decreased and the production of ET-1 increased. But when the attachments of endothelial cells and activated leucocytes were blocked by the filter, productions of EDRF and ET-1 had no change.
As for protecting effects of endothelial cells by Ca^<++> blockers, TMB-8 and ruthenium red which are intercellular Ca^<++> blockers had the most protecting effect at the level of 10muM/L1. But nicardipine which is one of Ca^<++>blockers at the level of membrane had no protecting effect. It was concluded that reperfusion injury was caused when activated leucocytes attached endothelial cells and then the production of EDRF decrease and the production of ET-1 increased, and that it was important to protect the increase of intercellular Ca^<++>.
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