| Project/Area Number |
08671521
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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 |
Thoracic surgery
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| Research Institution | Mie University |
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Principal Investigator |
TANI Kazuhiro Mie University, Hospital Assistant, 医学部・附属病院, 助手 (80263010)
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| Project Period (FY) |
1996 – 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: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1996: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Cardiopulmonary by pass / Platelet / Glycoprotein Ib / Glycocalicin / Heparin coated circuits / 血小板膜表面糖蛋白 / GPIb / ヘパリンコーティング / ずり応力下血小板凝集率 / ヘパリンレコーティング体外循環 / Nafamostant mecilate / 血小板GPIb / 血漿Glycocalicin / TAT / PIC / PET1+2 |
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| Research Abstract |
Cardiopulmonary bypass (CPB) induces the activation of multiple biologic systems as a consequence of blood contact with the synthetic surfaces. It produces functional defects in platelets and coagulofibrinolytic abnormalities. The previous study reviled the platelet surface membrane glycoprotein Ib (GP Ib) decrease during CPB,but the mechanism of this reaction is not clear. In this study, we detect the locational change of GP Ib in the platelet and also evaluate the effect of heparin coated circuits on the coagulo fibrinolytic system and platelet membrane GP Ib.
1.During CPB at open heart surgery, thrombin/antithrombin III complex、prothrombin fragment F1+2 and alpha2 plasmin inhibit or/plasmin complex in creased and platelet surface GP Ib decreased but there was no significant change in the amount of serum glycocalicin.
2.In vitro study, high shear stress induced platelet aggregation, ristocetin induced platelet aggregation and platelet surface GP Ib significantly decrease during human blood circulation of experimental circuit. We measured a amount of GP Ib contained in platelet membrane skeleton and cytoskeleton using the westem blot method. Platelet membrane skeleton GP Ib decreased and cytoskeleton GP Ib increased during circulation of experimental circuit.
3.These changes was observed in group of heparin coated circuits, but was more smaller than in group of non coated circuit.
We conclude that platelet dysfunction caused by CPB results from redistribution of GP Ib from platelet surfaces on to surfaces connected to open canalicular system. Heparin coated circuits reduces these change and may preserve platelet function during CPB.
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