2012 Fiscal Year Final Research Report
Pathology and treatment of acute coagulopathy just after trauma
| Project/Area Number |
23792068
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Emergency medicine
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| Research Institution | Hokkaido University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2012
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| Keywords | 組織因子 / 線溶 / 凝固 / フィブリノゲン分解 |
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| Research Abstract |
Hypotension, hypoxemia and lactic acidosis were not observed in any of the three groups. In proportion to the doses of TF, the platelet counts, coagulation and fibrinolysis variables deteriorated in line with DIC. The alpha 2-plasmin inhibitor levels significantly decreased in the high dose group compared to the other groups. The amounts of FgDP increased in proportion to the doses of TF. The plasmin-alpha2-plasmin inhibitor complex level in the high dose group increased more than that of the other groups. In conclusions, TF can induce DIC associated with fibrinolysis and fibrinogenolysis without tissue hypoperfusion. The decrease in the alpha 2-plasmin inhibitor level and the significant increase in the plasmin level may be the two main factors underlying the pathogenesis of hyper-fibrin(ogen)olysis after TF administration.
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