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Massive amounts of tissue factor induce fibrinogenolysis without tissue hypoperfusion in rats

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Title: Massive amounts of tissue factor induce fibrinogenolysis without tissue hypoperfusion in rats
Authors: Hayakawa, Mineji Browse this author →KAKEN DB
Gando, Satoshi Browse this author →KAKEN DB
Ieko, Masahiro Browse this author →KAKEN DB
Honma, Yoshinori Browse this author
Homma, Taeko Browse this author
Yanagida, Yuichiro Browse this author
Kubota, Nobuhiko Browse this author
Uegaki, Shinji Browse this author
Sawamura, Atsushi Browse this author →KAKEN DB
Asakura, Hidesaku Browse this author →KAKEN DB
Keywords: Fibrin fibrinogen degradation products
fibrinolysin
fibrinolysis
multiple trauma
thromboplastin
Issue Date: Jun-2013
Publisher: Lippincott Williams & Wilkins
Journal Title: Shock
Volume: 39
Issue: 6
Start Page: 514
End Page: 519
Publisher DOI: 10.1097/SHK.0b013e318293980d
PMID: 23542400
Abstract: Trauma-induced tissue factor (TF) release into the systemic circulation is considered to play an important role in the development of disseminated intravascular coagulation (DIC) immediately after severe trauma. However, the relationship between TF and hyperfibrinolysis, especially fibrinogenolysis, has been unclear. A total of 18 rats were divided into three groups: (a) the control group was infused with normal saline; (b) the low-dose group was infused with 4 U/kg TF; and (c) the high-dose group was infused with 16 U/kg TF. Arterial blood was drawn immediately and 2 and 4 h after the start of TF infusion. At each sampling point, arterial blood gases, platelet counts, and coagulation variables were measured. The fibrinogen degradation products were evaluated by a Western blot analysis. 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 with the other groups. The amounts of fibrinogen degradation products increased in proportion to the doses of TF. The plasmin-alpha 2-plasmin inhibitor complex level in the high-dose group increased more than that of the other groups. In conclusion, 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 hyperfibrin(ogen)olysis after TF administration.
Rights: This is a non-final version of an article published in final form in Shock. 39(6):514-519, June 2013.
Relation: http://www.shockjournal.com
Type: article (author version)
URI: http://hdl.handle.net/2115/56243
Appears in Collections:北海道大学病院 (Hokkaido University Hospital) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 早川 峰司

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