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Noble-Collip Drum Trauma Induces Disseminated Intravascular Coagulation But Not Acute Coagulopathy of Trauma-Shock

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/60737

Title: Noble-Collip Drum Trauma Induces Disseminated Intravascular Coagulation But Not Acute Coagulopathy of Trauma-Shock
Authors: Hayakawa, Mineji Browse this author →KAKEN DB
Gando, Satoshi Browse this author →KAKEN DB
Ono, Yuichi Browse this author
Wada, Takeshi Browse this author
Yanagida, Yuichiro Browse this author
Sawamura, Atsushi Browse this author →KAKEN DB
Ieko, Masahiro Browse this author →KAKEN DB
Keywords: Fibrinolysis
fibrinogenolysis
procoagulant
thrombin
fibrinolytic phenotype
ACoTS acute coagulopathy of trauma-shock
DIC disseminated intravascular coagulation
F factor
FDP fibrinogen
fibrin degradation products
FgDP fibrinogen degradation products
ETP endogenous thrombin potential
tPA tissue-type plasminogen activator
TIC trauma-induced coagulopathy
Issue Date: Mar-2015
Publisher: Lippincott Williams & Wilkins
Journal Title: Shock
Volume: 43
Issue: 3
Start Page: 261
End Page: 267
Publisher DOI: 10.1097/SHK.0000000000000281
PMID: 25423126
Abstract: Background: There are two opposing possibilities for the main pathogenesis of trauma-induced coagulopathy: an acute coagulopathy of trauma shock and disseminated intravascular coagulation with the fibrinolytic phenotype. Objective: The objective of this study was to clarify the main pathogenesis of trauma-induced coagulopathy using a rat model of Noble-Collip drum trauma. Methods: Eighteen rats were divided into the control, trauma 0, and trauma 30 groups. The trauma 0 and 30 groups were exposed to Noble-Collip drum trauma. Blood samples were drawn without, immediately after, and 30 min after Noble-Collip drum trauma in the control, trauma 0, and trauma 30 groups, respectively. Coagulation and fibrinolysis markers were measured. Thrombin generation was assessed according to a calibrated automated thrombogram. Results: Spontaneous thrombin bursts resulting from circulating procoagulants were observed in the nonstimulated thrombin generation assay immediately after trauma. Soluble fibrin levels (a marker of thrombin generation in the systemic circulation) were 50-fold greater in the trauma groups than in the control group. The resultant coagulation activation consumed platelets, coagulation factors, and antithrombin. Endogenous thrombin potential and factor II ratio were significantly negatively correlated with antithrombin levels, suggesting insufficient control of thrombin generation by antithrombin. High levels of active tissue-type plasminogen activator induced hyperfibrin(ogen)olysis. Soluble thrombomodulin increased significantly. However, activated protein C levels did not change. Conclusions: The systemic thrombin generation accelerated by insufficient antithrombin control leads to the consumption of platelets and coagulation factors associated with hyperfibrin(ogen)olysis. These changes are collectively termed disseminated intravascular coagulation with the fibrinolytic phenotype.
Rights: This is a non-final version of an article published in final form in "Shock", 43(3):261-267, March 2015.
Relation: http://www.shockjournal.com/
Type: article (author version)
URI: http://hdl.handle.net/2115/60737
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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