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)
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