The roles of activated protein C in experimental trauma models.
10.1016/j.cjtee.2018.07.005
- Author:
Satoshi GANDO
1
;
Toshihiko MAYUMI
2
;
Tomohiko UKAI
3
Author Information
1. Acute and Critical Care Center, Department of Acute and Critical Care Medicine, Sapporo Higashi Tokushukai Hospital, Japan. Electronic address: gandoicoud@icloud.com.
2. Department of Emergency Medicine, School of Medicine, University of Occupational and Environmental Health, Japan.
3. Department of Social Medicine, Graduate School of Medicine, Osaka University, Japan.
- Publication Type:Journal Article
- Keywords:
Activated protein C;
Coagulopathy;
Disseminated intravascular coagulation;
Thrombin;
Trauma
- MeSH:
Acute Disease;
Animals;
Blood Coagulation Disorders;
etiology;
Disease Models, Animal;
Disseminated Intravascular Coagulation;
etiology;
Humans;
Mice;
Plasminogen Activator Inhibitor 1;
Protein C;
physiology;
Thrombin;
Wounds and Injuries;
complications
- From:
Chinese Journal of Traumatology
2018;21(6):311-315
- CountryChina
- Language:English
-
Abstract:
Trauma-induced coagulopathy is classified into primary and secondary coagulopathy, with the former elicited by trauma and traumatic shock itself and the latter being acquired coagulopathy induced by anemia, hypothermia, acidosis, and dilution. Primary coagulopathy consists of disseminated intravascular coagulation and acute coagulopathy of trauma shock (ACOTS). The pathophysiology of ACOTS is the suppression of thrombin generation and neutralization of plasminogen activator inhibitor-1 mediated by activated protein C that leads to hypocoagulation and hyperfibrinolysis in the circulation. This review tried to clarify the validity of activated protein C hypothesis that constitutes the main pathophysiology of the ACOTS in experimental trauma models.
