活化蛋白C在实验性创伤模型中的作用。
The roles of activated protein C in experimental trauma models.
作者信息
Gando Satoshi, Mayumi Toshihiko, Ukai Tomohiko
机构信息
Acute and Critical Care Center, Department of Acute and Critical Care Medicine, Sapporo Higashi Tokushukai Hospital, Japan.
Department of Emergency Medicine, School of Medicine, University of Occupational and Environmental Health, Japan.
出版信息
Chin J Traumatol. 2018 Dec;21(6):311-315. doi: 10.1016/j.cjtee.2018.07.005. Epub 2018 Dec 11.
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.
创伤性凝血病分为原发性和继发性凝血病，前者由创伤和创伤性休克本身引起，后者是由贫血、低温、酸中毒和稀释导致的获得性凝血病。原发性凝血病包括弥散性血管内凝血和创伤性休克急性凝血病（ACOTS）。ACOTS的病理生理学是凝血酶生成受抑制以及活化蛋白C介导的纤溶酶原激活物抑制剂-1被中和，从而导致循环中低凝状态和高纤溶状态。本综述试图阐明活化蛋白C假说在实验性创伤模型中作为ACOTS主要病理生理学的有效性。
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