• Mineji Hayakwa, Takayoshi Ooyasu, Yoshihiro Sadamoto, Tomoyo Saito, Tomonao Yoshida, Kenichi Katabami, Takeshi Wada, Kunihiko Maekawa, and Masahiro Ieko.
• Department of Emergency Medicine, 163693Hokkaido University Hospital, Sapporo, Japan.
• Clin. Appl. Thromb. Hemost. 2020 Jan 1; 26: 1076029620950825.

AbstractWe investigated the relationships between circulating procoagulants and trauma severity, including cellular destruction, and the effects of thrombin generation on procoagulants in a rat blunt trauma model. The rats were subjected to tumbling blunt trauma, where they were tumbled for 0, 250, 500, or 1000 revolutions. Creatine kinase, nucleosome, and microparticle plasma levels increased gradually with trauma severity. Strong interrelationships were observed among creatine kinase, nucleosome, and microparticle levels. Time to initiation of thrombin generation shortened with increasing trauma severity. In accordance with trauma severity, prothrombin activity decreased, but the thrombin generation ratio increased. Time to initiation of thrombin generation and the thrombin generation ratio correlated with creatine kinase levels. In an in vitro study, a homogenized muscle solution, which included massive nucleosomes and microparticles, showed accelerated thrombin generation of plasma from healthy subjects. Procoagulants, such as microparticles and nucleosomes, are released from destroyed parenchymal cells immediately after external traumatic force, activating the coagulation cascade. The procoagulants shorten the time to initiation of thrombin generation. Furthermore, although coagulation factors are consumed, the thrombin generation ratio increases.

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