EA4324-ORPHY, Université de Bretagne Occidentale, IBSAM, UFR Sciences et Techniques, 6 Avenue Le Gorgeu, CS 93837, 29238 Brest Cedex 3, France, Brest, France.
Department of emergency medicine, CHU Pontchaillou, 2 Rue Henri le Guilloux, 35000, Rennes, France.
Sci Rep. 2018 Apr 10;8(1):5783. doi: 10.1038/s41598-018-24225-1.
Acute traumatic coagulopathy (ATC) is an acute and endogenous mechanism triggered by the association of trauma and hemorrhage. Several animal models have been developed, but some major biases have not yet been identified. Our aim was to develop a robust and clinically relevant murine model to study this condition. Anesthetized adult Sprague Dawley rats were randomized into 4 groups: C, control; T, trauma; H, hemorrhage; TH, trauma and hemorrhage (n = 7 each). Trauma consisted of laparotomy associated with four-limb and splenic fractures. Clinical variables, ionograms, arterial and hemostasis blood tests were compared at 0 and 90 min. ATC and un-compensated shock were observed in group TH. In this group, the rise in prothrombin time and activated partial thromboplastin was 29 and 40%, respectively. Shock markers, compensation mechanisms and coagulation pathways were all consistent with human pathophysiology. The absence of confounding factors, such as trauma-related bleeding or dilution due to trans-capillary refill was verified. This ethic, cost effective and bias-controlled model reproduced the specific and endogenous mechanism of ATC and will allow to identify potential targets for therapeutics in case of trauma-related hemorrhage.
急性创伤性凝血病（ATC）是一种由创伤和出血共同引起的急性内源性机制。已经开发了几种动物模型，但一些主要的偏差尚未被识别。我们的目的是开发一种稳健且与临床相关的小鼠模型来研究这种情况。麻醉的成年 Sprague Dawley 大鼠随机分为 4 组：C，对照组；T，创伤组；H，出血组；TH，创伤和出血组（每组 n=7）。创伤包括剖腹术，伴有四肢和脾脏骨折。在 0 和 90 分钟时比较临床变量、离子谱、动脉和止血血液测试。在 TH 组观察到 ATC 和未代偿性休克。在该组中，凝血酶原时间和活化部分凝血活酶时间分别升高 29%和 40%。休克标志物、代偿机制和凝血途径均与人类病理生理学一致。已经证实没有混杂因素，例如与创伤相关的出血或由于毛细血管再充盈引起的稀释。这种符合伦理、具有成本效益且偏差得到控制的模型再现了 ATC 的特定和内源性机制，并将有助于确定与创伤相关的出血情况下治疗的潜在靶点。
