Huang S, Tang Y, Lin W, et al. - In view of the global health issue concerning traumatic coagulopathy with undefined mechanisms, researchers established rat models of hemorrhagic shock (HS), multiple injury (MI) and traumatic brain injury (TBI) examining the diversity of traumatic coagulopathy, particularly platelet dysfunction. They divided 70 male SD rats randomly into seven groups(n = 10): control, HS_30min, HS_3h, MI_30min, MI_3h, TBI_30min, and TBI_3h. For conventional coagulation tests, thromboelastography and platelet mapping, they collected plasma or whole blood and to confirm the injuries of rats model, they conducted X-ray, 7T magnetic resonance imaging and hematoxylin-eosin staining of injured tissues. Outcomes suggest a possible contribution of the failure of forming a strong clot, instead of the prolonged clot time, in traumatic coagulopathy. Possibly, the main reason for HS-induced coagulopathy was the loss of platelets. Inhibition of arachidonic acid-dependent pathway seemed to account for MI-induced coagulopathy. For TBI-induced coagulopathy, the major contributor suggested was adenosine diphosphate-dependent pathway inhibition.