ArticlePloS one2016
Inducing Acute Traumatic Coagulopathy In Vitro: The Effects of Activated Protein C on Healthy Human Whole Blood.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Risk prediction of sepsis-associated acute kidney injury: development, validation of a machine learning model with multicenter data.BMC medical informatics and decision making · 2026Article
- Radiation-induced multi-organ injury.International journal of radiation biology · 2024Article
- The Multitarget Action of Vitamins in the Ischemic Stroke.Current topics in medicinal chemistry · 2024Review
- circ_0001274 Competitively Binds miR-143-3p to Upregulate VWF Expression to Improve Acute Traumatic Coagulopathy.Oxidative medicine and cellular longevity · 2023Article
- Article
- Variability in international normalized ratio and activated partial thromboplastin time after injury are not explained by coagulation factor deficits.The journal of trauma and acute care surgery · 2019Article
- Trauma-induced coagulopathy: The past, present, and future.Journal of thrombosis and haemostasis : JTH · 2019Review
- New considerations on pathways involved in acute traumatic coagulopathy: the thrombin generation paradox.World journal of emergency surgery : WJES · 2019Article
- The roles of activated protein C in experimental trauma models.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2018Review
- A clinically relevant and bias-controlled murine model to study acute traumatic coagulopathy.Scientific reports · 2018Article
- Activated protein C plays no major roles in the inhibition of coagulation or increased fibrinolysis in acute coagulopathy of trauma-shock: a systematic review.Thrombosis journal · 2018Review
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
introductionAcute traumatic coagulopathy has been associated with shock and tissue injury, and may be mediated via activation of the protein C pathway. Patients with acute traumatic coagulopathy have prolonged PT and PTT, and decreased activity of factors V and VIII; they are also hypocoagulable by thromboelastometry (ROTEM) and other viscoelastic assays. To test the etiology of this phenomenon, we hypothesized that such coagulopathy could be induced in vitro in healthy human blood with the addition of activated protein C (aPC).
methodsWhole blood was collected from 20 healthy human subjects, and was "spiked" with increasing concentrations of purified human aPC (control, 75, 300, 2000 ng/mL). PT/PTT, factor activity assays, and ROTEM were performed on each sample. Mixed effect regression modeling was performed to assess the association of aPC concentration with PT/PTT, factor activity, and ROTEM parameters.
resultsIn all subjects, increasing concentrations of aPC produced ROTEM tracings consistent with traumatic coagulopathy. ROTEM EXTEM parameters differed significantly by aPC concentration, with stepwise prolongation of clotting time (CT) and clot formation time (CFT), decreased alpha angle (α), impaired early clot formation (a10 and a20), and reduced maximum clot firmness (MCF). PT and PTT were significantly prolonged at higher aPC concentrations, with corresponding significant decreases in factor V and VIII activity.
conclusionA phenotype of acute traumatic coagulopathy can be induced in healthy blood by the in vitro addition of aPC alone, as evidenced by viscoelastic measures and confirmed by conventional coagulation assays and factor activity. This may lend further mechanistic insight to the etiology of coagulation abnormalities in trauma, supporting the central role of the protein C pathway. Our findings also represent a model for future investigations in the diagnosis and treatment of acute traumatic coagulopathy.
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