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• W2496248742 abstract "Essentials•Acidosis, an outcome of traumatic injury, has been linked to impaired procoagulant efficiency.•In vitro model systems were used to assess coagulation dynamics at pH 7.4 and 7.0.•Clot formation dynamics are slightly enhanced at pH 7.0 in blood ex vivo.•Acidosis induced decreases in antithrombin efficacy offset impairments in procoagulant activity.Summary: BackgroundDisruption of hydrogen ion homeostasis is a consequence of traumatic injury often associated with clinical coagulopathy. Mechanisms by which acidification of the blood leads to aberrant coagulation require further elucidation.ObjectiveTo examine the effects of acidified conditions on coagulation dynamics using in vitro models of increasing complexity.MethodsCoagulation dynamics were assessed at pH 7.4 and 7.0 as follows: (i) tissue factor (TF)‐initiated coagulation proteome mixtures (±factor [F]XI, ±fibrinogen/FXIII), with reaction progress monitored as thrombin generation or fibrin formation; (ii) enzyme/inhibitor reactions; and (iii) TF‐dependent or independent clot dynamics in contact pathway‐inhibited blood via viscoelastometry.ResultsRate constants for antithrombin inhibition of FXa and thrombin were reduced by ~ 25–30% at pH 7.0. At pH 7.0 (+FXI), TF‐initiated thrombin generation showed a 20% increase in maximum thrombin levels and diminished thrombin clearance rates. Viscoelastic analyses showed a 25% increase in clot time and a 25% reduction in maximum clot firmness (MCF). A similar MCF reduction was observed at pH 7.0 when fibrinogen/FXIII were reacted with thrombin. In contrast, in contact pathway‐inhibited blood (n = 6) at pH 7.0, MCF values were elevated 6% (95% confidence interval [CI]: 1%–11%) in TF‐initiated blood and 15% (95% CI: 1%– 29%) in the absence of TF. Clot times at pH 7.0 decreased 32% (95% CI: 15%–49%) in TF‐initiated blood and 51% (95% CI: 35%–68%) in the absence of TF.ConclusionsDespite reported decreased procoagulant catalysis at pH 7.0, clot formation dynamics are slightly enhanced in blood ex vivo and suppression of thrombin generation is not observed. A decrease in antithrombin reactivity is one potential mechanism contributing to these outcomes. Essentials•Acidosis, an outcome of traumatic injury, has been linked to impaired procoagulant efficiency.•In vitro model systems were used to assess coagulation dynamics at pH 7.4 and 7.0.•Clot formation dynamics are slightly enhanced at pH 7.0 in blood ex vivo.•Acidosis induced decreases in antithrombin efficacy offset impairments in procoagulant activity. •Acidosis, an outcome of traumatic injury, has been linked to impaired procoagulant efficiency.•In vitro model systems were used to assess coagulation dynamics at pH 7.4 and 7.0.•Clot formation dynamics are slightly enhanced at pH 7.0 in blood ex vivo.•Acidosis induced decreases in antithrombin efficacy offset impairments in procoagulant activity. Disruption of hydrogen ion homeostasis is a consequence of traumatic injury often associated with clinical coagulopathy. Mechanisms by which acidification of the blood leads to aberrant coagulation require further elucidation. To examine the effects of acidified conditions on coagulation dynamics using in vitro models of increasing complexity. Coagulation dynamics were assessed at pH 7.4 and 7.0 as follows: (i) tissue factor (TF)‐initiated coagulation proteome mixtures (±factor [F]XI, ±fibrinogen/FXIII), with reaction progress monitored as thrombin generation or fibrin formation; (ii) enzyme/inhibitor reactions; and (iii) TF‐dependent or independent clot dynamics in contact pathway‐inhibited blood via viscoelastometry. Rate constants for antithrombin inhibition of FXa and thrombin were reduced by ~ 25–30% at pH 7.0. At pH 7.0 (+FXI), TF‐initiated thrombin generation showed a 20% increase in maximum thrombin levels and diminished thrombin clearance rates. Viscoelastic analyses showed a 25% increase in clot time and a 25% reduction in maximum clot firmness (MCF). A similar MCF reduction was observed at pH 7.0 when fibrinogen/FXIII were reacted with thrombin. In contrast, in contact pathway‐inhibited blood (n = 6) at pH 7.0, MCF values were elevated 6% (95% confidence interval [CI]: 1%–11%) in TF‐initiated blood and 15% (95% CI: 1%– 29%) in the absence of TF. Clot times at pH 7.0 decreased 32% (95% CI: 15%–49%) in TF‐initiated blood and 51% (95% CI: 35%–68%) in the absence of TF. Despite reported decreased procoagulant catalysis at pH 7.0, clot formation dynamics are slightly enhanced in blood ex vivo and suppression of thrombin generation is not observed. A decrease in antithrombin reactivity is one potential mechanism contributing to these outcomes." @default.
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• W2496248742 date "2016-10-01" @default.
• W2496248742 modified "2023-10-05" @default.
• W2496248742 title "Effects of an acidic environment on coagulation dynamics" @default.
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• W2496248742 doi "https://doi.org/10.1111/jth.13418" @default.
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