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Updated: May 9, 2026
05:03
Brain Death Induction in Mice Using Intra-Arterial Blood Pressure Monitoring and Ventilation via Tracheostomy
Published on: April 17, 2020
Hypercoagulation following brain death cannot be reversed by the neutralization of systemic tissue factor
Christine L Hvas1, Christian Fenger-Eriksen, Søren Høyer
1Department of Anaesthesiology and Intensive Care Medicine, Aarhus University Hospital, 8000 Aarhus C, Denmark; Institute of Clinical Medicine, Aarhus University Hospital, 8200 Aarhus N, Denmark.
Thrombosis Research
|August 6, 2013
Summary
Brain death causes hypercoagulation, but inhibiting tissue factor (TF) does not reverse it. This suggests TF is not the primary cause of coagulopathy after brain injury.
Area of Science:
- Neuroscience
- Hematology
- Transplantation
Background:
- Cerebral injury and brain death are linked to hypercoagulation and poor organ outcomes.
- This study investigates if brain death causes hypercoagulation and microvascular thrombosis.
- It also examines if inhibiting tissue factor (TF) can reverse this coagulable state.
Purpose of the Study:
- To investigate the coagulopathic profile following brain death in a validated animal model.
- To determine the role of tissue factor (TF) in brain death-induced hypercoagulation.
- To assess the efficacy of TF inhibition in reversing coagulopathy.
Main Methods:
- A pig model of intracranial hemorrhage and brain death was used.
- Coagulation parameters were assessed using thromboelastometry (ROTEM) and thrombin generation.
- In vitro experiments with a TF inhibitor (ASIS) were conducted, and kidneys were examined for microvascular thrombosis.
Main Results:
- Brain death induced hypercoagulation, confirmed by ROTEM and thrombin generation assays.
- In vitro TF inhibition with ASIS did not reverse the observed hypercoagulation.
- No microvascular thromboses were detected in the kidneys.
Conclusions:
- Brain death leads to hypercoagulation, but TF inhibition is ineffective in reversing it.
- TF release is unlikely to be the primary driver of brain death-associated coagulopathy.
- The protein C pathway may play a role in the observed coagulopathy.
Keywords:
APTTASISActivated partial thromboplastin timeBDBSABovine serum albuminBrain deathCCPCTCTICerebral perfusion pressureClotting timeCorn trypsin inhibitorETPExperimental animal modelsHypercoagulabilityICPIntracerebral hemorrhageMAPMCFMaxVelMaximum clot firmnessMaximum velocityMean arterial pressurePAI-1PCTPTPlasminogen activator inhibitor-1Protein CProthrombin timeROTEMSDTFTime to maximum velocityTime to peakTissue factorTissue plasminogen activatorbrain deadendogenous thrombin potentialintracranial pressureplasma clotting timerecombinant active site-inhibited factor VIIastandard deviationtt, MaxVeltPatimetissue factorttPeakwhole blood thromboelastometry
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