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Platelet Function Changes in a Time-Dependent Manner Following Traumatic Brain Injury in a Murine Model
Grace E Martin1, Brent Xia, Young Kim
1Division of Research and Institute for Military Medicine, Department of Surgery, University of Cincinnati, Cincinnati, Ohio.
Shock (Augusta, Ga.)
|November 16, 2017
Summary
Traumatic brain injury (TBI) causes initial platelet dysfunction, followed by hyperaggregation and increased clotting. These changes correlate with systemic inflammation after TBI.
Area of Science:
- Neuroscience
- Hematology
- Immunology
Background:
- Traumatic brain injury (TBI) induces systemic coagulation and inflammation, impacting patient outcomes.
- The interplay between platelets and cytokines post-TBI in coagulation and thrombosis remains unclear.
Purpose of the Study:
- To investigate the dynamic changes in platelet function and coagulation following TBI.
- To determine the relationship between platelet aggregation, pro-inflammatory cytokines, and hemostasis after TBI.
Main Methods:
- A murine weight-drop model was used to induce moderate TBI.
- Measurements included platelet aggregation, cytokine levels, fibrinogen, and thromboelastometry at various time points post-injury.
Main Results:
- TBI induced transient platelet dysfunction within 10 minutes, followed by hyperaggregation at 6 hours.
- Increased maximal clot firmness and elevated pro-inflammatory cytokines were observed at 6 hours post-TBI.
- Platelet function and coagulation markers returned to baseline by 24 hours.
Conclusions:
- TBI triggers a biphasic response in platelet aggregation: initial dysfunction followed by hyperaggregation.
- Post-TBI coagulation alterations are reflected in thromboelastometry and linked to the systemic inflammatory response.
