• Victoria A Ploplis, Deborah L Donahue, Mayra J Sandoval-Cooper, Maria MorenoCaffaro, Patrick Sheets, Scott G Thomas, Mark Walsh, and Francis J Castellino.
• 1 W. M. Keck Center for Transgene Research, University of Notre Dame , Notre Dame, Indiana.
• J. Neurotrauma. 2014 Oct 1; 31 (19): 1672-5.

AbstractCoagulopathy after severe traumatic brain injury (TBI) has been extensively reported. Clinical studies have identified a strong relationship between diminished platelet-rich thrombus formation, responsiveness to adenosine diphosphate agonism, and severity of TBI. The mechanisms that lead to platelet dysfunction in the acute response to TBI are poorly understood. The development of a rodent model of TBI that mimics the coagulopathy observed clinically has recently been reported. Using immunohistochemical techniques and thromboelastography platelet mapping, the current study demonstrated that the expression of coagulation (tissue factor and fibrin) and platelet activation (P-selectin) markers in the injured brain paralleled the alteration in systemic platelet responsiveness to the agonists, adenosine diphosphate and arachodonic acid. Results of this study demonstrate that local procoagulant changes in the injured brain have profound effects on systemic platelet function.

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