Systemic platelet dysfunction is the result of local dysregulated coagulation and platelet activation in the brain in a rat model of isolated traumatic brain injury

Victoria A. Ploplis, Deborah L. Donahue, Mayra J. Sandoval-Cooper, Maria Morenocaffaro, Patrick Sheets, Scott G. Thomas, Mark Walsh, Francis J. Castellino

Research output: Contribution to journalArticle

13 Scopus citations

Abstract

Coagulopathy 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.

Original languageEnglish (US)
Pages (from-to)1672-1675
Number of pages4
JournalJournal of neurotrauma
Volume31
Issue number19
DOIs
StatePublished - Oct 1 2014

Keywords

  • brain injury
  • coagulopathy
  • platelet dysfunction

ASJC Scopus subject areas

  • Clinical Neurology
  • Medicine(all)

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