Early Platelet Dysfunction in a Rodent Model of Blunt Traumatic Brain Injury Reflects the Acute Traumatic Coagulopathy Found in Humans
| Autor: | Julia Beck, Victoria A. Ploplis, Robert A. Yount, Francis J. Castellino, Braxton Fritz, Mayra J. Sandoval-Cooper, Deborah L. Donahue, Scott Thomas, Mark Walsh, Patrick Davis |
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| Rok vydání: | 2014 |
| Předmět: |
Blood Platelets
Male Subarachnoid hemorrhage Platelet Aggregation Traumatic brain injury Wounds Nonpenetrating Rats Sprague-Dawley Thrombin medicine Coagulopathy Animals Platelet medicine.diagnostic_test business.industry Brain Original Articles Blood Coagulation Disorders Hirudins Subarachnoid Hemorrhage medicine.disease Recombinant Proteins Thromboelastography Blood Cell Count Rats Thrombelastography nervous system diseases Adenosine Diphosphate Kinetics Direct thrombin inhibitor Brain Injuries Anesthesia Hemostasis Acute Disease Partial Thromboplastin Time Prothrombin Neurology (clinical) business medicine.drug |
| Zdroj: | Journal of Neurotrauma. 31:404-410 |
| ISSN: | 1557-9042 0897-7151 |
| DOI: | 10.1089/neu.2013.3089 |
| Popis: | Acute coagulopathy is a serious complication of traumatic brain injury (TBI) and is of uncertain etiology because of the complex nature of TBI. However, recent work has shown a correlation between mortality and abnormal hemostasis resulting from early platelet dysfunction. The aim of the current study was to develop and characterize a rodent model of TBI that mimics the human coagulopathic condition so that mechanisms of the early acute coagulopathy in TBI can be more readily assessed. Studies utilizing a highly reproducible constrained blunt-force brain injury in rats demonstrate a strong correlation with important postinjury pathological changes that are observed in human TBI patients, namely, diminished platelet responses to agonists, especially adenosine diphosphate (ADP), and subarachnoid bleeding. Additionally, administration of a direct thrombin inhibitor, preinjury, recovers platelet functionality to ADP stimulation, indicating a direct role for excess thrombin production in TBI-induced early platelet dysfunction. |
| Databáze: | OpenAIRE |
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