refludan and Brain-Injuries

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.

Topics: Acute Disease; Adenosine Diphosphate; Animals; Blood Cell Count; Blood Coagulation Disorders; Blood Platelets; Brain; Brain Injuries; Hirudins; Kinetics; Male; Partial Thromboplastin Time; Platelet Aggregation; Prothrombin; Rats; Rats, Sprague-Dawley; Recombinant Proteins; Subarachnoid Hemorrhage; Thrombelastography; Thrombin; Wounds, Nonpenetrating