title: Effects of low temperature on shear-induced platelet aggregation and activation.
abstract: BACKGROUND
  Hemorrhage is a major complication of trauma and often becomes more severe in hypothermic patients. Although it has been known that platelets are activated in the cold, studies have been focused on platelet behavior at 4 degrees C, which is far below temperatures encountered in hypothermic trauma patients. In contrast, how platelets function at temperatures that are commonly found in hypothermic trauma patients (32-37 degrees C) remains largely unknown, especially when they are exposed to significant changes in fluid shear stress that could occur in trauma patients due to hemorrhage, vascular dilation/constriction, and fluid resuscitation.
  
  
  METHODS
  Using a cone-plate viscometer, we have examined platelet activation and aggregation in response to a wide range of fluid shear stresses at 24, 32, 35, and 37 degrees C.
  
  
  RESULTS
  We found that shear-induced platelet aggregation was significantly increased at 24, 32, and 35 degrees C as compared with 37 degrees C and the enhancement was observed in whole blood and platelet-rich plasma. In contrast to observation made at 4 degrees C, the increased shear-induced platelet aggregation at these temperatures was associated with minimal platelet activation as determined by the P-selectin expression on platelet surface. Blood viscosity was also increased at low temperature and the changes in viscosity correlated with levels of plasma total protein and fibrinogen.
  
  
  CONCLUSIONS
  We found that platelets are hyper-reactive to fluid shear stress at temperatures of 24, 32, and 35 degrees C as compared with at 37 degrees C. The hyperreactivity results in heightened aggregation through a platelet-activation independent mechanism. The enhanced platelet aggregation parallels with increased whole blood viscosity at these temperatures, suggesting that enhanced mechanical cross-linking may be responsible for the enhanced platelet aggregation.
authors.affiliation: Section of Thrombosis Research, Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA.
authors.forename: Jian-ning
authors.initials: JN
authors.lastname: Zhang
authors.forename: Jennifer
authors.initials: J
authors.lastname: Wood
authors.forename: Angela L
authors.initials: AL
authors.lastname: Bergeron
authors.forename: Latresha
authors.initials: L
authors.lastname: McBride
authors.forename: Chalmette
authors.initials: C
authors.lastname: Ball
authors.forename: Qinghua
authors.initials: Q
authors.lastname: Yu
authors.forename: Anthony E
authors.initials: AE
authors.lastname: Pusiteri
authors.forename: John B
authors.initials: JB
authors.lastname: Holcomb
authors.forename: Jing-fei
authors.initials: JF
authors.lastname: Dong
mesh_terms: D000704:Analysis of Variance; D001798:Blood Proteins / Q000378:metabolism; D001809:Blood Viscosity; D003080:Cold Temperature / Q000009:adverse effects*; D005340:Fibrinogen / Q000378:metabolism; D005440:Fluid Therapy / Q000009:adverse effects / Q000379:methods; D006438:Hemodilution / Q000009:adverse effects / Q000379:methods; D018056:Hemorheology; D006470:Hemorrhage / Q000097:blood / Q000209:etiology / Q000628:therapy; D006801:Humans; D007035:Hypothermia / Q000097:blood / Q000209:etiology; D009102:Multiple Organ Failure / Q000209:etiology; D019007:P-Selectin / Q000502:physiology; D015539:Platelet Activation / Q000502:physiology*; D010974:Platelet Aggregation / Q000502:physiology*; D012151:Resuscitation / Q000009:adverse effects / Q000379:methods; D012307:Risk Factors; D033081:Shear Strength; D013314:Stress, Mechanical; D013696:Temperature; D013921:Thrombocytopenia / Q000209:etiology; D014947:Wounds and Injuries / Q000150:complications
chemical_list: D001798:Blood Proteins; D019007:P-Selectin; D005340:Fibrinogen