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The coagulation phase is a critical part of the body's process to prevent blood loss following injury to blood vessels. It involves chemical reactions that form a clot to seal the injured area. The clotting process begins shortly after injury, within 15-20 seconds for severe damage and 1-2 minutes for minor injuries.
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Microfluidics in Assessing Platelet Function
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Complement Activation in Trauma Patients Alters Platelet Function.

Gelareh Atefi1, Omozuanvbo Aisiku, Nathan Shapiro

  • 1*Departments of Medicine and Emergency Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts †Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts ‡Institute of Surgical Research, San Antonio, Texas.

Shock (Augusta, Ga.)
|June 30, 2016
PubMed
Summary
This summary is machine-generated.

Trauma impairs platelet function, leading to coagulopathy. Complement activation in trauma patients paradoxically reduces platelet responsiveness, despite complement enhancing platelet aggregation.

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Area of Science:

  • Immunology and Hematology
  • Trauma Pathophysiology

Background:

  • Trauma is a leading cause of death, often complicated by trauma-associated coagulopathy.
  • Coagulopathy involves inflammation, coagulation, and platelet dysfunction.
  • The role of complement activation in trauma-associated coagulopathy is not fully understood.

Purpose of the Study:

  • To investigate the involvement of complement activation in trauma-associated coagulopathy.
  • To determine the effect of trauma sera on platelet function and complement deposition.

Main Methods:

  • Prospective study of 40 trauma patients and 30 healthy donors.
  • Incubation of healthy platelets with trauma sera, measuring responsiveness to thrombin receptor-activating peptide.
  • Flow cytometry to quantify complement deposition (C3a, C4d) on platelets.

Main Results:

  • Trauma sera rendered normal platelets hypoactive, despite increased agonist-induced calcium flux.
  • Complement deposition (C3a, C4d) was significantly higher on platelets from trauma patients.
  • Complement depletion reversed the hypoactivity of platelets incubated with trauma sera.

Conclusions:

  • Complement activation enhances platelet aggregation but trauma sera induce platelet hypoactivity.
  • The defect in platelet activation is distal to receptor activation, linked to complement deposition.
  • Complement plays a complex role in trauma-associated coagulopathy, contributing to platelet dysfunction.