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Related Experiment Videos

Platelet function in sepsis.

A Yaguchi1, F L M Lobo, J-L Vincent

  • 1Departments of Intensive Care Medicine and Hematology, Erasme Hospital, Free University of Brussels, Brussels, Belgium.

Journal of Thrombosis and Haemostasis : JTH
|December 23, 2004
PubMed
Summary
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Sepsis impairs platelet aggregation and hemostatic function, while increasing vascular endothelial growth factor (VEGF) release. Platelet adhesion molecule expression remains intact, suggesting sepsis alters platelet function independently of thrombin generation.

Area of Science:

  • Hematology
  • Critical Care Medicine
  • Immunology

Background:

  • Severe sepsis commonly presents with coagulation abnormalities and thrombocytopenia.
  • The specific impact of sepsis on platelet function remains incompletely understood.
  • Investigating sepsis-induced changes in platelet behavior is crucial for understanding disease pathophysiology.

Purpose of the Study:

  • To investigate the effects of sepsis on platelet aggregation.
  • To assess sepsis-induced alterations in platelet adhesiveness.
  • To determine changes in growth factor release from platelets during sepsis.

Main Methods:

  • Platelet aggregation was measured in response to agonists in septic patients.
  • Platelet adhesion molecule expression was analyzed using flow cytometry.

Related Experiment Videos

  • Vascular Endothelial Growth Factor (VEGF) and Platelet-Derived Growth Factor (PDGF) release was quantified via ELISA.

    • Main Results:

    • Septic patients exhibited significantly reduced platelet aggregation compared to controls, irrespective of platelet count or disseminated intravascular coagulation (DIC) status.
    • Platelet adhesion molecules and alpha-granule secretion (P-selectin) were unchanged in sepsis.
    • VEGF release was elevated, while PDGF release remained unchanged following agonist activation in septic patients.

    Conclusions:

    • Sepsis compromises the hemostatic function of circulating platelets.
    • Platelet adhesion molecule expression and secretion capabilities are preserved during sepsis.
    • Sepsis modulates growth factor production, notably increasing VEGF release in a thrombin-independent pathway.