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Endothelial cell dysfunction and coagulation.

B Vallet1, E Wiel

  • 1Department of Anesthesiology and Intensive Care, Lille University Hospital, Fance.

Critical Care Medicine
|July 11, 2001
PubMed
Summary
This summary is machine-generated.

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Monocyte activation and tissue factor expression are critical in sepsis-induced coagulation disorders. Endothelial cell injury, exacerbated by coagulation, also plays a significant role in sepsis.

Area of Science:

  • Sepsis research
  • Coagulation disorders
  • Endothelial cell biology

Background:

  • Endothelial cells normally maintain anticoagulant activity.
  • Sepsis and inflammatory stimuli can shift endothelial cells to a procoagulant state.
  • Sepsis profoundly impacts endothelial cell function and coagulation pathways.

Purpose of the Study:

  • To review endothelial properties and their role in anticoagulant activity.
  • To determine the contributions of endothelial cells and monocytes to sepsis-induced coagulation changes.

Main Methods:

  • Literature review of MEDLINE and other sources.
  • Analysis of endothelial cell and monocyte functions in sepsis.
  • Assessment of published data on sepsis-induced coagulation alterations.

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Main Results:

  • Sepsis induces procoagulant behavior in endothelial cells and increases tissue factor.
  • Monocytes also upregulate tissue factor expression during sepsis.
  • Endothelium protection did not reduce monocyte tissue factor, but reduced monocyte tissue factor lessened endothelial injury.

Conclusions:

  • Monocyte activation and tissue factor expression are crucial in sepsis-associated injuries.
  • Coagulation activation may contribute to endothelial cell injury during sepsis.
  • Endothelial injury further worsens sepsis-induced coagulation abnormalities.