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Microthrombosis in sepsis.

B Vallet1

  • 1Department of Anesthesiology and Intensive Care, University Hospital of Lille, Rue Michel Polonovski, 59037 Lille, France.

Minerva Anestesiologica
|May 29, 2001
PubMed
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Strategies targeting coagulation pathways can reduce organ dysfunction and mortality in septic shock. Treatments like tissue factor pathway inhibitors and activated protein C show promise in animal models and early clinical studies.

Area of Science:

  • Endothelial cell biology
  • Coagulation cascade
  • Septic shock pathophysiology

Background:

  • Normal endothelial cells possess anticoagulant properties via tissue factor pathway inhibitors (TFPI), thrombomodulin (TM), nitric oxide, and prostacyclin.
  • Septic stimuli can induce a procoagulant state by decreasing anticoagulant membrane components and activating bacterial endotoxins.
  • Impaired fibrinolysis alongside coagulation activation leads to fibrin deposition, tissue ischemia, and necrosis in sepsis.

Purpose of the Study:

  • To review strategies for modulating coagulation activity to reduce organ dysfunction and mortality in septic shock.
  • To evaluate the efficacy of TFPI, antithrombin (AT), and activated protein C (APC) in septic shock models and clinical trials.
  • To explore the potential of l-arginine, perindopril, and anti-glycoprotein IIb/IIIa agents in preventing endothelial injury and improving outcomes in sepsis.

Related Experiment Videos

Main Methods:

  • Review of animal models and clinical studies (Phase II and III) investigating anticoagulant therapies.
  • Analysis of data on the impact of TFPI, AT, APC, l-arginine, perindopril, and anti-glycoprotein IIb/IIIa on organ dysfunction, mortality, and endothelial injury in sepsis.
  • Examination of the role of monocytes in disseminated intravascular coagulation (DIC) and the effect of anti-glycoprotein IIb/IIIa agents.

Main Results:

  • TFPI, AT, and APC reduced organ dysfunction and mortality in various animal models and Phase II clinical studies.
  • Phase III trials indicated no efficacy for AT but a reduced relative risk of death with APC.
  • Animal studies showed l-arginine and perindopril prevented septic shock-associated endothelial injury, while anti-glycoprotein IIb/IIIa agents reduced endothelial injury and improved survival by attenuating monocyte roles in DIC.

Conclusions:

  • Modulating coagulation activity presents a viable therapeutic strategy for septic shock.
  • Activated protein C demonstrates potential in reducing mortality, though further investigation is warranted.
  • Preventing endothelial injury through agents like l-arginine, perindopril, and anti-glycoprotein IIb/IIIa may improve survival in septic shock.