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A Reproducible Intensive Care Unit-Oriented Endotoxin Model in Rats
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A Reproducible Intensive Care Unit-Oriented Endotoxin Model in Rats

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Polymicrobial sepsis and endotoxemia promote microvascular thrombosis via distinct mechanisms

K N Patel1, S H Soubra, F W Lam

  • 1Medical Care Line, Michael E. DeBakey VA Medical Center, Houston, TX, USA.

Journal of Thrombosis and Haemostasis : JTH
|March 30, 2010
PubMed
Abstract

Insights

Polymicrobial sepsis and endotoxemia cause microvascular thrombosis through different pathways. Sepsis-induced thrombosis requires toll-like receptor 2 (TLR2), not TLR4 or VWF, and is mitigated by fluid replacement.

Area of Science:

  • Vascular biology
  • Immunology
  • Sepsis research

Background:

  • Endotoxemia promotes microvascular thrombosis in wild-type mice.
  • This effect is absent in mice lacking toll-like receptor 4 (TLR4) or von Willebrand factor (VWF).

Purpose of the Study:

  • To investigate if polymicrobial sepsis, induced by cecal ligation/perforation (CLP), causes similar microvascular thrombosis responses as endotoxemia.
  • To determine if these responses involve the same biological mechanisms.

Main Methods:

  • Comparison of wild-type mice with TLR4-, TLR2-, and VWF-deficient mice.
  • Induction of thrombosis using a light/dye-injury model in the cremaster microcirculation.
  • Administration of CLP, sham surgery, endotoxin (LPS), or saline, with assessment of fluid replacement effects in the CLP model.

Main Results:

  • Both CLP and LPS increased thrombotic occlusion in wild-type mice.
  • CLP, unlike LPS, induced thrombosis in TLR4- and VWF-deficient mice.
  • CLP-induced thrombosis was absent in TLR2-deficient mice, while LPS still induced thrombosis in these mice. Fluid replacement prevented CLP-induced thrombosis and hemoconcentration but not LPS-induced thrombosis.

Conclusions:

  • Polymicrobial sepsis (CLP) and endotoxemia (LPS) promote microvascular thrombosis via distinct mechanisms.
  • CLP-induced thrombosis requires TLR2, but not TLR4 or VWF.
  • Intravenous fluid replacement benefits microvascular thrombosis in sepsis, but the precise mechanisms require further study.

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