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Recombinant factor XIII mitigates hemorrhagic shock-induced organ dysfunction.

Sergey B Zaets1, Da-Zhong Xu, Qi Lu

  • 1Novo Nordisk, Inc, Princeton, New Jersey 08540, USA. seza@novonordisk.com

The Journal of Surgical Research
|February 1, 2011
PubMed
Summary

Recombinant factor XIII (FXIII) treatment reduced multiple organ dysfunction (MOD) in rats experiencing trauma-hemorrhagic shock (THS). FXIII preserved gut barrier function and modulated inflammatory responses, improving outcomes after severe injury.

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Area of Science:

  • Biochemistry
  • Physiology
  • Trauma Research

Background:

  • Plasma factor XIII (FXIII) stabilizes fibrin clots and modulates inflammation.
  • FXIII has shown potential in mitigating organ dysfunction after gut ischemia-reperfusion injury.

Purpose of the Study:

  • To investigate the efficacy of recombinant human FXIII A(2) subunit (rFXIII) in reducing multiple organ dysfunction (MOD) caused by trauma-hemorrhagic shock (THS).

Main Methods:

  • Rats underwent 90-minute trauma-hemorrhagic shock (THS) or sham shock (TSS) and received rFXIII or placebo post-resuscitation.
  • Evaluated lung permeability, myeloperoxidase (MPO) activity, gut histology, neutrophil activity, microvascular blood flow, and cytokine levels 3 hours post-shock.

Main Results:

  • rFXIII treatment significantly reduced lung permeability and MPO activity in lungs and gut compared to placebo.
  • rFXIII administration led to lower neutrophil respiratory burst, less ileal injury, and improved liver microvascular blood flow.
  • FXIII levels remained stable throughout the study period in THS rats.

Conclusions:

  • Recombinant FXIII administration effectively diminishes THS-induced MOD in rats.
  • FXIII likely acts by preserving gut barrier function, limiting polymorphonuclear leukocyte activation, and modulating cytokine responses.