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Defining Endotheliopathy in Murine Polytrauma Models
Taylor E Wallen1, Kathleen E Singer, Nora C Elson
1Department of Surgery, University of Cincinnati, Cincinnati, Ohio.
Shock (Augusta, Ga.)
|June 27, 2022
Summary
This study shows that polytrauma in mice, including traumatic brain injury and hemorrhagic shock, causes endotheliopathy. Biomarker analysis in serum reveals distinct patterns of cellular injury following trauma, aiding in understanding patient outcomes.
Area of Science:
- Trauma research
- Endothelial dysfunction
- Biomarker analysis
Background:
- Endotheliopathy, or endothelial dysfunction, is a critical factor in poor outcomes following traumatic injury.
- Acute post-traumatic endothelial cell dysfunction is linked to significant physiological, hemodynamic, and coagulation disturbances.
Purpose of the Study:
- To define the generation and extent of endotheliopathy in murine polytrauma models.
- To evaluate the post-traumatic release of serum biomarkers indicative of ongoing cellular injury.
Main Methods:
- Mice underwent moderately severe concussive traumatic brain injury (TBI), 60-minute hemorrhagic shock with resuscitation, or midline laparotomy with rectus muscle crush.
- Serum biomarker evaluation was performed at 1, 4, and 24 hours post-injury.
- Specific biomarkers analyzed included soluble thrombomodulin, syndecan-1, UCHL-1, and hyaluronic acid.
Main Results:
- Serum biomarkers demonstrated differential timing and injury-dependent release patterns.
- Soluble thrombomodulin, syndecan-1, UCHL-1, and hyaluronic acid showed significant elevations at various time points and in different polytrauma combinations.
- Polytrauma models reliably indicated endotheliopathy through distinct biomarker changes.
Conclusions:
- A murine polytrauma model incorporating TBI, hemorrhagic shock, and abdominal crush effectively models endotheliopathy.
- Differential changes in serum biomarkers serve as reliable indicators of trauma-induced endothelial dysfunction.
