Cardiac Depression in Pigs after Multiple Trauma - Characterization of Posttraumatic Structural and Functional
M Kalbitz1, S Schwarz2, B Weber3
1Department of Traumatology, Hand-, Plastic-, and Reconstructive Surgery, Center of Surgery, University of Ulm, Ulm, Germany. miriam.kalbitz@uniklinik-ulm.de.
Scientific Reports
|December 21, 2017
Summary
Multiple trauma significantly impairs cardiac function by altering heart tissue at cellular and subcellular levels. This study reveals key molecular changes, including extracellular histones and connexin 43 alterations, explaining post-trauma cardiac depression.
Area of Science:
- Cardiovascular Research
- Trauma Medicine
- Molecular Biology
Background:
- Cardiac dysfunction following multiple trauma remains poorly understood.
- The mechanistic basis of depressed cardiac function after trauma is elusive.
Purpose of the Study:
- To define the relationship between cardiac depression and morphological/immunological alterations in cardiac tissue post-multiple trauma.
- To elucidate molecular mechanisms of cardiac dysfunction after trauma.
Main Methods:
- Utilized a porcine polytrauma model (blunt chest trauma, liver laceration, femur fracture, hemorrhage).
- Performed serial trans-thoracic echocardiography.
- Correlated cardiac function with cellular injury markers (H-FABP, troponin I, extracellular histones) and postmortem cardiac tissue analysis.
Main Results:
- Left ventricular ejection and shortening fractions were significantly impaired 4-27 hours post-trauma.
- Elevated extracellular histones, H-FABP, and troponin I were observed early post-trauma.
- Cardiac tissue showed increased nitrotyrosine, IL-1β, apoptosis, altered connexin 43 (Cx43) and α-actinin, with increased desmin.
Conclusions:
- Multiple trauma induces significant cardiac depression through morphological and immunological alterations.
- Changes in Cx43, extracellular histones, and cardiomyocyte structural proteins contribute to cardiac dysfunction.
- This study provides novel insights into the molecular mechanisms of post-traumatic cardiac depression.
