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Updated: Nov 8, 2025

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An Intact Pericardium Ischemic Rodent Model
Published on: September 2, 2021
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Left Ventricular Impaired Relaxation and Interstitial Myocarditis Identified in Sepsis-Associated Cardiac
David J Sturgess1, Shannon Morrison1, Brian Haluska2
1Mater Research Institute (MRI-UQ), University of Queensland, Brisbane, Queensland, Australia.
Summary
Sepsis induces left ventricular diastolic dysfunction and myocarditis in a rodent model. This study links structural and functional cardiac changes in sepsis, aiding future research into treatments.
Area of Science:
- Cardiology
- Pathology
- Animal Models
Background:
- Sepsis is a systemic response to infection, with left ventricular (LV) diastolic dysfunction contributing to mortality.
- Animal models are crucial for studying sepsis-induced cardiac dysfunction, controlling for clinical confounders.
- Endotoxemia models offer insights into sepsis-associated cardiac pathology.
Purpose of the Study:
- To evaluate an endotoxemia (LPS) rodent model for left ventricular (LV) diastolic dysfunction using echocardiography and tissue Doppler.
- To assess histopathological changes in the myocardium following LPS administration.
- To correlate structural and functional cardiac alterations in sepsis.
Main Methods:
- Male Sprague-Dawley rats were randomized to LPS or saline (control).
- Echocardiography with tissue Doppler assessed LV diastolic function.
- Mean arterial blood pressure (MAP) was monitored.
- Histopathology and immunohistochemistry examined myocardial tissue post-mortem.
Main Results:
- LPS administration induced hypotension (MAP 81.86±31.67 mmHg vs. 124.29±20.16 mmHg).
- Impaired LV relaxation was observed (early diastolic velocity [e'] 0.06±0.02 m/s vs. 0.09±0.02 m/s).
- Histopathology revealed interstitial myocarditis, including hydropic changes and inflammation.
Conclusions:
- The LPS rodent model demonstrated both LV diastolic dysfunction and interstitial myocarditis.
- These findings establish a link between structural and functional cardiac changes in sepsis.
- This model facilitates further investigation into the mechanisms and treatments for sepsis-associated cardiac dysfunction.

