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Biphasic changes in left ventricular function during hyperdynamic endotoxemia.

S Ishihara1, J A Ward, O Tasaki

  • 1United States Army Institute of Surgical Research, Fort Sam Houston, Texas 78234, USA.

The American Journal of Physiology
|May 8, 1999
PubMed
Summary
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This study in pigs reveals cardiac contractility changes during endotoxemia. Cardiac function initially improved then declined, mimicking human responses and highlighting complex endotoxemia hemodynamics.

Area of Science:

  • Cardiovascular Physiology
  • Critical Care Medicine
  • Animal Models

Background:

  • Endotoxemia significantly impacts cardiovascular function.
  • Understanding cardiac contractility during sepsis is crucial for clinical management.
  • Swine models offer relevant hemodynamic simulation for human endotoxemia.

Purpose of the Study:

  • To investigate cardiac contractility using end-systolic elastance (EES) in a conscious swine model during endotoxemia.
  • To compare swine hemodynamic responses to human endotoxemia.
  • To explore the relationship between tumor necrosis factor-alpha (TNF) and cardiac contractility.

Main Methods:

  • Utilized a chronic instrumentation swine model with ultrasonic crystals and pressure sensors.
  • Measured left ventricular pressure-volume relationships to determine EES, a load-independent contractility index.

Related Experiment Videos

  • Administered Escherichia coli endotoxin intravenously for 24 hours to simulate sepsis.

    • Main Results:

    • End-systolic elastance (EES) showed a biphasic response, increasing early and decreasing after 7 hours.
    • Later hemodynamic changes in pigs closely mirrored human cardiovascular performance during endotoxemia.
    • No direct correlation was found between plasma tumor necrosis factor-alpha (TNF) levels and EES changes.

    Conclusions:

    • Cardiac contractility exhibits a biphasic response during prolonged endotoxemia in a swine model.
    • The swine model effectively replicates human cardiovascular dynamics in later stages of endotoxemia.
    • Tumor necrosis factor-alpha (TNF) does not appear to be the sole determinant of cardiac contractility changes in this model.