Key Points
- To determine whether sepsis-induced myocardial depression is caused by an inadequate supply of intracellular free energy available for cardiac work.
- Implanted Escherichia coli-infected (n = 18) or sterile control (n = 16) fibrin clots intraperitoneally into beagles.
- Assessed cardiac structure and function using radionuclide ventriculography, echocardiography, and light and electron microscopy.
- Measured myocardial energy metabolism via the phosphocreatine-to-adenosine triphosphate ratio (PCr:ATP) using 31P-magnetic resonance spectroscopy alongside catecholamine-induced increases in myocardial oxygen consumption (MVO2) and rate pressure product (RPP).
- Septic animals developed significant myocardial depression, showing decreased left ventricular ejection fraction on day 1 (P < 0.0001) and decreased fractional shortening on day 2 (P < 0.0003) compared with controls.
- Septic hearts exhibited pronounced morphological abnormalities under light and electron microscopy, but maintained stable PCr:ATP ratios on day 2 without statistically significant decreases relative to controls.
- Intracellular PCr:ATP levels remained preserved even during catecholamine-stimulated stress, which produced mean maximal increases in MVO2 of 135 ± 31% and RPP of 51 ± 10% in septic animals.
Structured PICO
PPopulationBeagles (n=34) implanted intraperitoneally with Escherichia coli-infected (n=18) or sterile (n=16) fibrin clots
IInterventionEscherichia coli-infected fibrin clots implanted intraperitoneally (sepsis model)
CComparatorSterile fibrin clots implanted intraperitoneally (control)
OOutcomeMyocardial energy metabolism (PCr:ATP ratio) and myocardial function (left ventricular ejection fraction and fractional shortening)surrogate
In a canine model of sepsis, myocardial depression occurs with morphological abnormalities but intracellular free energy levels are maintained, suggesting high-energy synthetic capabilities do not limit cardiac function.