Key Points
- The study aims to examine mitochondrial function and integrity in a canine model of pacing-induced cardiac failure.
- Evaluated respiratory complex I-V and citrate synthase activities in myocardial and skeletal muscle tissues.
- Assessed large-scale mtDNA deletions and peptide content of mitochondrial enzyme subunits.
- Measured circulating and cardiac tumor necrosis factor-alpha (TNF-alpha) levels and total aldehyde content in the left ventricle.
- Specific activity levels of complex III and V were significantly lower in paced animals compared to controls (p<0.05).
- Large-scale mtDNA deletions were found in myocardial tissue of paced animals, less than 0.01% of wild-type mtDNA.
- Increased plasma and cardiac TNF-alpha levels were correlated with reductions in complex III and V activities.
Structured PICO
PPopulationCanine model of pacing-induced cardiac failure
IInterventionPacing-induced cardiac failure
CComparatorControl animals
OOutcomeLevels of respiratory complex I-V and citrate synthase activities, large-scale mtDNA deletions, and peptide content of specific mitochondrial enzyme subunits in myocardium and skeletal musclesurrogate
In a canine model, pacing-induced heart failure reduces specific mitochondrial respiratory enzyme activities in both cardiac and skeletal muscle, suggesting a systemic role for mitochondrial dysfunction.