Introduction
Sepsis is often accompanied by myocardial depression; one of the possible mechanisms includes mitochondrial injury. We hypothesized that opening of the mitochondrial permeability transition pore (mPTP) may occur during sepsis-induced myocardial depression. We investigated the opening of the mPTP in septic hearts by measuring cytochrome C release into the cytosol.
Methods
Sepsis was induced in rats by 7.5 mg/kg lipopolysaccharide injection intraperitoneally. After 4 hours, hearts were excised and mounted in a Langendorff setup to study myocardial contractility ex vivo. Subsequently, hearts were frozen and 5 μm cryostat sections were made. Sections were stained for cytochrome C using immunohistochemistry. Healthy rats served as controls.
Results
Septic animals showed a decreased contractility (P < 0.005) and lower developed pressure (P < 0.001) when compared with healthy controls. Immunohistochemistry revealed no release of cytochrome C in healthy or septic hearts.
Conclusion
Cytochrome C is not released during sepsis-induced myocardial depression. These results indicate that the mitochondrial permeability pore may not be involved in the development of myocardial dysfunction during sepsis.