The pathogenesis of septic myocardial depression is complicated.
Mitochondrial dysfunction has been suggested to be one of the main reasons for the reduced cardiac function. As
melatonin is an
antioxidant with the potential to scavenge radicals in mitochondria, we therefore employed a
sepsis model, that is, cecal
ligation and double
puncture (CLP) in rats, to study the
melatonin effects on: (i), myocardial mitochondrial function; (ii), heart systolic function; and (iii), prognosis of septic rats. We demonstrate that
melatonin treatment (30 mg/kg, 3, 6, 12, 18, 24 hr after CLP) (i) improved myocardial
cytochrome c oxidase (CcOX) activity and blood
lactate level, (ii) attenuated heart dysfunction with a higher left ventricular ejection fraction (EF), and (iii) promoted 48-h survival of the rats compared to CLP animals with no
melatonin treatment. In conclusion, our results show that rat myocardial mitochondrial CcOX activity was depressed during
severe sepsis accompanied by myocardial depression characterized by the decline of EF. In septic rats,
melatonin increased the CcOX activity, improved heart systolic function, and lowered mortality rate. The clinical use of
melatonin in septic myocardial depression should be tested in the future.