Sepsis triggers the failure of cardiac mitochondria and this deleterious effect could be prevented by omega-3 polyunsaturated fatty acids (PUFA).

To evaluate the influence of eicosapentaenoic acid (C20: 5 omega-3 or EPA) on the mechanical and mitochondrial functions of the heart during early sepsis.

Four month-old female Wistar rats were subdivided in 4 groups (n=8 per group) according to: (i) the 4-week diet given (deficient in omega-3 PUFA [DEF] or enriched with EPA); (ii) the surgery performed (caecal ligation at 1cm of the apex of the heart and puncture in order to induce sepsis [CLP] or sham). The cardiac mechanical function was studied in vivo by NMR 48h after the surgery. Immediately after, part of the myocardium was used in order to extract mitochondria and another part was frozen in order to subsequently analyse the fatty acid composition of cardiac phospholipids.

The EPA groups display a large decrease in the omega-6/omega-3 PUFA ratio of cardiac phospholipids. Sepsis increases the mRNA expression of IL-1beta in the DEF group but not in the EPA one. The mechanical function is altered neither by the diets nor by the surgeries. The DEF/CLP animals have a deficient oxidative phosphorylation compared to the DEF/Sham rats: reduced mitochondrial oxygen consumption (−42%, P<0.001) and ATP production (−37%, P<0.05). The sepsis-induced mitochondrial damages in this group is due to an increase reactive oxygen species (ROS) release (+130 and +63% for the ROS/respiration and ROS/ATP ratios, P<0.01 and P<0.05, respectively). The dietary EPA prevents these damages (P<0.05).

A sufficient EPA intake favours the upholding of the mitochondrial function during early sepsis, which could delay the subsequent development of heart failure. We plan to verify this beneficial effect of EPA in Humans affected by acute endocarditis.