Only two studies published so far addressed the myocardial mitochondrial respiratory dysfunction in porcine models of peritonitis-induced sepsis: one of them reported reduced activity of Complex I determined spectrophotometrically at 30°C and expressed per citrate synthase activity (Li et al., 2007); the other documented no difference in myocardial mitochondrial oxygen consumption between control and septic animals treated with antibiotics for at least 48 h (Corrêa et al., 2012). The gene discussed is CS; the disease is Sepsis.