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Hepatic mitochondrial dysfunction in fluid-resuscitated porcine septic shock


Sepsis-induced multiple organ failure may crucially depend on the development of mitochondrial dysfunction and consequent cellular energetic failure. We investigated whether hepatic mitochondrial dysfunction was present in a clinically relevant porcine model of fluid-resuscitated septic shock.


Anesthetized and ventilated pigs (40 ± 3 kg) were randomly assigned to septic shock by fecal peritonitis (F, n = 3) or control (C, n = 3) after placement of portal/hepatic vein catheters and portal vein and hepatic artery flow probes. F and C received 8 ± 13 ml/kg/hour and 5 ± 7 ml/kg/hour ringer lactate + starch, respectively. The mean arterial pressure (MAP), total liver flow (TLF), hepatic O2 delivery (DO2,h) and hepatic O2 consumption (VO2,h) were recorded at baseline (BL), 12 and 24 hours (ml/kg/min). Activities of mitochondrial respiratory chain enzymes (complex I–IV) were assessed by spectrophotometry in snap-frozen liver samples. Data are presented as the mean ± SD.


Hyperdynamic circulation developed in F with increasing DO2,h and decreasing VO2,h (Table 1). Complex II activity significantly decreased from 19.3 ± 4.2 to 9.5 ± 2.6 (P < 0.05 vs BL and between groups) in F compared with C. Complex I–III–IV function decreased in parallel in F.

Table 1 abstract P258


While increasing DO2,h far exceeded decreasing VO2,h in the setting of hyperdynamic fluid-resuscitated septic shock, hepatic mitochondrial function was significantly impaired compared with control.

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Wauters, J., Vanhorebeek, I., Dieudonne, A. et al. Hepatic mitochondrial dysfunction in fluid-resuscitated porcine septic shock. Crit Care 11 (Suppl 2), P259 (2007).

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