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Muscle versus liver mitochondrial respiration in experimental three-hit endotoxemia


Endotoxemia and hemorrhage may both affect mitochondrial function. We aimed to characterize the impact of a short-term, three-hit hemorrhage/endotoxemia model on liver and skeletal muscle mitochondrial respiration.


Seven anesthetized pigs were bled (blood loss 20%) and retransfused to euvolemia before and after endotoxin infusion (0.4 μg/kg/hour for 2 hours). The cardiac index (CI) (thermodilution) and systemic mean arterial pressure (MAP) were recorded. State 3/4 respiration (nanoatom O2/min/mg protein for glutamate) was assayed from tissue samples at baseline (muscle) and the end of the experiment (muscle and liver). Hepatic mitochondrial respiration was compared with controls (n = 6).


One pig died earlier (not included). Data are presented as the median (range). P < 0.05, Friedman test. Muscle mitochondrial respiration was similar at baseline and the end of experiment; state 3 (317 (222–594) vs 409 (295–468)), state 4 (29 (22–58) vs 40 (31–49)), respiratory control ratio (11 (7–15) vs 10 (9–11)) (not significant). Hepatic mitochondrial state 4 was higher (27 (16–31) vs 19 (13–22)) and respiratory control ratio lower (3 (3–4) vs 5 (4–6)) in the hemorrhage/endotoxemia group, compared with controls.


Repeated ischemia/reperfusion episodes plus short-term endotoxemia decreased the efficiency of hepatic but not muscle mitochondrial respiration. Mitochondrial dysfunction under these experimental circumstances seems to be organ specific.

Table 1 abstract P258


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Borotto, E., Tüller, D., Krähenbühl, S. et al. Muscle versus liver mitochondrial respiration in experimental three-hit endotoxemia. Crit Care 11 (Suppl 2), P258 (2007).

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