It has been previously demonstrated that mitochondria isolated from the livers of septic rats display an oxidative phosphorylation capability similar to that of mitochondria from normal hepatocytes. The present study was performed to determine whether this is also true at the level of the whole tissue or was perhaps the result of mitochondrial isolation. To study this, sepsis in rats was produced by cecal ligation and puncture (CLP). 16-19 hr after CLP (late sepsis) rats were sacrificed and the livers removed and placed in ice-cold Krebs Ringer's phosphate buffer. Slices less than 1-mm thick were prepared and placed in the well of a temperature controlled O2 monitor. O2 consumption by liver slices was monitored in buffer equilibrated with 100% O2 (high O2) or room air (low O2). Slices from both septic and sham-operated rats exhibited high initial rates of respiration in high O2 environment (34.3 +/- 3.4 and 31.5 +/- 2.5 microliters/min/gm, respectively). Rates of oxygen consumption were significantly lower after 20 min in high O2 and initially in low O2. Under each environmental condition there was no significant difference in O2 consumption between liver slices from sham-operated and septic rats. The decline in O2 consumption in high O2 was not reversed by resuspending in high O2 buffer but was further inhibited by KCN. These results support the view that depressed O2 consumption in late sepsis is secondary to decreased O2 delivery rather than a primary deficit in oxidative capability of the hepatocytes.