Our results demonstrate that endotoxic shock induces a
very early and severe impairment in exogenous whole
body net lactate clearance that is not related to total
liver hypoperfusion or evident biochemical dysfunction.
However, the very low portohepatic vein lactate differences
suggest at least a liver metabolic inability to handle in-
creased lactate loads. This appears to be a specific rather
than generalized metabolic dysfunction in LPS animals as
the clearance of sorbitol, a polyol molecule with a 96% first
pass liver extraction, was preserved. This finding might
lead to reconsider the role of the liver in persistent hyper-
lactatemia, and opens new perspectives for translational
and clinical research on a complex potential resuscitation
target, such as lactate.