Liver lactate uptake in correcting of hemorrhagic shock with crystalloid, colloid, or whole blood.

A controversy still exists on whether the liver changes to a lactate producer during hemorrhagic shock. Considerable disagreement has been reported on the question whether crystalloids or colloids should be used when treating hemorrhagic shock. The present study tries to clarify both questions, using an animal shock model. Severe arterial hypotension after hemorrhage in pigs was corrected with infusion of blood or a crystalloid or a colloid solution. The liver did not seem to produce lactate at any stage of the shock level, but during early retransfusion it changed transiently to a lactate producer. Later during the resuscitation period, the correction of arterial hypotension seemed to be unstable and the correction of acidosis incomplete after crystalloid infusion compared to transfusion or colloid substitution.