The role of the liver in lactate metabolism in an experimental low flow state induced by cardiac tamponade was investigated in dogs.
Arterial and venous lactate, and pyruvate levels and arterio-venous oxygen content differences were measured for the liver, gut, forequarter and hind limbs. Cardiac output and regional blood flows were determined by electromagnetic flow probes.
The contribution of the liver to the development of lactic acidosis was found to be variable. When hepatic oxygen consumption was decreased, the liver was documented as the major site of lactate production with an associated increase in the lactate-pyruvate ratio of hepatic venous blood. In some experiments, however, the hepatic oxygen consumption was maintained, or even increased slightly; in these circumstances the liver was, in part, responsible for the development of lactic acidosis by impaired lactate consumption.
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