Abstract
The clinical entity of lactic acidosis was recently described by Huckabee<sup>1,2</sup>as a severe, uniformly fatal, metabolic acidosis, characterized by the appearance of markedly increased levels of lactate in the blood. Additionally it was pointed out by Huckabee that not only was blood lactate elevated, but that the levels present far exceed those which could be predicted from the blood pyruvate levels under normal circumstances. Huckabee showed that while increased blood lactate levels could be produced in humans and animals by a variety of procedures, including the production of alkalosis by the infusion of bicarbonate or hyperventilation, the administration of epinephrine, and glucose or pyruvate infusions, these increases accompany a rise in blood pyruvate levels and the increased lactate levels can be attributed to the increased pyruvate. Increased lactate concentrations which significantly exceed the levels which can be attributed to the pyruvate alone were seen in situations resulting in
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