Abstract
Marked lactate production and accumulation was found in dogs and men in the absence of hypoxia as a result of pyruvate, bicarbonate, or glucose infusions and of hyperventilation alkalosis. All these forms of lactic acidemia were secondary to changes in body pyruvate which were brought about by the stimuli. The relationships between lactate and pyruvate were such as to indicate that no change in the steady-state position of the lactic dehydrogenase system had occurred. It was concluded that tissue lactic acid production does not imply tissue hypoxia.