Abstract
The accumulation of lactate in the blood has long been recognized as a normal response to vigorous exercise and as a manifestation of acute hypoxia secondary to shock or asphyxia. However, it was not until 1961 that Huckabee called attention to the occurrence of hyperlactatemia in a variety of clinical circumstances lacking evidence of either circulatory failure or hypoxemia.1 , 2 Since then, a large and still growing literature on this subject has appeared, and some experts now suspect that lactic acidosis may be the most frequent form of acute metabolic acidosis. It is also a not uncommon cause of congenital or . . .

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