Transient arterial lactic acid changes in unanesthetized dogs at 21,000 feet

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Abstract
Blood lactic acid levels have been reported by some to be elevated during exposure to altitude and by others to be unaffected. Both the hyperventilation caused by hypoxia and tissue hypoxia itself should cause a rise in blood lactic acid, the latter factor being reflected primarily as excess lactate. After a 3-hr control period at ground level, unanesthetized dogs were exposed for 8 hr to 21,000 ft simulated altitude (Pb = 335 mm Hg). Arterial blood samples were drawn frequently from a Teflon T-cannula surgically placed in a carotid artery 1 or 2 days prior to the experiment. Lactic and pyruvic acid concentrations, Pco2, Po2, and pH were measured. At altitude, the average arterial Po2 was 32 mm Hg, Pco2 was 24 mm Hg, and pH was 7.50. All control values fell in normal ranges. Although the magnitude of changes differed among animals, arterial lactic acid reached a peak value within the first 2 hr at altitude and gradually declined thereafter and, in most animals, closely approached the control value during the 8th hr at altitude. Excess lactate changed in a similar manner. The decline in lactic acid, with no concomitant relief of arterial hypoxia and hypocapnia, remains unexplained.