Metabolic effects of sodium bicarbonate in hypoxic lactic acidosis in dogs

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Abstract
The metabolic effects of NaHCO3 therapy in hypoxic lactic acidosis were evaluated in the anesthetized dog. Hypoxic lactic acidosis was induced by ventilating the dogs with a hypoxic gas mixture of 8% O2/92% N2, resulting in arterial PO2 of less than 30 mm Hg, pH below 7.20, bicarbonate less than 12 mM, and lactate more than 7 mM. In this situation lactate accumulates because of overproduction of lactate by gut and carcass in the presence of a diminished capacity of the liver to extract lactate. After the development of hypoxic lactic acidosis the dogs were treated for 60 min with either NaHCO3 or NaCl or had no therapy. Sixty minutes of either treatment resulted in further declines of blood pH and bicarbonate that were similar in all three groups. NaHCO3-treated animals, however, showed an increase in blood lactate that were significantly higher than those treated with NaCl or those that had no therapy. This could be explained by a significantly higher gut lactate production with NaHCO3 therapy than in the NaCl-treated group. Concomitantly NaHCO3-treated animals showed a decrement in liver and gut blood flow that did not occur with NaCl treatment. Only NaHCO3 therapy was associated with a further decrease of liver intracellular pH, which could be attributed to both an increase in the CO2 load to the liver and increased tissue lactate levels, which were not observed with NaCl or no therapy. Additionally, liver lactate extraction was not improved by administration of NaHCO3 or NaCl. Thus, NaHCO3 administration in dogs with hypoxic lactic acidosis does not increase blood pH or bicarbonate, but it increases blood lactate to a greater extent than either NaCl or no treatment. In the dog model of hypoxic lactic acidosis bicarbonate administration results in detrimental effects on blood flow to liver and gut and increases both the quantity of CO2 delivered to the liver and the liver tissue lactate levels, resulting in a further decrease in liver intracellular pH.

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