LACTATE METABOLISM IN DOG DURING SHOCK FROM HEMORRHAGE, CARDIAC-TAMPONADE OR ENDOTOXIN

  • 1 January 1976
    • journal article
    • research article
    • Vol. 143  (4) , 581-586
Abstract
The elevated arterial lactate concentration in shock was investigated by measuring lactate production and clearance rate using a constant infusion of 14C-labeled lactate. The pathways of lactate metabolism also were characterized by determining the percentage of lactate undergoing oxidation and the percentage of the total CO2 production which was derived from lactate. These measurements were performed on 16 normal dogs and on 23 dogs in a state of shock. Shock was induced by hemorrhage in 10, by controlled cardiac tamponade in 7 and by endotoxin injection in 6. In all of the dogs in a state of shock, there was a statistically significant increase in both the arterial lactate concentration and lactate turnover, while the lactate clearance decreased significantly. The percentage of the arterial lactate which underwent oxidation remained normal. The percentage of the total CO2 production which was derived from lactate increased significantly, P < 0.05, from 4.7% in the normal dogs to 22.7% in the dogs in a state of shock. Since both O2 uptake and CO2 production remain unchanged in shock, these data are consistent with an increased metabolism of substrates which form pyruvate and lactate as intermediary metabolites (carbohydrates and certain amino acids) and with a concomitant decrease in the metabolism of substrates which do not form pyruvate (free fatty acids). In both the normal and shocked dogs, the arterial lactate concentration rose as the lactate production rate increased. The elevated arterial lactate in shock was apparently due to an increase in the lactate production and not to a lack of O2.

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