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Effect of acid‐base alterations on hepatic lactate utilization
Author(s) -
Goldstein Philip J.,
Simmons Daniel H.,
Tashkin Donald P.
Publication year - 1972
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1972.sp009846
Subject(s) - chemistry , base (topology) , biochemistry , medicine , mathematics , mathematical analysis
1. The effect of acid‐base changes on hepatic lactate utilization was investigated in anaesthetized, mechanically ventilated dogs. 2. Portal vein flow and hepatic artery flow were measured with electromagnetic flowmeters, lactate concentration of portal vein, arterial and mixed hepatic venous blood was determined by an enzymatic technique, and hepatic lactate uptake was calculated using the Fick principle. 3. Respiratory alkalosis (Δ pH 0·25 ± 0·02) in four dogs resulted in a significant fall in total hepatic blood flow (−22 ± 4%) and a significant rise in both arterial lactate concentration (2·18 ± 0·32 m‐mole/l.) and hepatic lactate utilization (3·9 ± 1·2 μmole/min.kg). 4. 0·6 M ‐Tris buffer infusion (Δ pH 0·21 ± 0·02) in four dogs produced no significant changes in liver blood flow, arterial lactate concentration or hepatic lactate uptake. 5. Respiratory acidosis (Δ pH −0·20 ± 0·03) in six dogs and metabolic acidosis (Δ pH −0·20 ± 0·02) in four dogs produced no significant changes in liver blood flow, decreases in arterial lactate concentration of 0·38 ± 0·09 m‐mole/l. ( P < 0·05) and 0·13 ± 0·13 m‐mole/l., respectively, and no significant changes in hepatic lactate uptake. 6. A significant correlation ( r = 0·63; P < 0·01) was found between hepatic lactate utilization and arterial lactate concentration during the hyperlactataemia associated with respiratory alkalosis. 7. Hyperlactataemia induced in four dogs by infusion of buffered sodium lactate (Δ pH 0·05 ± 0·01;% Δ liver blood flow 29 ± 7%) was also significantly correlated with hepatic lactate utilization ( r = 0·70; P < 0·01) and the slope of the regression was similar to that during respiratory alkalosis. 8. These data suggest that the hyperlactataemia of alkalosis is not due to impaired hepatic utilization of lactate and that the principal determinant of hepatic lactate uptake during alkalosis or lactate infusion is blood lactate concentration, rather than liver blood flow or acid‐base status.