Effect of haematocrit value and pO2 on the redox state and metabolism of the perfused liver

Abstract

The hematocrit [hct] value and pO2 of blood perfusing the isolated liver were varied. Provided O2 content of the blood was not rate-limiting, O2 consumption was related to hct value rather than O2 saturation or pO2. Hypoxia caused the blood-glucose concentration and ketogenesis to increase and the output of very-low-density (d < 1.006) lipoproteins to decrease. A decrease in pO2 caused an increase in both the [lactate]/[pyruvate] and [3-hydroxybutyrate]/[acetoacetate] and a decrease in [ATP]/[ADP] ratios, independently of O2 consumption. The more reduced redox state was associated with a shift in the balance between the oxidation and esterification of free fatty acids in favor of oxidation. Acetoacetate may be an important H acceptor during hypoxia of the liver.