Effect of haematocrit value and pO2 on the redox state and metabolism of the perfused liver.
1. The haematocrit 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 haemotocrit value rather than O2 saturation or pO2. 2. Hypoxia caused the blood-glucose concentration and ketogenesis to increase and the output of very-low-density (d less than 1.006) lipoproteins to decrease. 3. 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. 4. The more reduced redox state was associated with a shift in the balance between the oxidation and esterification of free fatty acids in favour of oxidation. 5. Acetoacetate may be an important hydrogen acceptor during hypoxia of the liver.
D000090:Acetoacetates / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005260:Female; D006400:Hematocrit; D008079:Lipoproteins, VLDL / Q000378:metabolism; D008099:Liver / Q000378:metabolism*; D010084:Oxidation-Reduction; D010100:Oxygen / Q000097:blood*; D010101:Oxygen Consumption; D051381:Rats
D000090:Acetoacetates; D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D008079:Lipoproteins, VLDL; D010100:Oxygen