Hepatic oxygen and lactate extraction during stagnant hypoxia

Area of Science:

• Physiology
• Hepatology
• Hypoxia Research

Background:

• Tissues increase oxygen (O2) extraction as O2 delivery declines to maintain O2 consumption.
• A critical O2 delivery threshold exists, below which O2 uptake becomes supply-dependent.
• Regional contributions to critical O2 delivery are not fully understood, particularly in the liver.

Purpose of the Study:

• To determine the relationship between O2 consumption and O2 delivery in the isolated canine liver.
• To investigate hepatic lactate extraction in relation to O2 consumption during falling O2 delivery.
• To assess the liver's O2 extraction capacity and its transition to O2 supply dependence.

Main Methods:

• Utilized pump-perfused canine livers sourced from support dogs.
• Inducted stagnant hypoxia by progressively lowering blood flow.
• Measured O2 consumption and lactate extraction across a range of O2 deliveries.

Main Results:

• The critical O2 delivery for the canine liver was determined to be 28 ± 5 ml.kg-1.min-1.
• Livers extracted 68 ± 9% of delivered O2 before becoming O2 supply-dependent.
• Hepatic lactate uptake decreased and transitioned to production at low O2 deliveries, coinciding with O2 supply dependence.

Conclusions:

• The isolated liver exhibits an O2 extraction capacity comparable to the whole body and other isolated tissues.
• Reductions in hepatic lactate uptake do not precede the liver's transition to O2 supply dependence.
• The liver's ability to extract O2 is a key factor in maintaining function during reduced O2 delivery.