Compensatory mechanisms in response to an elevated hepatic oxygen consumption in chronically ethanol-fed rats.

During conditions that elevate hepatic oxygen consumption (VLO2), oxygen delivery, or oxygen extraction may also increase, acting as compensatory mechanisms. VLO2 was quantitated by an in vivo method in chronically ethanol-fed rats to establish whether VLO2 was increased and what compensatory mechanisms might ensue. VLO2 was increased 45% (0.32 +/- 0.02 ml O2 X min-1 X 100 g body wt-1; P less than 0.001) in rats chronically fed ethanol for 8 wk, while VLO2 (0.28 +/- 0.04; P = NS) was not increased in chronically ethanol-fed rats withdrawn from ethanol 20 h before study compared with control rats (0.22 +/- 0.01). Oxygen delivery was increased 31% (P less than 0.05) in ethanol-fed rats and adequately compensated for the increased VLO2. Hepatic artery blood flow did not increase in ethanol-fed rats, indicating a lack of hepatic artery vasodilation in response to the elevated VLO2. As a result, a greater percentage of oxygen delivery was supplied via portal venous blood flow that has a reduced oxygen content. These observations might suggest that ethanol-fed rats may have a decreased reserve for maintaining an adequate oxygen supply to the liver and may be at an increased liability for developing hepatic hypoxia if oxygen delivery and/or extraction were compromised.