AJP - Gastrointestinal and Liver Physiology, Vol 248, Issue 5 507-G511, Copyright © 1985 by American Physiological Society
Compensatory mechanisms in response to an elevated hepatic oxygen consumption in chronically ethanol-fed rats
J. E. Bredfeldt, E. M. Riley and R. J. Groszmann
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chronically ethanol-fed rats withdrawn from ethanol 20 h before study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.
