AJP - Gastrointestinal and Liver Physiology, Vol 258, Issue 3 411-G418, Copyright © 1990 by American Physiological Society
Acute and chronic ethanol on hepatic oxygen ethanol and lactate metabolism in cats
C. V. Greenway and W. W. Lautt
Department of Pharmacology, University of Manitoba, Winnipeg, Canada.
The effects of increasing blood ethanol levels on hepatic hemodynamics and
O2, ethanol, and lactate metabolism were studied in two groups of
anesthetized cats: a control group and a group whose prior fluid intake
contained 2, 4, then 8% ethanol for 24 days. Within each group, responses
were compared in cats with acutely denervated and innervated livers. A
hepatic venous long-circuit technique with an extracorporeal reservoir was
used to allow hemodynamic measurements and repeated sampling of arterial,
portal, and hepatic venous blood without depletion of the cats' blood
volume. Vmax for ethanol was 105 +/- 9 and 91 +/- 6 mumol.min-1 g liver-1
and Km was 136 +/- 18 and 168 +/- 24 microM for control and chronic alcohol
groups, respectively. There was no stimulation of ethanol metabolism after
chronic administration. O2 uptake by the liver was not altered during acute
ethanol administration in any group and base-line O2 uptakes before acute
administration of ethanol were not different between normal and chronic
ethanol groups. No evidence for a hypermetabolic state induced by chronic
ethanol administration was seen in innervated or acutely denervated livers.
Oxidation of ethanol required 40-45% of normal O2 uptake; thus other
oxidative processes must have been suppressed during ethanol metabolism.
Hepatic lactate uptake remained unaltered when ethanol metabolism was less
than 0.5 Vmax, but was suppressed on an equimolar basis with ethanol
metabolism when ethanol metabolism rose to greater than 0.5 Vmax. Thus
lactate metabolism is one process that can be suppressed to allow ethanol
metabolism without additional O2 uptake by the liver.
