The contribution of the stomach to ethanol oxidation in the rat.
To estimate the amount of ethanol that can be oxidized in the stomach, steady-state conditions were created in a group of fed rats by giving a loading dose of ethanol (2 g/kg body wt I.V.) followed by continuous infusion either intravenously or intragastrically. The rate of ethanol oxidation was calculated from the rate of infusion required to maintain steady blood levels of approximately 30 mM for at least 3 hours. Gastrointestinal ethanol concentrations and total contents also remained steady. The rate of ethanol oxidation was 19.3% faster during intragastric than during intravenous infusion (p less than 0.01). When measured at the prevailing luminal ethanol concentration (145 mM) and expressed per body weight, the gastric ADH activity represented 14% of the hepatic activity at 30 mM ethanol, suggesting that gastric ADH activity could account for most of the increased rate of oxidation when ethanol is given intragastrically. Thus, gastric ethanol oxidation by a high Km ADH in the rat represents a significant fraction of the total rate of ethanol oxidation and it is therefore one of the factors which determines the bioavailability of orally administered ethanol.
D000426:Alcohol Dehydrogenase / Q000378:metabolism*; D000818:Animals; D000431:Ethanol / Q000008:administration & dosage / Q000378:metabolism*; D005753:Gastric Mucosa / Q000378:metabolism*; D007262:Infusions, Intravenous; D007441:Intubation, Gastrointestinal; D008297:Male; D010084:Oxidation-Reduction; D051381:Rats; D011919:Rats, Inbred Strains
D000431:Ethanol; D000426:Alcohol Dehydrogenase