Abstract
The liver is the primary site for the oxidation of ethanol-derived acetaldehyde (AcH) in the rat. Only a small amount of the total AcH formed in this organ escapes into the rest of the body, but this amount increases with increasing hepatic ethanol concentrations. The bulk of the hepatic AcH output is eliminated extrahepatically, thus drastically changing the AcH level from that initially leaving the liver. Nevertheless, the extrahepatic blood AcH levels can be used as relatively accurate indicators of the corresponding hepatic AcH levels, since they are highly correlated with them. Significant levels of brain AcH occur only at very high arterial blood AcH concentrations.
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