[Physiopathology of acute alcoholic intoxication and alcoholic withdrawal]

Ethanol blood levels are the result of alcohol absorption and the process of its distribution, metabolism and excretion. Kinetics are complex and not yet well known. They can be influenced by acquired factors (type of alcohol ingested, association with fasting or eating, induction or inhibition of ethanol metabolism) or by genetically determined differences in the activity of alcohol and of acetaldehyde dehydrogenase. The presence of ethanol in the organism leads to various consequences. On the one hand, hydropic changes on membranes modify their function and thus that of membrane proteins (particularly receptors); on the other, ethanol can affect neurotransmitter metabolism. Such modification of the major neurotransmitter systems (cholinergic, aminergic and GABA) in some cerebral regions explains the pharmacologic consequences of acute alcohol ingestion. In chronic alcohol dependence, adaptation phenomena occur, in both the membranes (increased rigidity) and the neurotransmitter systems. They are reflected by the hyperexcitability (catecholaminergic hyperactivity and GABA hypoactivity) observed after disappearance of the tranquilizing effect of ethanol and are clinically expressed by the withdrawal syndrome.