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Liver acute alcohol ingestion

In a study of the effects of acute alcohol ingestion in plasma Bj, we gave 80 g of ethanol, as vodka, over a 30-min period to six normal male volunteers who drank infrequently and nine male heavy drinkers who consumed between 720 and 2000 g of alcohol per week. None of the subjects had clinical evidence of liver disease (H33). [Pg.337]

Both alcohol and the barbiturates are CNS depressants, and simple additive CNS depression provides part of the explanation. Acute alcohol ingestion may inhibit the liver enzymes concerned with the metabolism of barbiturates such as phenobarbital and pentobarbital, but chronic exposure to alcohol increases hepatic microsomal enzyme activity and may reduce sedation from barbiturates in patients without liver impairment. - Similarly, chronic exposure to a barbiturate such as phenobarbital may increase alcohol metabolism due to enzyme induction and consequently reduce blood-alcohol levels. ... [Pg.52]

Most, if not all, of the tissues and organs in the body are adversely affected by chronic ingestion of excessive amounts of alcohol, including the liver, pancreas, heart, reproductive organs, central nervous system, and the fetus. Some of the effects of alcohol ingestion, such as the psychotropic effects on the brain or inhibition of vitamin transport, are direct effects caused by ethanol itself. However, many of the acute and chronic pathophysiologic effects of alcohol relate to the pathways of ethanol metabolism (see Chapter 25). [Pg.116]

Acute effects of alcohol ingestion arise principally from the generation of NADH, which greatly increases the NADHINAD ratio of the liver. As a consequence, fatty acid oxidation is inhibited, and ketogenesis may occur. The elevated NADHINAD ratio may also cause lactic acidosis and inhibit gluconeogenesis. [Pg.458]

Chronic liver disease reduces cortisol clearance and the production of urinary metabolites. Cortisol concentrations are elevated by acute ingestion of alcohol. Individuals with alcoholic cirrhosis have normal to elevated basal cortisol concentrations, blunted circadian rhythms, and prolonged clearance rates. [Pg.2012]

Theoretically, when blood and liver levels of vitamin A are reduced as in alcoholic hepatitis and alcoholic cirrhosis, subjects should receive supplemental vitamin A. Such supplementation, as high as 3000-10,(X)0 xg daily, has been shown to correct abnormal dark adaptation in some alcoholic cirrhotics uncomplicated by zinc deficiency (Morrison et aL, 1978 Russell et aL, 1978 Mobarhan et aL, 1981). Some studies in rats, however, indicate that acute and chronic administration of ethanol impairs hepatic and/or peripheral tissue uptake of newly ingested retinyl ester and/or causes the release of retinyl esters from hepatic tissue... [Pg.323]

On the other hand, the ethiology of fatty livers caused by alcohol is still debated and manifold effects of alcohol have been reported. In man a fatty liver can result from acute or chronic ethanol ingestion. In the rat a single dose of ethanol or the chronic administration causes an increase in liver lipids (Dilxjzio 1958 Mallov 1955). Mallov (1961) demonstrated an increased mobilization of free fatty acids from the depots, caused by alcohol administration. On the other hand, ScHAPiRO et al. (1964) showed in the perfused liver, that addition of ethanol to the perfusate decreased the secretion of neutral glycerides by the liver. However, with ethanol no decrease in protein synthesis could be shown (Seakins and Robinson 1964), and normal or elevated plasma lipids were found. [Pg.63]

Ethanol is usually ingested through the gastrointestinal tract, but can be absorbed as vapor by the alveoli of the lungs. This alcohol is oxidized metaboHcally, first to acetaldehyde (discussed later in this section), then to CO2. Ethanol has numerous acute effects resulting fi-om central nervous system depression. These range from decreased inhibitions and slowed reaction times at 0.05% blood ethanol, through intoxication, stupor, and—at more than 0.5% blood ethanol—death. Ethanol also has a number of chronic effects, of which the addictive condition of alcoholism and cirrhosis of the liver are the most prominent. [Pg.755]


See other pages where Liver acute alcohol ingestion is mentioned: [Pg.297]    [Pg.458]    [Pg.263]    [Pg.616]    [Pg.405]    [Pg.73]    [Pg.140]    [Pg.323]    [Pg.180]    [Pg.198]    [Pg.434]    [Pg.83]    [Pg.543]    [Pg.2426]    [Pg.21]    [Pg.2542]    [Pg.276]    [Pg.647]    [Pg.658]    [Pg.137]    [Pg.319]    [Pg.74]    [Pg.370]    [Pg.65]    [Pg.377]   
See also in sourсe #XX -- [ Pg.336 , Pg.337 , Pg.338 , Pg.339 , Pg.340 , Pg.341 , Pg.342 , Pg.343 , Pg.344 , Pg.345 , Pg.346 , Pg.347 ]




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