PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Ethanol”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1975

Intestinal lymph formation and fat absorption: stimulation by acute ethanol administration and inhibition by chronic ethanol administration and inhibition by chronic ethanol feeding.

The acute administration of ethanol, either in lipid emulsions administered intraduodenally or in liquid diets given by gastric tube, increased the flow of intestinal lymph and the output of proteins and dietary lipids into the lymph, mainly in the 1st hr after administration. During this time, the intraduodenal administration of ethanol (0.75 g per kg of body weight), without exogenous lipids, increased the flow of lymph without changing the lymph lipid output. Stimulation of the lymph flow with neostigmine or by increasing the fluid load also enhanced the output of lymph proteins and the transport of exogenous lipids from the intestinal lumen into the lymph. To study the chronic effects of ethanol, rats were pair-fed liquid diets containing either ethanol (36% of calories) or isocaloric carbohydrate for 3 to 4 weeks. Thereafter, the lymph changes were measured after administration of equal lipid loads with and without ethanol. The administration of an acute ethanol dose to rats chronically fed alcohol moderately increased the lymph flow, but did not change the output of dietary lipids. Furthermore, rats chronically fed alcohol responded to a dietary challenge devoid of ethanol with increases in both lymph flow and dietary lipid output which were not as great as those of pair-fed controls. Thus, acute ethanol administration has a marked stimulatory effect both on the formation of intestinal lymph and on the transport of deitary fat. By contrast, chronic ethanol feeding inhibits these acute effects of ethanol, and, in addition, appears to have moderate inhibitory effect on lipid absorption.

Acute Disease↗
PubMed1979

Free-choice ethanol intake and ethanol metabolism in the hamster and rat.

Hamsters, as previously reported, demonstrated greater ethanol intake and preference than rats. However, as ethanol was gradually added to a sweet solution, hamster ethanol intakes did not consistently exceed ethanol metabolic capacity for prolonged periods. In ethanol-naive hamsters and rats, alcohol dehydrogenase activities and ethanol metabolic rates of isolated hepatocytes in vitro and blood ethanol elimination rates in vivo show consistent large interspecific differences corresponding to the species' differences in ethanol intake and preference. The data suggest a limiting role of ethanol metabolism in the regulation of maximized free-selection ethanol intake by rodents, and provide an explanation for the absence of continuously elevated blood ethanol levels and alcohol withdrawal syndrome in hamsters during periods of comparatively high daily ethanol intake.

Alcohol Drinking↗
PubMed1979

Metabolism of palmitate in perfused rat liver. Effect of ethanol in livers from rats fed on a high-fat diet with or without ethanol.

1. Rats were treated for 4 weeks with liquid diets that contained, on the basis of energy content, 35% fat, 18% protein and 47% carbohydrate (high-fat diet) or 35% fat, 18% protein, 11% carbohydrate and 36% ethanol (high-fat/ethanol diet). 2. The livers were perfused with 1mm-[1-(14)C]palmitate and with 0, 10mm- or 80mm-ethanol. The oxidation and esterification of palmitate was measured. Two subcellular pools of triacylglycerol were separated; one contained triacylglycerol from cytoplasmic lipid droplets and the other contained triacylglycerol from the endoplasmic reticulum and Golgi apparatus. 3. In the presence of ethanol, liver from rats fed on the high-fat diet esterified about 70% of the [1-(14)C]palmitate taken up compared with 90% in liver from rats fed chow (containing 11% fat on the basis of energy content). Compared with chow diet the high-fat diet did not potentiate the effect of ethanol on storage of [1-(14)C]palmitate in hepatic triacylglycerol. The relation between the fat content of the diet and the degree of fatty liver induced by by ethanol [Lieber & DeCarli (1970) Am. J. Clin. Nutr.23, 474-478] is discussed. 4. The ethanol-containing diet increased the hepatic content of triacylglycerol 4-fold and the increase was exclusively found in the fraction suggested to contain lipid from cytoplasmic lipid droplets. The ethanol-induced fatty liver, perfused with ethanol, esterified and oxidized palmitate at rates that were quite similar to the rates found in high-fat control livers perfused without ethanol. This suggests that the fatty liver had adapted to the presence of ethanol with respect to palmitate metabolism. 5. O(2) and ethanol uptake by the livers were not affected by the ethanol-containing diet.

Animals↗
PubMed1979

Pyrithiamin shortens ethanol-induced narcosis and increases voluntary ethanol drinking in rats.

To investigate the role of thiamin deficiency in increasing voluntary ethanol intake in rats the effect of ethanol on the central nervous system was studied by measuring the duration of ethanol narcosis in pyrithiamin-treated rats. The duration of ethanol-induced narcosis was significantly shorter and blood ethanol concentration at the moment of righting reflex recovery was higher in pyrithiamin-treated rats than in controls. Thus, the shorter ethanol narcosis of pyrithiamin-treated rats was not a result of a change in ethanol metabolism but rather suggests changes in the central effects of ethanol. Treatment with thiamin increased the duration of ethanol narcosis to the initial level in rats pretreated with pyrithiamin. During the same pyrithiamin treatment as used for the narcosis test voluntary ethanol intake of rats was higher than during optimal treatment by thiamin. The results suggest that there might be a decrease in central sensitivity to ethanol in pyrithiamin treated rats, which may have a role in increasing their voluntary ethanol drinking.

Alcohol Drinking↗
PubMed1979

Activities of hepatic enzymes related to ethanol oxidation and effects of ethanol on hepatic metabolites in rats with chronic liver injury.

To study the effects of ethanol on liver chronically injured by CCl4, activities of hepatic enzymes related to ethanol oxidation, influences of ethanol on hepatic metabolites, and blood ethanol disappearance were observed. (1) Activities of alcohol dehydrogenase, low- and high-Km aldehyde dehydrogenase, microsomal ethanol-oxidizing system and drug-metabolizing enzyme were remarkably decreased in the injured liver. (2) Increases in lactate/pyruvate and beta-hydroxybutyrate/acetacetate ratios were shown in control liver 2 h after ethanol ingestion. Similar but less pronounced effects of ethanol on the 'redox state' were also seen in rats with chronic liver injury. (3) Delay in ethanol disappearance was not observed until 12 h after ethanol ingestion. The ethanol-induced changes in the redox state in the injured liver were similar to those in controls. Higher ethanol concentrations in blood from rats with chronic liver injury could be related to potentiate the injured liver.

Animals↗
PubMed1978

Dietarily-induced changes in voluntary ethanol consumption and ethanol metabolism in the rat.

1. The voluntary ethanol consumption, ethanol elimination rate and blood acetaldehyde level after intraperiotoneal injection of ethanol were studied in rats receiving diets with highly imbalanced proportions of dietary protein, carbohydrate and fat. 2. The rats, which received the low-protein diet containing 0.05 of the total energy as protein, 0.80 as carbohydrate and o.15 as fat, drank only approximately half as much ethanol as did the control group, which received 0.30 of its total food energy from protein, 0.55 from carbohydrate and 0.15 from fat. Ethanol elimination rate in the low-protein group was decreased and the blood acetaldehyde level after ethanol injection was markedly increased. 3. On the high-fat diet, which contained 0.30 of the total energy from protein, 0.05 from carbohydrate and 0.65 from fat, the rats drank significantly more ethanol than did the rats on the control diet; their ethanol elimination rate was decreased but their blood acetaldehyde level was not affected. 4. In conclusion, the strong decrease in voluntary ethanol drinking by the low-protein group may have been caused by the increased acetaldehyde accumulation in the blood, but a particularly low blood acetaldehyde level was not one of the factors inducing excessive ethanol drinking in the high-fat group.

Acetaldehyde↗
PubMed1977

Concentrations of free amino acids in brains of mice during the induction of physical dependence on ethanol and during the ethanol withdrawal syndrome.

Chronic administration of ethanol to mice by inhalation for 10 days produced physical dependence demonstrated by a characteristic syndrome of withdrawal. Free amino acid concentrations in whole brain were measured at intervals during the induction of dependence and during withdrawal. During the induction of dependence there was an initial increase in brain glycine, a sustained increase in brain tyrosine and reductions in brain GABA and proline. Serine and isoleucine concentrations were consistently reduced during the induction of dependence, but this change was not significant (P less than 0-05) at any single time interval studied. After the withdrawal of ethanol only the reductions in GABA and proline persisted during the withdrawal syndrome. In addition to these changes an increase in brain glycine concentration was observed during the ethanol withdrawal syndrome. In an attempt to discriminate between the immediate, metabolic effects of ethanol on central amino acid concentrations and those changes associated with the induction of ethanol dependence, the results were compared with those obtained when mice were exposed to a high concentration of ethanol vapour for 3 h. Although this produced similar blood ethanol concentrations, no evidence of physical dependence was observed. The changes in central amino acid concentrations differed from those seen during the induction of dependence in that no change in isoleucine concentration occurred, and that the reduced concentrations of GABA and proline very rapidly reverted to control values when ethanol was removed. The possible role of central amino acids in ethanol dependence is discussed.

Alcoholism↗
PubMed1979

The calcium carbimide-ethanol interaction: effects of ethanol dose.

In a double-blind, placebo-controlled study involving five male alcoholic volunteers, oral administration of 0.7 mg/kg of calcium carbimide (CC) 12 hr before ingestion of ethanol (0.125, 0.25, and 0.5 gm/kg) produced an interaction consisting of increased blood acetaldehyde level, tachycardia, and decreased diastolic blood pressure. The order of intensity of the interaction with regard to ethanol dose was 0.5 greater than 0.25 greater than 0.125 k gm/kg. The subjects were aware of a CC-ethanol interaction only for 0.25 and 0.5 gm/kg of ethanol, for which heart rate was elevated above 100 bpm. With the criterion of heart rate above 100 as indicative of the CC-ethanol interaction, the onset was 0.25 and 0.38 hr for the 0.5 and 0.25 gm/kg ethanol doses and the duration of the interaction was 1.0 and 0.38 hr, respectively. There were positive linear correlations between blood acetaldehyde level and both heart rate and pulse pressure. There was appreciable individual variability in the intensity and duration of the interaction. Pretreatment with CC reduced the rate of ethanol metabolism at the 0.5 gm/kg ethanol dose.

Acetaldehyde↗
PubMed1977

Common mechanism for the adaptive increase in hepatic ethanol and acetaldehyde metabolism due to chronic pretreatment with ethanol.

Perfused livers from ethanol pretreated rats utilized ethanol and acetaldehyde at higher rates than appropriate controls. This adaptive increase in hepatic ethanol and acetaldehyde uptake was associated with a marked (greater than 60%) increase in hepatic oxygen uptake. Ethanol uptake in both ethanol-treated and control livers was similarly sensitive to inhibition by 4-methylpyrazole, rotenone, and antimycin A. The adaptive increase in ethanol uptake was apparently specifically abolished by ouabain, an inhibitor of the sodium-plus potassium-activated ATPase. The data are consistent with the hypothesis that chronic treatment with ethanol increases ATPase activity. The ADP produced from these initiating events enters the mitochondrial space and stimulates electron transport and oxygen uptake. As a consequence of these events, a greater rate of NADH reoxidation occurs, resulting in a greater rate of production of NAD+ which stimulates ethanol oxidation via alcohol dehydrogenase and acetaldehyde oxidation via aldehyde dehydrogenase(s).

Acetaldehyde↗
PubMed1979

Attenuation of ethanol intake by 5-hydroxytryptamine uptake blockade in laboratory rats. I. Involvement of brain 5-hydroxytryptamine in the mediation of the positive reinforcing properties of ethanol.

The role of 5-hydroxytryptamine (5-HT) uptake blockade in the mediation of the positive reinforcing peroperties of ethanol in male wistar rats was investigated. It was demonstrated that treatment with zimelidine (H102/09) a 5-HT uptake inhibitor, specifically attenuated ethanol consumption. In an attempt to extinguish the ethanol drinking response, ethanol preferring animals in a second experiment, were provided with ethanol as the only source of fluid in combination with zimelidine treatment. Animals treated in such a manner subsequently reduced their ethanol consumption when presented with a free-choice between ethanol and water. These results were attributed to an increased availability of central 5-HT, suggesting that central 5-HT mechanisms may in some way be involved in the mediation of the positive reinforcing properties of ethanol.

Alcohol Drinking↗
PubMed1978

Comparison of the excitatory and anaesthetic effects of ethanol in C57BL/6 and BALB/c mice; relation to blood ethanol concentration.

Ethanol increased the exploratory locomotion of BALB/c mice over a wide dose range (1.15--3.1 g/kg orally), whereas only a 2.31 g/kg dose of ethanol increased the locomotion of C57BL/6 mice. After 1.15 g/kg of ethanol the blood concentrations in BALB/c and C57BL/6 mice were 65 +/- 11 and 68 +/- 13 mg %, respectively, and after 2.3 g/kg--the corresponding concentrations were 156 +/- 26 and 142 +/- 14 mg % (mean +/- SEM). Doses of 3.8 and 4.6 g/kg inhibited the exploratory locomotion of mice of both strains to an equal extent. The induction time and the duration of ethanol-induced anaesthesia, as well as the blood ethanol concentrations (428 +/- 40 and 446 +/- 40 mg %, respectively, at the onset of anaesthesia) were similar in mice of both strains after a 5.4 g/kg dose. However, motor excitement before anaesthesia was observed only in the BALB/c mice. It is suggested that the observed strain differences in response to ethanol are due to low responsivity of C57BL/6 mice to the excitatory action of ethanol and are not caused by differences in the rate of its metabolism. Apparently, the excitatory and anaesthetic effects of ethanol are under separate genetic control mechanisms.

Administration, Oral↗
PubMed1979

Electrophysiological responses to ethanol, pentobarbital, and nicotine in mice genetically selected for differential sensitivity to ethanol.

Cortical electroencephalographic (EEG) changes induced by ethanol (4.3 and 1.4 g/kg, ip), pentobarbital (50 and 16 mg/kg), and nicotine (1.0 g/kg) were examined in long-sleep (LS) and short-sleep (SS) mice that were genetically selected for differential sleep times induced by a hypnotic dosage of ethanol. Ethanol (4.3 g/kg) caused EEG changes that paralleled the behavioral differences, whereas no differences between selected lines were observed following the activating dose (1.4 g/kg). Data support the notion that the known difference in ethanol sleep times is due not to greater SS sensitivity to ethanol activation but rather to greater LS sensitivity to ethanol hypnosis. No differences between selected lines were observed following 50 mg/kg pentobarbital, which again parallels previous behavioral data. The SS mice were more responsive to pentobarbital activation (16 mg/kg). Nicotine more severely reduced EEG power and heart rate in LS mice; a continuous iv infusion of nicotine elicited a distinct pattern of behavioral stereotypy for each selected line, with more profound motor and reflex depression in LS mice. The lines do not differ in rate of nicotine metabolism, hence they must differ in central nervous system sensitivity to nicotine. Thus, lines of mice selectively bred for differential sensitivity to ethanol also display marked differences in electrophysiological and behavioral responses to nicotine.

Animals↗
PubMed1979

Rats bred for ethanol sensitivity: impairment of swimming by ethanol and pentobarbital.

Rats selectively bred for disparate degrees of ethanol-induced depression of spontaneous locomotor activity ('most affected' = MA; 'least affected' = LA) were trained on a swim task. Undrugged rats of the MA line swam significantly faster than rats of the LA line. Ethanol, 0.0--2.25 g/kg i.p., produced dose-dependent increases in swim time in rats of the 13 generation (F13). Averaged over trials, these increases were greater in LA than in MA rats and greater in males than in females, but there was no sex difference in peak impairment. Increases in swin time were uncorrelated with predrug performance. These findings were confirmed in younger F17 rats receiving 1.75 g EtOH/kg i.p. Although the lines differed in ethanol-induced impairment, F17 males of the two lines were not differentially impaired by pentobarbital (12.5--22.5 mg/kg, i.p.). The existence of task-dependent line differences in ethanol sensitivity emphasizes the nonunitary nature of ethanol-induced 'behavioral depression.'

Animals↗
PubMed1978

Effect of adrenergic beta receptor blockade on ethanol elimination and on ethanol-induced changes in carbohydrate and lipid metabolism in man.

The effect of adrenergic beta receptor blockade on the elimination rate of ethanol was studied in seven healthy young men. The studies were performed before and after 14 days of propranolol 240 mg/day: the ethanol was given per-orally--0.8 mg/kg b.w. The blood concentration of ethanol, glucose, lactate and glycerol, and the plasma concentration of free fatty acids and triglycerides were followed in samples from the superior vena cava taken every 20 min for four hours. The splanchnic hepatic blood flow was estimated with a single i.v. injection of indocyanine green. The absorption rate, absorption fraction and elimination rate of ethanol were not changed by propranolol. The splanchnic hepatic blood flow was significantly reduced (mean 19 per cent) during beta receptor blockade. The ethanol-induced change in the concentration of glucose, lactate and free fatty acids was affected by propranolol, the time-concentration curves for glucose and lactate being significantly elevated and that for free fatty acids being significantly reduced. The time-concentration curves for glycerol and triglycerides did not differ in the two studies.

Adolescent↗