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Acute alcohol intoxication paired with appetitive reinforcement: effects upon ethanol intake in infant rats.

A recent study suggested that infant rats process alcohol odor and/or taste during acute ethanol intoxication probably due to ethanol elimination via respiration and salivation. The present set of experiments was meant to analyze the possibility that this orosensory processing may act as a conditioned stimulus when an appetitive reinforcer is paired with the state of intoxication. In the first experiment it was observed that intragastric administration of a mildly intoxicating ethanol dose (1.5 g/kg), paired during postabsorptive time intervals with oral infusion of sucrose, was sufficient to promote a significant preference to ethanol. In Experiment 2 different doses of ethanol were either paired or explicitly unpaired with sucrose administration. The result reported in Experiment 1 was replicated and it was observed that a higher dose (3.0 g/kg) unpaired with the reinforcer resulted in alcohol aversions in terms of alcohol consumption patterns. However, when the reinforcer was paired with this dose, the aversion was inhibited. Finally, in the third experiment results indicated that preexposure to alcohol odor eliminates sucrose-conditioned alcohol preferences. These results indicate that, in physiologically immature rats, alcohol preference can be regulated by prior associative experiences involving the state of intoxication and consequences internal and/or inherent to this state.

Alcohol Drinking↗

[Adenylate deaminase of the liver mitochondria in normal state and in alcoholic intoxication].

AMP-deaminases were isolated and partially purified from subfractions of soluble mitochondrial proteins of rat liver under normal conditions and in ethanol intoxication. Repeated freezing and thawing of the mitochondrial fractions from liver of rats, which were treated with ethanol (1 ml of 32% solution daily for 7 days, intraperitoneally), liberated into the subfraction of soluble mitochondrial proteins significantly less AMP-deaminases, as compared with the control animals. The enzyme preparations obtained from intoxicated and intact animals were quite similarly inactivated by controlled heating, deaminated at similar rates AMP, ADP, FAD and some other nitrogenous compounds (but did not deaminate adenosine and some structural analogues of AMP). However, an inhibitory effect of the structural analogues of AMP and of nucleosides was significantly higher towards the AMP-deaminase from healthy rats as compared with the corresponding enzyme preparations obtained from the ethanol-treated animals. The increase in velocity of enzymatic AMP deamination in the subfraction of soluble mitochondrial proteins apparently does not represent a suitable target for possible therapeutic approaches to control the phenomenon, observed in the experimental ethanol intoxication, of stimulation of the deaminating activity in total mitochondrial fraction of rat liver.

AMP Deaminase↗

[Antistressor effect of ethanolamine in acute alcoholic intoxication].

Experiments on albino female rats have shown that ethanol, administered intragastrically at a single dose of 2 g/kg, demonstrates steroidogenic properties. Ethanolamine (a natural metabolic product), administered at a dose of 100 mg/kg, increases the basal level of corticosterone in the rat plasma suppressing the steroidogenic activity of ethyl alcohol.

Alcoholic Intoxication↗

Difficult temperament, acute alcohol intoxication, and aggressive behavior.

The purpose of this study was to investigate the influence of a difficult temperament on alcohol-related aggression in men and women. Subjects were 330 (164 men and 166 women) healthy social drinkers between 21 and 35 years of age. Temperament was measured using the dimensions of temperament survey-revised (DOTS-R). Following the consumption of either an alcohol or a placebo beverage, subjects were tested on a modified version of the Taylor aggression paradigm in which mild electric shocks were received from, and administered to, a fictitious opponent during a competitive task. Aggressive behavior was operationalized as the shock intensities administered to the fictitious opponent under conditions of low and high provocation. Of all the variables, provocation was the strongest elicitor of aggression. Overall, a difficult temperament was positively related to the aggression for all subjects. The finding of greatest importance was that alcohol only increased aggression for men with a difficult temperament. The results highlight the fact that alcohol consumption does not increase aggression in all persons and in all situations. An important goal for future research is to identify which individual difference and which contextual factors are most important in determining who will, and who will not, behave in an aggressive manner when intoxicated.

Acute Disease↗

[Problem of abnormal alcoholic intoxication in forensic psychiatric judgment].

The problem of pathological intoxication is discussed. Also considered by the authors in their present paper is the fact that various designations are used in the literature to describe abnormal intoxications of which the intensity is less than that of real pathological intoxication. However, phenomenological or symptomatological classifications provide no information whatsoever about the ability to take decisions and about mental responsibility. An attempt is made to establish criteria for the concept of "pathologically colored intoxication" which is primarily oriented, not in a phenomenological context, but toward a substantially diminished ability to take meaningful decisions.

Alcoholic Intoxication↗

After-effects of acute alcohol intoxication.

Female, Long-Evans hooded rats (N = 10, 4 months of age) were given ethanol via intragastric intubation in doses of 2.0, 3.0 or 4.0 g/kg (repeated measures design). After-effects (hypothermia, free operant activity, motor performance) were measured at six, twelve and sixteen hours, respectively, for the above doses and were compared to the effects observed after the intubation of equivolume amounts of tap water. The after-effects of ethanol on rectal temperature were varied. Both rotarod performance and free operant activity were impaired after each of the above doses of ethanol. Blood ethanol analyses revealed low blood levels of ethanol (range 6.6 +/- 1.5 to 24.6 +/- 3.4 mg/100 ml) at the time behavioral tests were performed. Thus, quantifiable behavioral impairment was observed after blood ethanol values had declined following acute intoxication episodes. These changes may be related to "hangover" symptomatology in man and may serve as a model for investigating the influence of a variety of factors related to drug dosage, rate of ethanol ingestion, type of alcoholic beverage, and prophylactic or acute intervention therapeutics.

Alcoholic Intoxication↗

[Reduced production of superoxide (02(-)] in peritoneal macrophages of the rat submitted to acute alcoholic intoxication].

Acute ethanol administration by intragastric tube caused an impairment of the superoxide anion production by rat peritoneal macrophages as compared to controls. Since the oxidative-dependent microbicidal system plays a crucial role, at cellular level, in the host defence mechanisms, this work may explain, at last in part, the reduced resistence of alcoholics to infections.

Alcoholic Intoxication↗

Impact of acute alcohol intoxication on patterns of non-fatal trauma: cause-specific analysis of head injury effect.

The impact of alcohol on injury patterns was studied by using 14,920 injured men aged 15-64 years seen in an emergency room in Helsinki, Finland. Blood alcohol was estimated by clinical evaluation and breath test, and was coded into a three-grade intoxication code. Intoxication was recorded in 19.7 per cent. Head injury was more common among the intoxicated (64.1 per cent) than among the sober (17.6 per cent). The odds of head injury, if 1.0 among the sober, was 8.3 among the intoxicated. This head injury effect (HIE) was found in every major external cause category: falls 15.4, traffic 3.0, other unintentional injury 3.4 and assault 2.6. A major difference in HIE was found by hospitalization status: 2.1 for hospitalized and 9.8 for ambulatory patients. Alcohol seems to produce mostly low-energy events (like falls) resulting usually in minor, though potentially dangerous, head injury.

Accidents↗

Percutaneous ethyl alcohol intoxication in a one-month-old infant.

A one-month-old child was referred to our hospital for unexplained lethargy. She was found to be intoxicated from ethanol-soaked gauze pads which had been applied to the umbilical stump and contiguous skin for several days for the purpose of promoting umbilical cord detachment. We emphasize the importance of considering the risk of percutaneous alcohol absorption, especially in young infants, and the necessity of toxicology screening in every child with drowsiness of unknown etiology.

Acute Disease↗

[The effect of acute alcoholic intoxication on the body's immunologic and biochemical indices].

Acute experimental intoxication in rats produced essential changes of the absorptive capacity of neutrophilic blood granulocytes, proteolytic activity, level of proteinase inhibitors and content of blood plasma fibrinogen. Female rats showed a distinct reduction of the activity of natural killer cells. Alcohol had no essential effect on the production of hemolytic antibodies as well as reagins in the respiratory organs.

Alcoholic Intoxication↗

The alcohol intoxicated child and its prognosis.

This article is a review of Swedish and international literature concerning children apprehended for drunkenness. The need for a thorough psychosocial investigation before deciding how to interpret the episode is stressed. A high-risk group of children, in whom the drunkenness is to be looked upon as a warning signal of developing alcoholism, is described. Increased co-operation between the Department of Paediatrics and of Child and Youth Psychiatry, Social Welfare Authorities and School Health Care regarding the treatment of these children is recommended.

Adolescent↗