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PubMed1994

[Concentrations of ethanol and ethanol metabolites and symptoms of acute alcohol-intoxicated patients].

Five patients who presented to an emergency room and did not have other injury and disease with acute alcohol intoxication were analyzed about blood and urine ethanol, acetaldehyde, acetate and acetone levels. The average concentrations of ethanol, acetaldehyde, acetate and acetone in blood were 37.0 mM (1.7 mg/ml), 18 microM, 1.00 mM and 18 microM, respectively and the concentrations in urine were 50.8 mM (2.3 mg/ml), 37 microM, 0.79 mM and 47 microM, respectively. Clinical symptoms were concerned with both ethanol concentration and concentrations of ethanol metabolites. Their symptoms of acute alcohol-intoxicated patients were caused by the ethanol concentrations which was less than the levels reported in early studies.

Acetaldehyde↗
PubMed1985

Measuring alcohol intoxication: the development, reliability and validity of an observational instrument.

This study presents an observational instrument designed to assess the presence or absence of alcohol intoxication as well as the level of intoxication. The Alcohol Symptom Checklist (ASC) was validated by comparing the blood alcohol level (BAL) of 672 subjects with the ASC score. The correlation between BAL and ASC for the final version of the scale was .84; alpha reliability = .92; interrater reliability = .93; and mean interitem correlation = .51. These results confirm the scale's reliability, its interrater consistency and its predictive validity. This instrument may be used in place of BAL measures in situations where it would be impractical to obtain samples of blood or alveolar air. The ASC will facilitate naturalistic studies of drinking behavior which previously have been limited by the lack of an unobtrusive method for assessing symptoms of intoxication. In addition, it has potential for use by law enforcement officials in situations where persons suspected of driving while intoxicated refuse to take an evidential breath test. This article examines requirements for training in the use of the ASC, and discusses other potential uses of the instrument.

Adolescent↗
PubMedDate not supplied

Influence of acute alcohol intoxication on the left ventricular pressure-volume relations of the rat heart.

In 17 Wistar rats isovolumetric pressure-volume diagrams, the rate of pressure rise, and the resting tension curve were recorded prior to and during acute alcohol intoxication. Ethyl alcohol was infused intravenously; parameters were recorded at blood alcohol levels between 0.6% and 0.2%. The following results were obtained. 1. In agreement with other authors, even slight amounts of alcohol induced significant cardiodepression. 2. At high blood alcohol levels the isovolumetric pressure-volume relation is shifted to higher enddiastolic volumes and pressures. 3. The alcohol-induced cardiodepression is dose-dependent. There is a linear correlation between the maximum rate of pressure rise and the blood alcohol level.

Alcoholic Intoxication↗
PubMedDate not supplied

[The evaluation of the effect of zinc sulfate on primary immune response indices under alcoholic intoxication].

Introduction of zinc sulfate in the composition of drinking liquid on the background of alcohol intoxication of animals increases the intensity of primary immune response to the sheep erythrocytes (ShE). This effect is manifested through an increase in the number of phagocytosing lymphocytes in peripheral blood, antibody forming cells in the spleen, antibody titer to ShE, and in an increase in the rosette-forming ability of lymphocytes. The data obtained indicate to the potential use of the zinc salts for immunity correction in conditions of chronic alcohol intoxication.

Adjuvants, Immunologic↗
PubMedDate not supplied

[Effect of alcohol intoxication on ascorbic and dehydroascorbic acid levels in rat tissue. and human blood].

It is found that acute ethanol intoxication is accompanied by a decrease in the ascorbic acid content in the brain, liver and kidneys. The content of dehydroascorbic acid in kidneys in this case increases and in the brain tends to decrease. The chronic alcohol intoxication of rats has an opposite (as compared to the acute intoxication) effect on changes in the content of ascorbic and dehydroascorbic acids in the studied organs. People with chronic alcohol intoxication have the lower content of ascorbic acid in blood plasma and the higher content in erythrocytes, the content of dehydroascorbic acid being increased.

Alcoholic Intoxication↗
PubMed1998

Alcohol intoxication and withdrawal: the role of nitric oxide.

Nitric oxide is an important messenger in the central nervous system and several types of evidence suggest that it mediates various alcohol effects. Treatment with a nitric oxide synthase inhibitor enhances the acute central depressant or anesthetic effect of alcohol and decreases some stimulatory effects of alcohol withdrawal after chronic alcohol treatment. Conversely, treatment with a nitric oxide donor inhibits the anesthetic effect of alcohol, blocks the effect of the nitric oxide synthase inhibitor on alcohol anesthesia, and enhances the severity of some alcohol withdrawal signs. These results indicate that changes in nitric oxide synthesis mediate some aspects of alcohol intoxication and withdrawal and that nitric oxide systems represent an important therapeutic target for the development of agents to treat alcoholism and alcohol intoxication.

Alcoholic Intoxication↗
PubMedDate not supplied

[Hemispheric lateralization of the visual-spatial function in chronic alcoholic intoxication in humans].

A series of behavioural and electrophysiological parameters was recorded in subjects with chronic alcohol intoxication during solving of visual-spatial nonverbalized task. It is shown that in comparison with the healthy subjects, their reaction time (RT) of correct decisions was increased; it was more expressed when stimuli were presented in the left visual field, i.e., directly to the right hemisphere, and the number of correct reactions decreased at stimuli presentation directly to the left hemisphere. During repeated tests there were no changes in the number of correct reactions and RT value in the group with chronic alcohol intoxication. It is found that long-term taking of alcohol produces an increase of latency and decrease of the amplitude of the late positive wave P300, more pronounced in the right cerebral hemisphere.

Adult↗
PubMed2002

Effect of alcoholic intoxication on water content and activity of Na,K-ATPase and Ca-ATPase in rat brain.

We studied the effect of 2-week alcohol intoxication on water exchange and activity of Na,K-ATPase and Ca-ATPase in rat brain. Alcohol intoxication increased water content in the brain due to cell hyperhydration. It is assumed that hyperhydration results from increased Na+ content in cells due to inhibition Na,K-ATPase activity, which in turn is caused by activation of lipid peroxidation under the effect of ethanol. A possible mechanism of Na,K-ATPase inhibition.

Alcoholic Intoxication↗
PubMed1986

[Effect of various types of artificial respiration on raised intracranial pressure, associated with acute alcoholic intoxication].

The effects of spontaneous respiration and mechanical ventilation on ICP were examined by investigating the interaction between elevated pressure and alcohol intoxication. 200 ml ethanol 48% were infused in 11 young pigs with elevated cerebral pressure during mechanical ventilation (Group 1), 7 young pigs with elevated intracranial pressure during spontaneous respiration (Group 2), and 4 young pigs without elevated intracranial pressure during spontaneous respiration (Group 3). While the behaviour of intracranial pressure during mechanical ventilation in the animals from Group 1 was inhomogeneous with a tendency to rise (29 mmHg to 34 mmHg), intracranial pressure (28 mmHg to 55 mmHg) increased dramatically in Group 2. This increase was associated with a sharp rise of paCO2 (37.6 mmHg to 73.3 mmHg) and a decline of paO2 (74 mmHg to 13 mmHg). None of the animals in Group 2 survived. paCO2 also rose in alcoholized animals without elevated ICP (Group 3) (41.9 mmHg to 63.9 mmHg); intracranial pressure, however, remained within the normal range. All animals in Group 3 survived. Our findings indicate that elevated intracranial pressure and alcohol intoxication have a cumulative or potentiating effect on depression of the respiratory centre. Respiratory depression can be prevented by mechanical ventilation and, therefore, a further rise of intracranial pressure can be generally avoided.

Alcoholic Intoxication↗
PubMed2003

Alcohol intoxication increases allopregnanolone levels in male adolescent humans.

RATIONALE: Teenage drinking is a cause of growing concern in industrialized countries, where almost 35% of alcohol drinkers are under 16 years old. Increased anxiety, irritability and depression among adolescents may induce them to seek the anxiolytic and rewarding properties of alcohol. Allopregnanolone is rewarding in rodents, and therefore may contribute to the effects of alcohol. OBJECTIVE: In this paper, we studied the effects of acute alcohol intoxication on the plasma levels of allopregnanolone in male adolescents. METHODS: Blood samples were drawn from male adolescents who arrived at the Emergency Department of the Hospital. Two groups were studied: one study group was formed by adolescents who arrived with evident behavioral symptoms of acute alcohol intoxication (AAI) and the other by those arriving for mild trauma (contusions, sprains) after no consumption of alcohol (Controls). RESULTS: Our results demonstrate that AAI significantly increases serum allopregnanolone levels in male adolescents. CONCLUSIONS: Because alcohol and allopregnanolone positively modulate gamma-aminobutyric acid type A (GABAA) receptors, allopregnanolone may play a major role in the anxiolytic and rewarding effects of alcohol, either directly or by influencing the sensitivity of GABAA receptors to alcohol.

Adolescent↗
PubMed1993

[Acute ethyl alcohol intoxication].

Excessive intake of ethyl alcohol leads to acute intoxication and necessitates the same management as other forms of intoxication. Diagnosis is based on clinical examination, medical history and course. Determination of alcohol level in the expired air is of limited interest. If low or absent, it should direct clinical investigation toward a disorder having similar symptoms; if high, it does not necessarily explain the clinical picture. The severity of the intoxication must always be assessed carefully. Severity is linked either to a complication of acute alcohol intoxication (coma, inhalation, pneumopathy), or to an associated disorder, observed in 50% of the patients (cranial trauma, drug intoxication). Means of treatment and patient management are simple and well established.

Alcoholic Intoxication↗
PubMed2001

[Human performance against acute alcohol intoxication].

Analyzed were quantitative literary data on the effects of acute alcohol intoxication on performance. Reviewed were impacts of various doses of alcohol on the psychophysiological parameters and intricate sensorimotor functions of flying human operator. Alcohol was found to be unfavorable to the vestibular function and, therefore, predisposing to traffic and flight accidents. Hence, the alcohol CNS effects give rise to behavioral and psychophysiological disturbances. The psychophysiological disturbances are impaired concentration and dynamic visual function as a whole, deteriorated light differentiation ability and information perception, short-term amnesia, altered alertness and block, and associated lack of self-criticism and self-control.

Acute Disease↗
PubMed2004

Alcohol intoxication impairs phosphorylation of S6K1 and S6 in skeletal muscle independently of ethanol metabolism.

BACKGROUND: The purpose of this study was to characterize the ability of alcohol to suppress insulin-like growth factor (IGF)-I stimulation of ribosomal S6 kinase 1 (S6K1) and 4E-BP1 phosphorylation, which are central elements in the signal transduction pathway used to coordinate the protein synthetic response and may contribute to the development of alcoholic myopathy. METHODS: In vivo studies examined the dose and time dependency of the ability of alcohol to impair signal transduction under basal and IGF-I-stimulated conditions. Additional studies examined the effect of gender, nutritional state, and route of alcohol administration. A separate study determined the direct effects of alcohol on muscle metabolism by using the isolated perfused hindlimb preparation. RESULTS: The phosphorylation of S6K1 and S6 in muscle was increased after injection of IGF-I in control rats. In contrast, IGF-I failed to stimulate S6K1 or S6 phosphorylation 2.5 hr after intraperitoneal administration of alcohol when the blood alcohol concentration was increased between approximately 165 and 300 mg/dl. With a maximal suppressive dose of alcohol, the inhibitory effect on S6K1/S6 phosphorylation was observed as early as 1 hr and for up to 8 hr. The ability of alcohol to impair phosphorylation of S6K1 and S6 was independent of gender (male versus female), nutritional status (fed versus fasted), and route of alcohol administration (intraperitoneal versus oral). Furthermore, the suppressive effect of alcohol was still observed in rats pretreated with 4-methylpyrazole, suggesting that the response was independent of the oxidative metabolism of ethanol. The direct effect of alcohol on IGF-stimulated S6K1/S6 phosphorylation was also present when the isolated hindlimb was perfused in situ with buffer containing alcohol. In contrast to S6K1, acute alcohol intoxication did not consistently impair the ability of IGF-I to stimulate 4E-BP1 phosphorylation under any of the experimental conditions. CONCLUSIONS: These data indicate that acute alcohol intoxication selectively impairs IGF-I signaling via S6K1, but not 4E-BP1, and that this defect is independent of gender, nutritional state, route of administration, and alcohol metabolism. The IGF-I resistance may represent a participating mechanism by which alcohol directly limits the translation of selected messenger RNAs and, ultimately, protein synthesis in skeletal muscle.

Alcoholic Intoxication↗
PubMed2000

Fatal acute alcohol intoxication in an ALDH2 heterozygote: a case report.

On an evening in November, a 25-year-old man was found dead in his bedroom. There were many empty snap-out sheets for flunitrazepam tablets in the trash at his bedside. He had been beaten by a gang of young people earlier in the morning of the same day. At the medico-legal autopsy, although there were many bruises and/or abrasions on the whole body, only slight subdural hemorrhage was observed, and none of them was thought to be the cause of death. Flunitrazepam and its metabolites were not detected in his body fluid by gas chromatography-mass spectrometry (GC-MS). Marked lung edema and a severe congestion of organs were observed. His blood alcohol concentration from the femoral vein was 2.00 mg/ml. Fatal cases of acute alcohol intoxication usually have shown higher alcohol concentration (2.25-6.23 mg/ml). Although the genotype of aldehyde dehydrogenase 2 (ALDH2) has not previously been mentioned as a contributing factor in determining the cause of death, in this case the genotype of ALDH2 was ALDH2*1/2 and thus is important. Those who possess the ALDH2*2 gene show high concentrations of acetaldehyde (AcH) at even comparatively lower alcohol levels. Consequently, the cause of death was considered to be acute alcohol intoxication including AcH poisoning.

Acetaldehyde↗