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Results for “Alcoholic Intoxication”

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PubMed1989

The effect of alcohol intoxication on primary and secondary processes in male social drinkers.

The acute effects of alcohol intoxication on cognitive style and on locus of control was investigated in an experimental setting. Sixty male subjects were randomly assigned to either an Alcohol, a Placebo, or a Control group. The alcohol dose was 1.0 ml of 100% alcohol/kg body weight. Subjects filled out a modified version of Rotter's locus of control scale and reported their perceptions to Street's Gestalt Completion Test. The latter test was scored in a standardized way for stimulus closeness, indicating a reality oriented and rational functioning, and stimulus distance, indicating a more primitive, irrational and pleasure oriented functioning. Alcohol made subjects less internally controlled and decreased the reality oriented functioning while the pleasure oriented functioning was not affected. Results were discussed in terms of pharmacological mechanisms, disinhibition, and creativity.

Adult↗
PubMed1978

[Subacute alcoholic intoxication in rats: effect of an intravenous injection of glucagon or adrenaline].

We have studied the hyperglycemic effect of glucagon (20 microgram/kg) and adrenaline (5 microgram/kg/mn/3 mn) on the rat subjected to a subacute alcoholic intoxication (6,4 g/kg by day during 12 days). The hyperglycemic action of the glucagon is increased while that of the adrenaline slightly decreased. So, the alcoholic intoxication allows to dissociate the both mechanisms of the glycogenolytic action of both hormones. Two hypothesis are brought forward in the discussion.

Alcoholism↗
PubMedDate not supplied

[Ethanol-oxidizing enzymes of the adrenal glands in acute alcoholic intoxication].

Complex morphological-and-histological examinations of the adrenal glands were performed on actual forensic-medical samples in acute alcoholic intoxication (AAI), i.e. 107 death cases of men and women, aged 17 to 60, due to mechanical trauma, lethal ethanol intoxication and somatic complications of chronic alcoholism. A differentiated distribution of ethanol-oxidizing enzymes was defined, i.e. of alcohol-dehydrogenase and acetyl-dehydrogenase in the structural-and-functional zones of the adrenal cortex and medullary substance. A differential activity of enzymes was established that correlated with the level of exogenous alcoholemia. Sets of morphological signs related with examinations of the adrenal glands, which enabled a differential diagnosis of death causes in AAI, were specified.

Adolescent↗
PubMed1985

Effects of maternal alcohol intoxication on fetal circulation and myocardial function: an experimental study in the ovine fetus.

To determine whether acute alcohol ingestion during pregnancy could affect fetal myocardial function, studies were carried in six chronically catheterized fetal sheep during maternal alcohol infusion. Absolute ethyl alcohol (0.8 ml/kg) was administered to the mother over 10 minutes via the jugular vein. These infusions were repeated every 30 minutes during 3 hours, and peak maternal and fetal blood concentrations close to 200 mg/dl alcohol were reached. Fetal PCO2 decreased from a baseline of 43.15 +/- 3.75 to 36.13 +/- 2.6 torr 1 hour after the start of alcohol infusion (P less than 0.05). Similarly, pH rose from 7.37 +/- 0.027 to 7.44 +/- 0.015 (P less than 0.05). Both values returned to baseline level at the end of alcohol infusion. PO2 remained within physiologic limits. The systolic time intervals of the fetal heart showed a rapid and prolonged modification. The pre-ejection period from 58 +/- 8 to 66 +/- 4 msec (P less than 0.05) during the infusion; this change was related to an increase in the isometric contraction period. The ratio of the pre-ejection period over the ejection time was also significantly increased (P less than 0.01), and remained elevated until the end of the experiment (12 hours). A rise in fetal systolic and diastolic pressures was observed at about 2 hours after the start of the alcohol infusion, and lasted 4 hours. This study suggests that an episode of maternal alcohol intoxication causes rapid depression of fetal myocardial contractility that is maintained several hours after cessation of alcohol ingestion.

Alcoholic Intoxication↗
PubMedDate not supplied

[Chronic alcoholic intoxication in animals as a model for the study of the safety of new anti-alcohol agents].

Experiments on 200 noninbred male rats have demonstrated that daily administration of ethanol per os in a dose of 8 g/kg (2/3 LD50) for a month produced pathological changes in organs and systems of the body, which were similar to the manifestations of chronic alcoholic intoxication in man. It is concluded that the model under consideration may be used during preclinical study of the safety of new antialcoholic agents.

Alcohol Deterrents↗
PubMed1990

Effects of amino acids on acute alcohol intoxication in mice--concentrations of ethanol, acetaldehyde, acetate and acetone in blood and tissues.

Condensation reactions between some SH-amino acids (L-and D-cysteine 1%) and acetaldehyde (50 microM) were studied in vitro experiment. In the aqueous solution, free acetaldehyde was reduced to 41.3% by L-cysteine and to 36.4% by D-cysteine. In the reaction with human blood medium, after the medium was deproteinized with perchloric acid reagent, acetaldehyde was reduced to 47.0% by L-cysteine and to 43.8% by D-cysteine. D-Cysteine appears to have great stability of reacting acetaldehyde. In vitro experiment reactability for D-cysteine exhibited 3-8% higher than that for L-cysteine. Next, effects of some amino acids on alcohol metabolism were studied in male ICR mice. The animals were given ethanol through a gastric catheter at a dose of 2 g/kg and they were intraperitoneally injected L-cysteine (300 mg/kg), D-cysteine (300 mg/kg), L-alanine (300 mg/kg) and control (saline), respectively in the period of one hour before the injection of ethanol. Blood and tissues samples were analyzed for ethanol, acetaldehyde, acetate and acetone during alcohol intoxication in mice by head space gas chromatography. In the groups administered D-cysteine and L-cysteine, the mice showed a definitely faster oxidation and disappearance of ethanol. Especially in the D-cysteine group, ethanol levels in blood, liver and brain remained lower than that in the other groups (p less than 0.01). Acetaldehyde levels in blood, liver and brain remained low by L-cysteine. Ethanol metabolites during alcohol oxidation by chemical reactabilities of L- and D-cysteine showed different distribution in the mice, respectively. In the mice received L-alanine, acetate and acetone levels in blood, liver and brain were distinctly reduced (p less than 0.01). L-Alanine is reported to supply an abundance of pyruvic acid that performs the NAD-generating system. NAD produced is introduced to alcohol metabolism and the TCA cycle. It was thus presumed that the L- or/and D-cysteine, and L-alanine was effective in acute alcohol intoxication by heavy drinking.

Acetaldehyde↗
PubMed1999

Effects of alcohol intoxication on parenting behavior in interactions with child confederates exhibiting normal or deviant behaviors.

Experimental analogue methods were used to study how acute alcohol intoxication in parents influences their perceptions of and reactions to child behaviors, as well as their strategies for management of those behaviors. All participating parents had a grade school-aged son, but in half the cases this target child had a diagnosed externalizing disorder, whereas for the remaining half neither the target son nor any other offspring of the parents evidenced any psychopathology. Equal numbers of married fathers, married mothers, and single mothers from each of these groups received either alcoholic or nonalcoholic beverages prior to videotaped interactions with male child confederates who, depending on condition, enacted behaviors characteristic of either normal boys or boys with attention deficit hyperactivity/conduct/oppositional defiant disorders (ADHD/CD/ODD). Results indicated that intoxicated parents rated their ADHD/CD/ODD child partners as less deviant than did sober parents. Alcohol intoxication caused all participant groups to exhibit less attention and productive work and more commands, indulgences, and off-task talk in the interactions. Implications for better understanding of the role of psychosocial factors in the correlation between adult drinking problems and childhood behavior disorders are discussed.

Adult↗
PubMed2003

Dose and time changes in liver alcohol dehydrogenase (ADH) activity during acute alcohol intoxication involve not only class I but also class III ADH and govern elimination rate of blood ethanol.

BACKGROUND: The elimination rate of blood ethanol usually depends on the activity of liver alcohol dehydrogenase (ADH). During acute alcohol intoxication, however, it is unclear how liver ADH activity changes with dose and time and what the involvement is of the two major isozymes of liver ADH: the classically known class I ADH and the very high Km class III ADH. We investigated dose- and time-wise changes in liver ADH activity and the contents of both ADHs by administering ethanol to mice, and analyzed the relationship among these ADH parameters to assess the contributions of these ADHs to liver ADH activity and ethanol metabolism in vivo. METHODS: Mice were given ethanol doses of 0, 1, 3 or 5 g/kg body weight and killed 0.5, 1, 2, 4, 8 or 12 h after administration. The elimination rate of blood ethanol was calculated from the regression line fitted to the blood ethanol curve. The liver ADH activity of crude extract was conventionally measured with 15 mM ethanol as a substrate. The liver class I and class III ADH contents were determined by enzyme immunoassay. These three ADH parameters were statistically analyzed. RESULTS: The change in liver ADH activity depended on both dose and time (P<0.001 by two-way ANOVA, n=74), but the change in the class I content depended on dose alone (P<0.0001). The class III content depended on both dose and time (P<0.001) with a time course similar to that of liver ADH activity for each dose. The sum of the class I and class III contents exhibited a higher correlation with liver ADH activity (r=0.882, P<0.0001) than the class I content alone did (r=0.825). The mean liver ADH activity during ethanol metabolism for each dose correlated significantly with the elimination rate of blood ethanol (r=0.970, P<0.0001). CONCLUSION: Liver ADH activity changes dose and time dependently during acute alcohol intoxication and governs the elimination rate of blood ethanol through the involvement not only of class I but also of class III ADH.

Alcohol Dehydrogenase↗