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PubMedDate not supplied

[Aspartate aminotransferase activity in the brain and spinal cord in acute and chronic alcoholic intoxication].

Resynthesis of aspartate via glutamate was decreased 6-8-fold in rat brain spinal cord tissues due to distinct inhibition of aspartate aminotransferase in acute alcohol intoxication. Consumption of glutamic acid was distinctly increased 1.5-2-fold in tissues of the central nervous system but its metabolism was altered. Normalization occurred within 12-24 hrs after the intake of alcohol. In the state of chronic alcohol intoxication the enzymatic activity was marked increased in brain and spinal cord; in this case the response to a single alcohol administration was altered as compared with acute alcohol intoxication.

Alcoholic Intoxication↗
PubMedDate not supplied

Ontogenetic differences in the expression of olfactory-conditioned aversions resulting from a state of acute alcohol intoxication in the rat.

Three experiments examined the effects of acute alcohol intoxication on olfactory conditioning in infant (16 days old) and adult rats (60-65 days old). In both age groups, alcohol administration (2 g/kg, IG) prior to conditioning procedures failed to affect subsequent expression of methyl-conditioned aversions in a two-way odor locational test. Nevertheless, whenever this same alcohol dose was administered prior to testing procedures, the expression of the olfactory conditioning was substantially impaired in infants but unaffected in adults. The factorial design allowed rejection of the possibility that ontogenetic differences in alcohol-induced state-dependent retention might explain this developmental difference (Experiment 1). A subsequent experiment (Exp. 2a) revealed major age related differences in terms of peak blood alcohol levels (BALs) that resulted from the 2 g/kg alcohol dose previously employed. As revealed by gas chromatography, infants exhibited significantly higher BALs than adults at time of conditioning and/or testing. Therefore in Experiment 2b, the alcohol dose administered in adults was increased until BALs were comparable to those attained in infants given 2 g/kg. This was accomplished with a 2.5 g/kg alcohol dose, employed in Experiment 2c to evaluate responsiveness of adults in conditioning circumstances identical to those of Experiment 1. Yet even with this dose the adults' expression of the conditioned olfactory aversion was unaffected by the alcohol at the time of testing. Experiment 3 analyzed the effects of alcohol intoxication on infantile and adult motor responses elicited by methyl and a novel odor (lemon), which might conceivably have affected performance in the two-way odor locational tests used to assess olfactory conditioning. The results failed to support the possibility that the previously observed ontogenetic differences in the expression of olfactory-conditioned aversions were due to alcohol's effect on sensorimotor responsiveness. In accordance with prior studies, the present results seem to indicate age-related sensitivity to alcohol's effects on cognitive processes.

Aging↗
PubMedDate not supplied

[The determination of the degree of alcoholic intoxication].

A present-day approach to assessment of the degree of alcoholic intoxication during examinations of corpses is offered, based on the fundamentals developed by narcologists. New data are presented about assessment of ethanol levels in the blood and urine and about their significance for assessment of the degree of alcoholic intoxication.

Alcoholic Intoxication↗
PubMed2001

Gender differences in the association of alcohol intoxication and illicit drug abuse among persons arrested for violent and property offenses.

PURPOSE: To explore the associations between violent and other crimes, and alcohol intoxication and recent use of cocaine, marijuana, and other drugs among men and women arrestees and examine gender differences in these relationships. METHODS: We conducted a secondary analysis of 1998 using Arrestee Drug Abuse Monitoring (ADAM) system data using a sample of 9242 male and 2594 women arrested for violent and property offenses in 35 cities. Logistic regression was used to predict arrest for a violent offense (rather than a property crime) from drug- and alcohol-related, and other variables. RESULTS: Both gender and alcohol intoxication are significantly related to arrest for a violent offense. However, the intoxication effects (in the absence of cocaine) are more than three times as great for female (Exp(beta) = 5.59) as male arrestees (Exp(beta) = 1.74), while the combined effects of alcohol and cocaine predict a property offense for women but are insignificant for men. IMPLICATIONS: To achieve further reductions in violent crime, intervention strategies need to focus on reducing alcohol intoxication as well as illicit drug use. Research on the role of alcohol on women's aggression and violence also is suggested.

Adult↗
PubMed1986

[Ultrastructural morphology of acute alcoholic intoxication].

Histologic and electron-microscopic examination of the liver, heart, kidneys, lungs of 32 individuals who died from acute alcoholic intoxication (alcoholemia from 2,9 to 7,2 0/00) and 16 people who died suddenly from a trauma being in the state of a severe alcoholic intoxication. Material was taken for the examination within 3 hours after death. The ultrastructural alterations detected in the organs reflect a deep metabolic disturbances resulting from an acute or chronic alcoholic intoxication. The relation of morphological changes with an age and an alcohol abuse duration is discussed.

Adult↗
PubMedDate not supplied

[Comparative evaluation of the effect of carbidine and levamisole on the E-rosette-forming activity of the lymphocytes in alcoholic intoxication].

The E-rosette formation activity of lymphocytes in human alcoholics treated with carbidine was studied. In experimental alcohol intoxication in animals the effect of carbidine on the E-rosette formation was compared with that of levamisole. The effects of the both drugs in the in vitro experiments were studied as well. The use of carbidine for treating alcoholism was shown to produce changes in the E-rosette formation indicating possible immunodulating properties of the drug. In experimental conditions of the immune response to ram erythrocytes during alcoholic intoxication the inhibitory effect of carbidine on the E-rosette formation was more pronounced. In the in vitro conditions carbidine changes the E-rosette formation in alcoholics similarly to levamisole suggesting the immunomodulating properties of carbidine.

Alcoholic Intoxication↗
PubMed1976

Alcoholism, alcohol, intoxication and assaultive behavior.

The use of alcohol and the role of alcohol intoxication in the crime was studied in 307 males entering the North Carolina prison system after conviction of serious assaultive crimes. The majority (80%) were convicted of homicide (1st and 2nd degree murder and manslaughter), and the remainder (20%) committed a variety of felony assaults. Only 8% of the subjects were abstainers, and 36% were problem drinkers. The problem drinkers often had previous arrests for alcohol offenses (70%) and also were more likely to have previous nonalcohol criminal records (67%) and previous serious assaults (50%) than were other subjects. The problem drinkers were unlikely to have been engaged in treatment of alcoholism (13%) and almost never voluntarily sought treatment. The majority (58%) of the subjects were definitely drinking at the time of the crime, and a substantial number (40%) of the victims were definitely drinking at the time of the assault. Amnesia for the cime was uncommon (13%) among those who were drinking; but of those subjects who did claim amnesia, almost all had been drinking. Alcohol use appeared to be a significant ingredient in the production of the assaultive behavior in the majority of the cases. The majority of the subjects who were intoxicated at the time of the crime did not consider their state of intoxication as relevant to their behavior in spite of the seeming advantage to do so.

Adolescent↗
PubMed1983

Acute alcohol intoxication: significance of the amylase level.

To evaluate the effects of acute alcohol intoxication on serum amylase and isoamylase levels, 58 clinically intoxicated patients with blood alcohol levels greater than 100 mg/dL were studied. Comparisons were made to normal control and a sober chronic alcoholic group. Admitting serum isoamylase levels were determined by cellulose acetate membrane electrophoresis and serum amylase levels measured by the Amylochrome technique. The average blood alcohol level in the intoxicated group was 301 +/- 99 mg/dL. Thirty of the 58 patients had hyperamylasemia (greater than 207 IU). Twenty-five of these 30 patients had hyperamylasemia from nonpancreatic sources (increased salivary isoamylase). Two of the 30 patients had pancreatic hyperamylasemia and three patients had elevated levels of both isoamylases. Neither of the patients with pancreatic hyperamylasemia had clinical evidence of acute pancreatitis. Although nine of the 58 patients had abdominal pain and clinical symptoms suggestive of acute pancreatitis, none of these patients had elevated pancreatic isoamylase. The finding of hyperamylasemia in acutely intoxicated patients is common. This is most frequently due to a rise in the salivary (nonpancreatic) isoamylase. The reliability of the total serum amylase as an indication of pancreatic disease in the intoxicated patient is questioned.

Acute Disease↗
PubMed1987

Left ventricular function during alcohol intoxication and autonomic nervous blockade.

Eight healthy young subjects (6 men, 2 women) entered a controlled investigation of left ventricular (LV) function during alcohol intoxication and autonomic nervous blockade. Radionuclide cardiography was performed at rest and during upright 50% submaximal bicycle exercise. During alcohol intoxication alone (serum ethanol 30 mmol/liter), heart rate at rest increased by 11% (p less than 0.05) and LV ejection fraction (EF) decreased by 6% because of end-systolic dilation. No significant alcohol-induced hemodynamic changes were observed during exercise. Plasma norepinephrine concentration increased by 29% (p less than 0.05), whereas plasma epinephrine concentration did not change. During subsequent autonomic nervous blockade with intravenous metoprolol and atropine infusion, heart rate at rest further increased and systolic blood pressure decreased. These changes were not, however, significantly different from those of a control experiment in which a nonalcoholic isocaloric drink was substituted for alcohol. Plasma norepinephrine levels at rest and during exercise were 25% and 32% higher (both p less than 0.05), respectively, than those during control conditions. Plasma epinephrine concentrations did not change. These findings suggest that alcohol intoxication has a depressant effect on LV function at rest that stimulates autonomic nervous blockade. The increased sympathetic nervous activity during exercise appears to be a toxic rather than a compensatory effect of alcohol.

Adult↗
PubMed1990

Mechanisms of alcohol intoxication in a rodent model: blunted alcohol-opposing reaction in "alcohol-sensitive" rats.

In this paper we describe new data and review some studies on the mechanisms of alcohol-induced motor impairment in rats. Habituation to handling did not affect the naive behavioural differences between the alcohol sensitive and alcohol insensitive rat lines. Nor was there any effect on the differential sensitivities of the lines to the motor impairing and hypnotic effects of alcohol. Peripheral mechanisms may be involved in the differential behaviours of these lines, as the plasma corticosterone response was much weaker in the alcohol sensitive animals, suggesting a limited capacity to react to stress and alcohol. A similar blunted response to acute ethanol exposure was found in the uptake of the benzodiazepine antagonist [3H]Ro 15-1788 in vivo by the cerebellum of alcohol sensitive rats. The finding that these rat lines do not have any general differences in their brain inhibitory GABAergic receptors was extended to the spinal cord inhibitory glycinergic receptors, which showed only a modest line difference in their dissociation constant. The apparent localisation of the two main receptor differences (high-affinity [3H]muscimol binding and diazepam sensitivity of [3H]Ro 15-4513 binding) to the cerebellar granule layer suggests a genetic modification in the granule cells of alcohol-sensitive rats. In conclusion, our studies on acute intoxication by moderate alcohol doses show that several central nervous and peripheral factors may be involved in this behaviour. As many of these factors mitigate the effects of alcohol, alcohol antagonistic treatments should be aimed at activating and supporting multiple adaptive phenomena.

Adrenal Glands↗
PubMed1992

Alcohol intoxication does not change [11C]cocaine pharmacokinetics in human brain and heart.

There is increasing evidence that the combined use of cocaine and alcohol produces enhanced behavioral and toxic effects. We have used PET and tracer doses of [11C]cocaine in 7 normal human volunteers to assess if the distribution and clearance of cocaine are altered by alcohol intoxication. Each subject received 2 PET studies with [11C]cocaine (3-11 micrograms), one before and one during alcohol intoxication (1 g/kg). Regions of interest included the brain (n = 3) and heart (n = 4). Arterial plasma was assayed for unchanged cocaine and for labeled cocaethylene, a metabolite of cocaine found in individuals using cocaine and alcohol in combination (Hearn et al., 1991a). Alcohol intoxication did not change uptake and clearance or the steady-state distribution volume of [11C] cocaine in brain (striatum, thalamus, and cerebellum) or in heart. Moreover, labeled cocaethylene was not detected in the 10 minute plasma sample. These results suggest that the acute enhancement of behavior and toxicity associated with the combined use of cocaine and alcohol is not due to an alteration in cocaine's organ distribution or to cocaethylene formation but may be related to an additive effect resulting from the direct actions of each of these drugs.

Adult↗
PubMed1985

Alcohol intoxication, an underdiagnosed problem?

To show that alcohol intoxication may be underdiagnosed in childhood, we describe four patients in whom it was not suspected until blood alcohol concentrations were measured as part of a toxicology screen.

Alcoholic Intoxication↗
PubMed1974

[Shifts in several aspects of phospholipid metabolism in the brain and liver of white rats during prolonged alcoholic intoxication].

Phosphatidic acid, total and individual phospholipids and ethanolamine levels of rat brain and liver are changed considerably following 40 and even more so after 80, days of alcohol intoxication. In brain the content of phosphatidic acid and total and individual phospholipids is increased and that of ethanolamine reduced. In liver exactly the opposite changes take place with the exception of inositol containing phospholipids, which are considerably reduced both in brain and liver. The study of the first stages of phospholipid synthesis showed that during 40 and 80 days of alcohol intoxication activity of enzymes participating in the metabolism of L-alpha-glycerophosphate (glycerokinase, glycerophosphate dehydrogenase) is increased several fold. This brings to the increase of L-alpha-glycerophosphate, the main product of phosphatidogenesis, through activation of its formation by glycerokinase and glycerophosphate dehydrogenase. Inspite of the fact that in liver activity of enzymes taking part in the metabolism of L-alpha-glycerophosphate is considerably increased during chronic alcohol intoxication its level is not raised. This indicates an activation of phosphatidic acid formation from L-alpha-glycerophosphate and the immediate inclusion of phosphatidic acid in the biosynthesis of neutral fats. The data obtained indicate that chronic alcohol intoxication activates biosynthetic processes of phospholipids in brain and accelerates their break down in liver, bringing to the fatty infiltration of liver.

Alcoholism↗
PubMed1995

Chronic alcohol intoxication enhances the expression of CD18 adhesion molecules on rat neutrophils and release of a chemotactic factor by Kupffer cells.

Chronic alcohol intoxication has been associated with increased migration of inflammatory leukocytes to the liver that may contribute to the development of alcoholic hepatitis in susceptible individuals. Thus, this work was performed to examine the mechanism by which neutrophils [polymorphonuclear neutrophils (PMNS)] are sequestered in the liver during prolonged consumption of alcohol. Male Sprague-Dawley rats were fed with Sustacal supplemented by 36% alcohol, or isocaloric diet for 16 weeks. Circulating blood PMNs were collected and examined for CD18 (beta 2-integrin) adhesion molecule expression. Monoclonal antibody 1F12, an anti-CD18 antibody and potent neutropenic agent, was used to detect CD18 on PMNs. More than 97% of neutrophils obtained from pair and ethanol-fed rats were positive for the antibody. Fluorescence intensity of fluorescein isothiocyanate-1F12 binding to PMNs from ethanol-fed rat was significantly enhanced 2-fold compared with the pair-fed controls. The release of chemoattractant and free radical-generating activity in culture supernatants of Kupffer cells was also examined. Twenty-four hr culture supernatants of Kupffer cells from chronic alcoholic rats enhanced the migration and superoxide anion generation by normal PMNs, compared with those of the pair-fed rats. Antirat interleukin-8 antiserum inhibited chemotactic activity and superoxide generating capacity of culture supernatants. These results suggest that upregulation of adhesion molecules on PMNs and chemotactic factor release from Kupffer cells may contribute, at least in part, to enhanced migration of inflammatory leukocytes to the liver during chronic alcohol intoxication.

Alcoholic Intoxication↗