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PubMed1989

[Should courses for alcohol intoxicated automobile drivers be legally introduced? An answer based on public economics].

The author is scientific collaborator at the Federal Road Traffic Institution and was a member of the project-group "courses for conspicuous motorists". He wants to put forward his following considerations as a basis for discussion. The courses are presumably without any effect, at best they have got a limited effect. In spite of this missing or very limited effect of the courses the calculation on cost and benefit has a positive result. The positive result is almost exclusively to be attributed to the shortening of the period of disallowance to drive. Post-schooling therefore may be seen as an expensive roundabout way to produce a shortening of periods of disallowance. If the given framework will not be changed, post-schooling in it's given area of measures fails to work for it's traffic-political aim and should not be legally validated. The quota of accidents caused by alcohol is presumably higher than the official traffic accident statistics shows. Therefore it can not be excluded that the costs of accidents caused by alcohol are up to 70 per cent higher than the calculations show, which are made on the basis of the number of alcohol-accidents statistically found out so far. The problem "alcohol in road traffic" is a part of the social problem "alcohol". Analyses on effectiveness and on cost and benefits, which are confined to the sector of road traffic, are reflecting the problems insufficiently and are leading to an undervaluation of the total dimension of cost and benefits. The failure of post-schooling for alcohol conspicuous motorists as well as the unsufficient effectiveness of the whole relevant measure practice should be a reason for a new valuation and new orientation of all of the measures in the area of "alcohol in road traffic". Position and effectiveness of post-schooling should be a matter of discussion in that process.

Accidents, Traffic↗
PubMed2002

Acute alcohol intoxication suppresses the CXC chemokine response during endotoxemia.

BACKGROUND: CXC chemokines play an important role in host defense against infections. Alcohol is a frequently abused drug that inhibits numerous immune functions of the host. This study investigated the effects of alcohol on CXC chemokine macrophage inflammatory protein-2 (MIP-2) and cytokine-induced neutrophil chemoattractant (CINC) responses in rats challenged with intravenous lipopolysaccharide (LPS). METHODS: Acute ethanol intoxication was induced by an intraperitoneal injection of 20% alcohol (5.5 g/kg). Thirty minutes thereafter, LPS (500 microg/kg) was administered intravenously. In another set of experiments, rats were intravenously administered an anti-tumor necrosis factor-alpha (TNFalpha) neutralizing antibody (10 mg per rat) 2 hr before the LPS challenge. RESULTS: At 1 and 2 hr after the LPS challenge, MIP-2, CINC, and TNFalpha concentrations in the plasma were significantly increased. Alcohol intoxication suppressed the MIP-2, CINC, and TNFalpha responses in the bloodstream during endotoxemia. Alcohol also suppressed the increase in plasma chemotactic activity and polymorphonuclear leukocyte adhesion molecule expression in rats with endotoxemia. MIP-2 and CINC messenger RNA (mRNA) expression was significantly increased 1 hr after endotoxemia in the lung, liver, and spleen. Alcohol suppressed the up-regulation of MIP-2 mRNA expression in all of these organs and CINC mRNA expression in the lungs of rats with endotoxemia. TNFalpha neutralization minimally inhibited plasma CINC and MIP-2 responses during endotoxemia and did not suppress the increase in plasma chemotactic activity. CONCLUSIONS: These results show that alcohol suppresses the systemic CXC chemokine response to LPS, which is not primarily mediated by ethanol-induced suppression of TNFalpha. This disruption of host-defense function may serve as one mechanism underlying the increased risk of infectious diseases in hosts who abuse alcohol.

Alcoholic Intoxication↗
PubMed1990

Impact of acute alcohol intoxication on the severity of injury: a cause-specific analysis of non-fatal trauma.

The impact of alcohol on the severity of injury was studied by using injured patients from an emergency room in Helsinki, Finland. Blood alcohol content was estimated either clinically or with a breath test and then was recorded using a three-grade intoxication code (Ethyl sign). The study population was comprised of 14,995 men aged 15-64 years. The Ethyl sign was positive in 19.7 per cent. Hospitalization was used as an indicator of the severity of injury. Hospitalization was almost as common among sober (9.3 per cent) as among intoxicated patients (9.6 per cent) and the odds of being hospitalized, if considered 1.0 among the sober, was 1.03 among the intoxicated. However, the severity of injury correlated positively with the alcohol intoxication in the injured car occupants with an odds ratio (OR) of 3.1 (95 per cent confidence interval (CI) 1.7-5.6) and in those injured in falls from stairs (OR = 2.6; 95 per cent CI 1.4-4.7), but negatively in those injured in unspecified falls on the same level (OR = 0.3; 95 per cent CI 0.2-0.6). The effect of alcohol on injury severity seems to vary with the cause of injury.

Accidents, Home↗
PubMedDate not supplied

Alcohol intoxication results in rapid loss in free magnesium in brain and disturbances in brain bioenergetics: relation to cerebrovasospasm, alcohol-induced strokes, and barbiturate anesthesia-induced deaths.

In vivo 31P-nuclear magnetic resonance (31P-NMR) spectroscopy and ion-selective electrode measurements were undertaken to determine if administration of acute doses of alcohol (ALC, 0.2-6.6 g/kg), and lethal doses of barbiturate anesthesia, exert any influence on: (1) brain cellular bioenergetics, intracellular free Mg ([Mg2+]i) and intracellular pH (pHi), and (2) serum levels of ionized Mg (IMg2+), ionized calcium (ICa2+) and K+. Approximately 20-30 min after intraperitoneal administration of ALC to anesthetized rats, brain phosphocreatine (PCr)/ATP and PCr/inorganic phosphate (P(i)) ratios dropped from 2.5 to 1.7 and from 6.6 to 2.2, respectively, P(i) rose 20-200% (depending upon ALC dose), and free ADP and creatine rose significantly. ALC induced rapid decreases in the cytosolic phosphorylation potential (CPP) and free energy of ATP hydrolysis (-delta G/delta E). Following ALC administration, brain [Mg2+]i dropped rapidly (within 4-30 min) and significantly; the greater the dose of ALC, the greater the loss in brain [Mg2+]. Correlations were found between [Mg2+]i, PCr/ATP, CPP and delta G/delta E after ALC but not in control brains. Rats that exhibited ALC-induced strokes and death (unlike barbiturate death) exhibited huge elevations in [Mg2+]i. Although ALC administration does not alter brain pHi at least (up to 70 min), ALC- and barbiturate-induced death produces rapid brain intracellular acidosis. Concomitant with ALC-induced alterations in [Mg2+]i and brain cellular bioenergetics, we noted that ALC administration results in rapid elevations in serum IMg2+ and K+ but not ICa2+. These results suggest that ALC administration and heavy or binge-drinking of ALC (1) can result in rapid alterations in brain bioenergetics, [Mg2+]i and pHi, and (2) result in rapid elevations in serum IMg2+ and K+ in rats. In addition, ALC- and barbiturate-induced deaths do not appear to produce identical alterations in brain bioenergetics and [Mg2+]i, and lastly binge or heavy drinking of ALC may result in stroke-like events and sudden death via rapid alterations in brain cellular bioenergetics.

Alcoholic Intoxication↗
PubMedDate not supplied

Alcohol intoxication reduces impulsivity in the delay-discounting paradigm.

AIMS: To examine the moderating effects of alcohol myopia on cognitive impulsivity in humans using the delay-discounting paradigm. METHODS: Seventy-six male undergraduate students were randomly assigned to sober, placebo or alcohol conditions. In the delay-discounting task, participants made a series of hypothetical choices between a small, immediate reward and a large, delayed reward. To test the predictions of alcohol myopia theory, participants completed a standard version of the task or one containing cues which impelled the impulsive choice (i.e. preference for the small, immediate reward). Participants also completed a personality measure of impulsivity and the go/no-go task, which assesses motor impulsivity. RESULTS: Intoxicated participants tended to discount delayed rewards at lower rates than sober participants, and blood alcohol level was inversely correlated with delay discounting. The impelling cues did not moderate the effects of alcohol on delay discounting. CONCLUSIONS: Alcohol intoxication does not always increase cognitive impulsivity and may lead to more cautious decision-making under certain conditions.

Adult↗
PubMedDate not supplied

[Effect of supplementary vitamin administration on free amino acids in the liver and brain of rats with alcoholic intoxication].

The authors studied combined action of ethanol, pyridoxine (3 mg/kg), and a mixture of thiamine (5 mg/kg), riboflavin (5 mg/kg), pyridoxine (3 mg/kg) and pantothenate (15 mg/kg) on the free amino acid reserve in the tissues of rats. Ethanol was given to the animals with a liquid semisynthetic diet (its calorific value comprised 36%) during 30 days. Both pyridoxine and the complex of vitamin B group produce normalizing action on the free amino acid pool by correcting the shifts induced by ethanol. It is especially manifested in the decreased levels of urea, isoleucine and GABA in the brain. The data obtained have shown that prevention with vitamins of shifts in the amino acid metabolism induced by ethanol, especially in respect to the central nervous system, should be recommended.

Alcoholic Intoxication↗
PubMed2004

Preservation of intestinal structural integrity by zinc is independent of metallothionein in alcohol-intoxicated mice.

Intestinal-derived endotoxins are importantly involved in alcohol-induced liver injury. Disruption of intestinal barrier function and endotoxemia are common features associated with liver inflammation and injury due to acute ethanol exposure. Zinc has been shown to inhibit acute alcohol-induced liver injury. This study was designed to determine the inhibitory effect of zinc on alcohol-induced endotoxemia and whether the inhibition is mediated by metallothionein (MT) or is independent of MT. MT knockout (MT-KO) mice were administered three oral doses of zinc sulfate (2.5 mg zinc ion/kg body weight) every 12 hours before being administered a single dose of ethanol (6 g/kg body weight) by gavage. Ethanol administration caused liver injury as determined by increased serum transaminases, parenchymal fat accumulation, necrotic foci, and an elevation of tumor necrosis factor (TNF-alpha). Increased plasma endotoxin levels were detected in ethanol-treated animals whose small intestinal structural integrity was compromised as determined by microscopic examination. Zinc supplementation significantly inhibited acute ethanol-induced liver injury and suppressed hepatic TNF-alpha production in association with decreased circulating endotoxin levels and a significant protection of small intestine structure. As expected, MT levels remained undetectable in the MT-KO mice under the zinc treatment. These results thus demonstrate that zinc preservation of intestinal structural integrity is associated with suppression of endotoxemia and liver injury induced by acute exposure to ethanol and the zinc protection is independent of MT.

Alanine Transaminase↗
PubMed2002

[Stereologic study of the cerebellar Purkinje cells submitted to alcoholic intoxication in Wistar rats].

BACKGROUND: to analyze the effect of the alcohol on the cells of Purkinje. METHOD: Wistar rats received alcoholic solutions orally in different concentrations 4%, 12% and 24%. The animals were sacrificed with 4, 8 and 12 weeks and the cerebella were randomly cut and embedded in paraffin. Sections of 6 micrometer (H&E) were stereologically analyzed. RESULTS: The differences among the density for area and density of surface of the cells of Purkinje of all of the experimental groups (E) and the respective controls (C) were significant. With 12 weeks the cell of Purkinje volume density decreased among the groups C and E in the concentrations of 4% and 12%, but not for the concentration of 24%, probably due to smaller liquid ingestion by the animals. CONCLUSION: The alcohol has toxic effect on the Purkinje cellular body in the three studied concentrations from 4 weeks.

Alcoholic Intoxication↗
PubMedDate not supplied

[Inositol containing phospholipids in brain and liver tissue of rats in prolonged alcoholic intoxication].

In brain and liver tissue of rats, treated repeatedly with alcohol, alterations in content of total phospholipids and polyphosphoinositols were reproducibly different. In the tissues studied content of polyphosphoinositols were distinctly decreased. Independent function of phosphoinositols in tissue metabolism as an auxiliary energy system in addition to the universal adenylate system is considered. These concepts are in agreement with observations on development of rough morphological alterations (fatty degeneration) in liver tissue. The fatty degeneration developed in the liver tissue in response to deficiency of oxidative potential in the organ.

Alcoholic Intoxication↗
PubMedDate not supplied

[Change in the functional state and tissue oxidative processes of the pancreas under the influence of alcoholic intoxication].

Experiments conducted with albino rats demonstrated that intragastrically introduced ethyl alcohol in a dose of 3 g/kg intensifies the external-secretary function of the pancreas and also increases the activity of the pancreatic juice amylase in the blood, this activity continuing to be elevated 24 hours after a single introduction of the alcohol. The action of the latter reduces the oxygen tension and the redox potential in the glandular tissue, lessens the activity of NAD-dependent dehydrogenases occurring against the background of the succinate-cytochrome-c-oxydoreductase complex activity, which bears evidence to the development of "hypoxy-like" shifts in the metabolic stade of the pancreas. The author concludes that the toxic action of alcohol on the pancreas is associated with disturbances in the redox processes and with the damage of cellular membranes.

Alcoholic Intoxication↗
PubMedDate not supplied

[Metabolic shifts during the repeated administration of analeptics in alcoholic intoxication].

It was shown in experiments on rabbits that under acute alcohol poisoning of medium degree, repeated administration of caffeine (10 mg/kg) and bemegrid in particular (5 mg/kg) promotes aerobization of the oxidative processes and mobilizes the respiratory mechanism of metabolic acidosis compensation. Under these conditions, ethimizol (10 mg/kg) stimulates the respiratory center and promotes (to a less measure) aerobization of the metabolic processes in tissues and ethanol elimination.

Acidosis↗
PubMed2003

Deleterious effects of alcohol intoxication: diminished cognitive control and its behavioral consequences.

The authors tested the hypothesis that impaired behavioral performance during intoxication results partly from alcohol's deleterious effects on cognitive control. The impact of alcohol on perseverative behavior was examined with an n-back working memory task that included manipulations of task complexity and prepotency of inclinations to respond or withhold responding. Thirty-two social drinkers (16 men) participated in either an alcohol (.075g/100ml) or a no-alcohol condition. Alcohol increased perseveration of prepotent, task-inappropriate response patterns only under cognitively demanding (heavy memory load) conditions. This effect was evident for both commission errors (response persistence despite contingencies altered to require restraint) and omission errors (failure to respond when contingencies were revised to encourage action). Findings suggested that alcohol-induced perseveration arises from impairments in cognitive control.

Adult↗