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PubMedDate not supplied

[Structural alterations in the human brain in acute alcohol intoxication].

Various regions of the brain were studied in 14 patients who suddenly died and in 20 patients who died from ethanol intoxication. Severe circulatory disorders with pronounced vascular pathology, blood diseases, degenerative and necrotic neurocytic changes were shown to develop in ethanol intoxication. The area of neurocytes in the hemispheric cortex, thalamus, and cerebellum reduced due to the death of some of them. In the medulla, they were found to be more resistant to ethanol. The diameter of capillaries in the studied regions of the brain decreased due to the fall in cerebral arterial tonicity, the number of these vessels on the standard area increased, which is due to the compensatory dilatation of reserve capillaries.

Alcoholic Intoxication↗
PubMedDate not supplied

[The effect of the preliminary intake of mineral waters in acute alcoholic intoxication (an experimental study)].

101 male Wistar rats (body mass 180-200 g) received a single dose of ethanol in two concentrations--96% and 30%. High ethanol concentrations produced a direct damage to gastric and duodenal mucosa. 30% ethanol inhibited secretion of glucagon, insulin and aldosterone. This inhibition rapidly changes for the hormones rise in the blood. Hydrocortisone was high over the experiment. Previous intake of mineral water prevents damage to the gastroduodenal mucosa induced by 96% ethanol and modifies the hormonal response provoked by 30% ethanol as evident from reduced expression of the two phases.

Alcoholic Intoxication↗
PubMed1990

[Changes in surface activity of surfactant and ultrastructure of the air-blood barrier in alcoholic intoxication in experimental animals].

In the results of complex investigation of the lungs of 26 white rats, it was established, that there is the suppression of surface active properties of surfactant under influence of ethanol. In acute poisoning this suppression is associated with direct injury of surfactant with ethanol and inactivation of surfactant with serum proteins, which appear in the alveolar space because of the edema of air-haematic barrier. In prolonged influence the suppression of the surface activity of surfactant is due to the increase of its catabolism with alveolar macrophages.

Alcoholic Intoxication↗
PubMed1977

[Development of liver glycogen reserves in rats subjected to chronic alcoholic intoxication].

Literature offers many but very different informations about the effects of alcohol on the hepatic carbohydrates metabolism. Therefore we have tried to observe, in process of time, the evolution of the hepatic glycogen reserves on rats intoxicated by ethanol 40% during variable durations. Stuffing is made by oesophageal way at the rate of 6,4 g/kg/day. During this period of poisoning, we note a significant increasing of the hepatic glycogen reserves.

Alcoholism↗
PubMed1976

A successful method for development of voluntary alcohol intoxication in mice.

Eight strains of male mice, C57BL, C3H SWM, SW, KK, KSB, KR and DBA, were fed on a standard pelletized diet and offered a choice of water or 10% sake solution (sake containing 10% alcohol). Both young (3 months of age) and old (8 months of age) groups were studied simultaneously. The degree of intoxication was measured by recording the drinking behavior on a pulse recorder, by calculating gaschromatographically the blood alcohol concentration, by taking depth electroencephalogram readings and so on. Intoxication, shown by lack of coordination such as grossly impaired gait, was observed only in the older mice of strain with a moderate natural alcohol preference such as C3H, SWM, SW, KK and KSB. In general, the intoxicated mice were over 9 months of age, tended to consume fluids regardless of the time of day or night and suffered a loss of body weight. The blood alcohol levels of them were over 4.6%. The threshold elevation of the ascending reticular activating system on electroencephalogram in a intoxicated mouse reached about 167%. The present study provides a successful method for the development of voluntary alcohol intoxication in mice.

Age Factors↗
PubMed2002

Accidental ingestion of cotton bud stick during alcohol intoxication: an unusual cause of caecal perforation.

A first reported case of caecal perforation by an ingested blunt foreign body is described. This 31-year-old female did not relate a history of accidental swallowing of a cotton bud stick on admission. The cause of her right iliac fossa pain (i.e. caecal perforation by a cotton bud stick) became only apparent when she underwent operation for suspected appendicitis. A simple closure of this caecal perforation was undertaken. The patient made a complete recovery from this ordeal. Caecal perforation by an ingested blunt foreign body can occur after it has safely negotiated the ileocaecal valve.

Adult↗
PubMed1993

[Cerebral infarct caused by compression of the carotid artery in an alcohol intoxicated patient].

A 49 year-old woman developed a left sided hemiparesis with hemineglect after lying in an intoxicated condition for approximately half an hour with the right side of her neck on the metal edge of her bed. Dopplersonography of the intra- and extracranial vessels showed no abnormality of blood flow. On the right side of the neck a strangulation mark 8 cm of length was visible for several weeks. The CCT scan initially showed slight oedema. After 6 weeks changes corresponding to selective parenchymal necrosis were to be seen predominantly in the territory of the right middle cerebral artery.

Alcoholic Intoxication↗
PubMed2000

Regional brain metabolism during alcohol intoxication.

BACKGROUND: Ethanol has a broad range of actions on many neurotransmitter systems. The depressant actions of ethanol in the brain are related in part to facilitation of gamma-aminobutyric acid (GABA) neurotransmission via its interaction with the benzodiazepine/GABA receptor complex. The purpose of this study was to evaluate the effects of ethanol on regional brain metabolism in 10 healthy right-handed men. The results were compared with those we previously published in a different group of 16 normal male subjects who received intravenous lorazepam, a benzodiazepine drug that also enhances GABA neurotransmission. METHODS: The subjects were scanned with positron emission tomography and [F-18] fluorodeoxyglucose twice: 40 min after the end of placebo (diet soda) or ethanol (0.75 g/kg) oral administration. Image data sets were analyzed by using both the region of interest and the statistical parametric mapping (SPM) approach. SPM was used to generate a difference image between baseline and ethanol, which we compared to the difference image between baseline and lorazepam (30 microg/kg). RESULTS: Ethanol significantly increased self-reports of "high" (p < or = 0.0001), dizziness (p < or = 0.004), and intoxication (p < or = 0.0001). Ethanol significantly decreased whole brain (-25 +/- 6%, p < or = 0.0001) and regional metabolism. Normalization of the regional measures by whole brain metabolism (relative measures) showed that ethanol decreased relative metabolic activity in occipital cortex (-4.9 +/- 4.1%, p < or = 0.006), whereas it increased relative metabolic act in left temporal cortex (+3.5 +/- 2.9%, p < or = 0.006) and left basal ganglia (+9 +/- 6.3%, p < or = 0.0009). SPM analyses revealed the same pattern of responses as the relative measures, showing decreases in occipital cortex and increases in left temporal cortex. Comparison of the relative measures and the SPM analyses obtained with lorazepam data revealed a similar pattern of effects, with relative decreases in occipital cortex (-7.8 +/- 4.8%) and relative increases in left temporal cortex (+3.8 +/- 5.7%). Lorazepam, but not ethanol, also decreased thalamic metabolism (-11.2 +/- 7.2%). CONCLUSIONS: These results support similar though not identical mechanisms for the effects of alcohol and benzodiazepines on brain glucose metabolism. The fact that lorazepam, but not alcohol, reduced thalamic metabolism, an effect associated with sleepiness, could explain the higher sedative effects of lorazepam than of alcohol.

Adult↗
PubMed1997

[Tubular necrosis after non-steroidal anti-inflammatory agents and acute alcoholic intoxication].

Acute nephrotoxicity due to nonsteroidal anti-inflammatory drugs is usually observed in clinical situations in which renal perfusion is compromised as in volume contraction. We report a case of a 20 year-old woman who suffered from acute tubular necrosis after concomitant ingestion of nonsteroidal anti-inflammatory drugs and binge drinking. This acute tubular necrosis is likely to have an hemodynamic origin due to nonsteroidal anti-inflammatory drugs in a patient with volume contraction secondary to binge drinking. The risk appears to be even more important since ethanol has been implicated in tubular necrosis by direct toxicity. This observation underlines the danger in associating nonsteroidal anti-inflammatory drugs and ethanol.

Acute Kidney Injury↗
PubMedDate not supplied

[The action of acute alcoholic intoxication on the antioxidant system and creatine kinase activity in the brain of rat embryos].

The activity of superoxide dismutase (SOD) was enhanced in the brain of 14-day rat embryos 1 and 3 hours after single administration of ethanol to pregnant rats. Concurrently, the levels of lipid peroxidation were changing in these periods. Ethanol, 1 g/kg, increased LPO levels in the 14-day embryonic brain, whereas its dose of 3 g/kg decreased them. It is concluded that with single administration of ethanol, free-radical processes are activated in the embryonic brain. It is suggested that the activity of creatine kinase decreases concurrently with an increase in SOD activity due to the damaging action of superoxide radicals on the enzyme molecule.

Alcoholic Intoxication↗
PubMed1977

Labeling of rat brain synaptosomal phosphatidyl serine in the after state of acute alcoholic intoxication and in the withdrawal state.

The synaptosomal phosphatidyl serine labeling by 14-C-serine after elimination of a single dose of 6 g EtOH/kg b.w. and after a prolonged ethanol period (8-11 g EtOH/kg b.w. for 8 days) was studied in vivo. In both experimental groups the 14-C-labeling of the phosphatidyl serine is decreased as compared with the controls. There is a great deal of evidence which implicates that phosphatidyl serine plays a major role in neural excitation providing ion exchanges sites which control the sodium current, known to be sensitive to ethanol. These ethanol induced changes in phosphatidyl serine labeling may be reflected functionally in the impulse conduction and increased sensitivity in the withdrawal state. These changes are suggested to be consequences of the primary membrane fluidity increasing properties of ethanol.

Alcoholic Intoxication↗
PubMed2005

An analysis of the genetics of alcohol intoxication in inbred mice.

We compared the behaviors of eight inbred mouse strains across 18 variables, using 11 behavioral assays, and gave ethanol (EtOH) as an intoxicant. Genetic influences on behavior and sensitivity to EtOH were pronounced, but strain sensitivities were generally only modestly correlated across tasks. Certain well-correlated clusters of responses suggested that some genes affect similar neurobiological substrates. No strains of mice were generally sensitive or resistant to intoxication across tasks. Anthropomorphically appealing concepts like 'muscle strength' had little explanatory power across tasks. A battery of selected tests was proposed for future studies. Overall, the results show that each mouse behavioral assay captures only a portion of ataxia, a genetically complex behavioral domain. Conversely, multiple behavioral capacities are apparently required for performance in each specific assay. Thus, if only one or two tests are used to evaluate motor function in genetically engineered mutant mice, only a small portion of the domain will be assessed and results may be misleading. This caveat likely extends to many behavioral domains (e.g. learning and memory, anxiety).

Alcoholic Intoxication↗
PubMed1993

Effect of flumazenil in a model of acute alcohol intoxication in rats.

The ability of high doses of flumazenil to antagonize ethanol-induced sedation was assessed via ethanol-induced loss of the righting reflex (LRR) in rats. Ethanol (3.5-5 g kg-1 i.p) produces a dose-dependent increase in the proportion of animals presenting a LRR response. Flumazenil (0.1 to 1 mg kg-1 i.p) was ineffective in preventing the suppression of the righting reflex and even aggravated it for ethanol dosages of 3.5 and 4.0 g kg-1. These data support the view that flumazenil has no effective 'anti-ethanol' properties. Conversely, the prolongation of mean sleep time provoked by the antidote could be related to the suppression of a putative endogenous inverse-agonist activity at the benzodiazepine receptor, which could be implicated in the mechanism of the acute tolerance to ethanol.

Alcoholic Intoxication↗
PubMed2002

Acute carbon monoxide poisoning and alcohol intoxication: a rare condition that is complex to manage.

Since the changeover in the gas used in domestic appliances, the prevalence of acute carbon monoxide (CO) poisoning has been dramatically reduced. In suicide attempts with car exhaust fumes lies the most common cause of the disorder. As a consequence, patients are more complex to manage as they often have other associated diagnoses such as substance use disorder, depressive disorder, or long-standing personality disorder. This report details such a case. The medical treatment was based on the carboxyhemoglobin (COHgb) levels at the time of admission. The patient developed permanent cognitive and functional deficits consistent with the observed brain scan changes. The author discusses the importance of an appropriate early diagnosis of the condition, the difficulties associated with it, and the validity of using the carboxyhemoglobin levels as a guide to treatment.

Acute Disease↗
PubMed1984

[Effect of acute alcoholic intoxication on the antigenic composition of soluble proteins in the rat brain].

Cross immunoelectrophoresis was used to study antigenic composition of the brain of rats preferring water, or 15% ethanol and of intermediate group animals. The rat brain showed 6 antigens, one of them was found to be neurospecific. The intermediate group animals and those preferring ethanol differed from those preferring water in that they demonstrated two antigens which were found to be neuro-nonspecific. The content of the neurospecific protein S-100 in the cerebellum measured by rocket immunoelectrophoresis was demonstrated to be the same in animals preferring water and ethanol. A single intraperitoneal injection of 25% ethanol (2.5 g/kg) to the intermediate group rats brought about a change in the composition of neuro-nonspecific soluble antigens of the brain.

Alcoholic Intoxication↗
PubMed1980

[Gamma-aminobutyric acid system and bioelectric activity of the brain of rats during alcoholic intoxication].

The changes of the GABA metabolizing enzyme activities in rat brain are connected with the phases of the functional condition of the central nervous system and doses of ethanol. Increase in the dose of ethanol caused the distinct decrease of locomotion degree and vertical component of motor activity. Chronic ethanol consumption caused an increase of the enzyme activities of GABA metabolism without any change of the brain GABA level. The brain glutamine concentration and the GAbA-T activity were increased but there was no change in the brain GABA level of rats after 24-hr ethanol withdrawal. Significant increases in mean energy content of EEG occurred throughout the withdrawal period in both dietary groups of rats receiving ethanol. In 24 hr after withdrawal, prodromal and ictal activity were apparent in the spontaneous EEG records of "ethanol" group.

4-Aminobutyrate Transaminase↗
PubMed1990

[Occasion and risk for detecting driving in alcoholic intoxication].

Detection of offenders driving while intoxicated (DW) (mandatory BAC limit at 0.50%) in Finland was investigated. Almost every fifth offender was detected at road blocks and every tenth of them because of abnormal driving. Compared to the local police the national traffic police had arrested much more offenders for traffic violation (38% vs. 11%) but much less because of accidents (12% vs. 23%). The reason of detection was in a significant way dependent on the following variables: BAC, stage of inebriation, vehicle, day of week and hour of day. The risk of detection is very low, i.e. about 1 to 300. However, the risk has doubled from 1979 to 1984, but thereafter slightly declined. The study provides information for the strategy of the police in traffic supervision.

Accidents, Traffic↗
PubMed1989

[Acute alcoholic intoxication in children in Vojvodina].

The aim of this work was to investigate the frequency and characteristics of acute ethanol poisoning in children in the territory of the Socialist Autonomous Province of Voivodina. In a retrospective study histories of poisoned children aged 0-15 years, who were hospitalized in all eleven stationary centres in Voivodina during 1985/86, were analysed. From 795 children, 52 were poisoned with ethanol (6.54%). With the exception of Novi Knezevac, where only eight cases of poisoning were recorded during the two-year period, the frequency of ethanol poisoning showed major regional differences varying from 3.03% in Zrenjanin to 11.45% in Subotica. Poisoning among boys was significantly more frequent than among girls, especially with ethanol. The average age of children poisoned with ethanol was 8.4 years i.e. almost twice that of children poisoned with other substances. The children's age and circumstances of ethanol poisoning point to the absence and failure of preventive measures.

Acute Disease↗