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PubMedDate not supplied

[Effect of acute alcohol intoxication on lipid peroxidation in testis and adrenal glands of rats].

Hormones level and lipid peroxidation processes under influence of acute alcohol intoxication are tested in testes and adrenals of rats. Ethanol marker effects--the rise of corticosterone biosynthesis and depression of testosterone concentration--were reproduced in the experiment. At the moment of maximal changes in steroid levels indices characterising lipid peroxidation didn't differ from the control. At the early stage of the experiment transient shifts in malonic dialdehyde and dienic conjugates levels were noted. The data obtained does not agree with the hypothesis of acute ethanol effects in testes and adrenals being mediated through the changes of lipid peroxidation rate.

Adrenal Glands↗
PubMed1990

Alcohol intoxication blunts sympatho-adrenal activation following brain injury.

In 46 patients experiencing traumatic brain injury, we studied the interactions of alcohol intoxication and severity of neurologic dysfunction on the resulting sympathetic nervous system activation. Sixty percent of the variation in norepinephrine (p less than 0.0001) and more than 50% of the variation in epinephrine (p less than 0.0001) were due to the initial ethanol concentrations and extent of brain injury assessed by the admission Glasgow Coma Score (GCS). As brain function deteriorated plasma cathecholamines rose (p less than 0.0001), but ethanol qualitatively and quantitatively modified this observation. The magnitude of the sympathetic response to worsening neurologic function was progressively diminished in association with increasing ethanol levels, i.e., the inverse relationship of GCS values with both norepinephrine and epinephrine was flattened. In comatose patients (GCS less than 8) increasing ethanol levels was associated with progressively decreasing norepinephrine and epinephrine responses (p less than 0.04), such that catecholamines were reduced by 80 to 90% at ethanol concentrations approaching 400 mg/dl (87.0 mmol/l). However, the impact of ethanol on the degree of sympathetic nervous system activation depended upon the degree of injury; the apparent ethanol suppression was greatest in patients with the most severe neurologic dysfunction (GCS 3 or 4), but it diminished as neurologic function improved. We conclude that the presence of alcohol appears to modify the rise in catecholamine levels following traumatic brain injury in a dose-dependent manner and alters the relationship between neurologic dysfunction and SNS activation. These alterations may have profound effects on patient morbidity in the immediate post-accident period.

Adolescent↗
PubMed1979

[Legal aspects of acute alcoholic intoxication (author's transl)].

This paper deals with the legal aspects of acute alcoholic intoxication. Everybody is obliged in case of helplessness to organise help. Every doctor confronted with an acute alcoholic should careful examine the situation not to overlook other concomitant acute diseases.

Alcoholism↗
PubMed1999

[Safety problems of occupational activity during alcoholic intoxication].

It has been established that work efficiency of persons occupied by machine operating duties degrades markedly under the action of an acute alcoholic intoxication--less on real machines and more on simulators and when operating simple technical devices. Work efficiency degradation is manifested by the task execution time increase (to a lesser degree) and by erroneous action quantity increase after taking alcohol, i.e. by work reliability decease. Most heavily it is manifested during the first 0.7-1.5 hr. After taking alcohol. And direct work efficiency index is usually improved 12-16 hr. after taking alcohol. Increase of erroneous action quantity is caused probably by a series of physiological, psychophysiological and psychological changes in the condition of a man under the action of alcohol. Time of the day when the activity takes place after taking that dose of alcohol is practically non valid for changing work efficiency index.

Accidents↗
PubMed1989

[Morphofunctional study of the myocardium in alcoholic intoxication].

An experimental model of acute and chronic ethanol poisoning is described. Electrocardiographic and morphologic changes in the hearts of white rats, exposed to alcoholic intoxication, have been assessed. Typical ECG features as well as muscle-cell and neuron ultrastructure have been identified, so that they could be used for morphologic and functional assessment of alcoholic poisoning.

Alcoholic Intoxication↗
PubMedDate not supplied

[Effect of lithium carbonate on glycolysis in different areas of the rat brain in acute alcoholic intoxication].

Selective activation of phosphofructokinase (PFK) and lactate dehydrogenase (LDG) in the cerebral cortex and an increase of glucose and lactate contents in all other brain areas were noted in acute alcoholic intoxication of rats (2.5 g/kg). Lithium carbonate potentiated the inhibitory action of alcohol on glycolysis in the brain tissue. In combination with ethanol it decreased the activity of PFK and LDG in all studied brain areas and increased glucose and lactate levels.

Alcoholic Intoxication↗
PubMed2000

Impaired myocardial protein synthesis induced by acute alcohol intoxication is associated with changes in eIF4F.

The purpose of the present study was to examine potential mechanisms for the known inhibitory effect of acute alcohol exposure on myocardial protein synthesis. Rats were injected intraperitoneally with either ethanol (75 mmol/kg) or saline, and protein synthesis was measured in vivo 2.5 h thereafter by use of the flooding-dose L-[(3)H]phenylalanine technique. Rates of myocardial protein synthesis and translational efficiency in alcohol-treated rats were decreased compared with control values. Free (nonpolysome bound) 40S and 60S ribosomal subunits were increased 50% after alcohol treatment, indicating an impaired peptide-chain initiation. To identify mechanisms responsible for this impairment, several eukaryotic initiation factors (eIF) were analyzed. Acute alcohol intoxication did not significantly alter the myocardial content of eIF2 alpha or eIF2B epsilon, the extent of eIF2 alpha phosphorylation, or the activity of eIF2B. Acute alcohol exposure increased the binding of 4E-binding protein 1 (4E-BP1) to eIF4E (55%), diminished the amount of eIF4E bound to eIF4G (70%), reduced the amount of 4E-BP1 in the phosphorylated gamma-form (40%), and decreased the phosphorylation of p70S6 kinase and the ribosomal protein S6. There was no significant difference in either the plasma insulin-like growth factor (IGF) I concentration (total or free) or expression of IGF-I or IGF-II mRNA in heart between the two groups. These data suggest that the acute alcohol-induced impairment in myocardial protein synthesis results, in part, from an inhibition in peptide-chain initiation, which is associated with marked changes in eIF4E availability and p70S6 kinase phosphorylation but is independent of changes in the eIF2/2B system and IGFs.

Acute Disease↗
PubMed2003

Alcohol intoxication increases allopregnanolone levels in female adolescent humans.

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. We studied the effects of acute alcohol intoxication (AAI) on the plasma levels of progesterone and allopregnanolone in female adolescents. Blood samples were drawn from female adolescents who arrived at the emergency department. One study group was formed by those who arrived with evident behavioral symptoms of AAI and the other by those arriving for mild trauma (contusions, sprains) after no consumption of alcohol (controls). Our results demonstrate that AAI significantly increases serum progesterone and allopregnanolone levels in both follicular and luteal phases of the ovarian cycle. Since alcohol and allopregnanolone positively modulate gamma-aminobutyric acid type A (GABA(A)) receptors, allopregnanolone may play a major role in the anxiolytic and rewarding effects of alcohol, either directly or by influencing the sensitivity of GABA(A)-receptors to alcohol.

Adolescent↗
PubMed1994

Acute alcohol intoxication among children and adolescents.

Severe toxicity from ethanol, manifested as coma, occurs at lower blood alcohol concentrations in young teenagers than in adults. Coma, vomiting and hypothermia are the commonest symptoms in young teenagers intoxicated by alcohol. The biochemical disturbances in children 11-16 years of age with alcohol intoxication resemble those of adults. Mild acidosis of a respiratory and metabolic origin and mild hypokalaemia are common findings in young teenagers. Young teenagers eliminate ethanol at the same rate as adults, whereas preschool age children are reported to eliminate ethanol twice as fast. The effect of ethanol on the state of consciousness is directly proportional to the blood alcohol concentration. Among small children the risk of hypoglycaemia is increased. Data on family history, social status, drinking habits, and children's motives for getting drunk are also of clinical importance. Fluid replacement with glucose-containing fluids and follow up are generally the only treatments needed for complete recovery. When children and adolescents are healthy, well-nourished and have not fasted, no severe complications are expected.

Acute Disease↗