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Results for “Alcoholic Intoxication”

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At least 19 recordsLinked to original sources
PubMed1978

Auditory brain stem potentials in chronic alcohol intoxication and alcohol withdrawal.

Auditory brain stem evoked responses were in unrestrained rats during periods of acute and chronic alcohol intoxication, alcohol withdrawal, and recovery. Acute alcohol administration altered the auditory brain stem potentials by a prolongation of both peak latency and central conduction time, beginning with early peaks. Similar but lesser effects affecting only the latter peaks were observed during chronic alcohol intoxication. By contrast, alcohol withdrawal resulted in a decrease in the peak latencies of auditory brain stem potentials and a facilitation of central conduction time. Recovery of the auditory brain stem potentials to the normal form required at least three to four weeks. The present study provides the first quantitative data, to our knowledge, on manifestations of alcohol tolerance and withdrawal.

Acoustic Stimulation↗
PubMed1977

Intravenous fructose treatment of acute alcohol intoxication. Effects on alcohol metabolism.

This study was designed to determine the efficacy of the intravenous administration of fructose in the treatment of acute alcohol intoxication. The study was prospective and double-blind, with glucose serving as the control. Treatment with glucose and fructose was determined by random selection. Fructose administration did not alter the clinical status or rate of alcohol metabolism as reflected by the decline in serum concentration. In addition, a significant elevation (P less than .05) in serum uric acid and lactate levels occurred in the patients receiving fructose. The results indicate that fructose is of no value in the treatment of acute alcohol intoxication, and produces metabolic abnormalities that could be harmful to the patient.

Adolescent↗
PubMed1978

Alcohol intoxication and the alcohol withdrawal syndrome.

Although acute alcohol intoxication can cause death, hepatic metabolism of ethanol is usually rapid, and in most cases general supportive care of the intoxicated patient is all that is required. Abrupt cessation of prolonged excessive alcohol intake gives rise to the alcohol withdrawal syndrome. The fundamentals of treatment are careful assessment of the patient and judicious use of a benzodiazepine.

Alcoholic Intoxication↗
PubMedDate not supplied

Forensic considerations on the comparison of "serum gamma-glutamyltranspeptidase" ("gamma-GT) activity in experimental acute alcoholic intoxication and in alcoholic car drivers who caused road accidents.

The authors studied blood alcohol levels and serum gamma-GT activity in 18 drivers who caused car accidents while intoxicated, and in 20 young volunteer subjects without any hepatic damage, in which an acute alcoholic intoxication was present. In most of the drivers the serum gamma-GT activity was significantly higher than in the volunteers, which strongly suggests a chronic alcoholic intoxication. In the 20 volunteers, who were occasional drinkers, the serum gamma-GT activity did not show pathological values even in a state of heavy intoxication. According to the authors, the serum gamma-GT determination could be made obligatory by law, in order to differentiate between acute or chronic alcoholic intoxication. Should an intoxicated driver be found guilty of an offense, this fact could aggravate the circumstances. Furthermore serum gamma-GT activity determination could be used as an evaluating parameter in granting driving licences.

Accidents, Traffic↗
PubMed1976

Management of potentially fatal alcohol intoxication.

Severely alcohol intoxicated patients pass through all stages of anesthesia according to the Guedel classification. Additional illnesses or injuries might be present, however. These require careful investigation. Blood alcohol levels are no criterion for the degree of intoxication. The treatment varies and is based on clinical symptoms. In our series of more than 100 alcohol intoxicated patients the treatment generally consisted o Apomorphine, unless unconsciousness was present, and peripheral vasopressors, if necessary. Occasionally endotracheal intubation was required. On gastric aspiration via nasogastric tube only minimal amounts of alcohol could be recovered. With correct diagnosis and effective treatment the cure rate of acute alcohol intoxication should be as high as that of other intoxications.

Adolescent↗
PubMed1978

[Adaptive changes in brain metabolism during chronic alcoholic intoxication].

Chronically alcoholized intoxication (1.5--2 months) induces adaptation of cerebral neurones to changing equilibrium states of biochemical processes by altering the activity of enzymes of GABA metabolism, reduction of alanine and aspartate transaminase activity and increase of LDH and succinate dehydrogenase activity. In the cerebellum and cerebral hemispheres during alcohol abstinacy the activity of GABA-T, succinate dehydrogenase and aspartate transaminase was reduced while that of LDH and alanine transaminase was increased. The administration of fusarinic acid (100 mg/kg i. p.) to control animals induced a sharp increase of GAD activity in both structures of the brain. The stimulatory effects of fusarinic acid were not observed when it was administered to animals receiving alcohol chronically. Motor activity or rats was markedly reduced during chronical alcoholism and the first days of alcohol abstinacy (24--48 h), as well as following injection fusarinic acid and homopantothenic acid. The increase of locomotion and the vertical component of motor activity was observed only following one week or one month after alcohol abstinacy.

4-Aminobutyrate Transaminase↗
PubMed1992

[Acute alcoholic intoxication--risk of complications].

Alcohol intoxication is the commonest cause of unconsciousness among patients admitted to hospital. Studies have shown that, of all acute admissions to medical wards, approximately 20 per cent are patients who are intoxicated or have alcohol-related damage. A study cited in the article showed patients in deep stupor generally to have a blood alcohol concentration above 70 mmol/l, and to be at increased risk of respiratory complications and aspiration of regurgitated stomach content. In cases of severe alcohol intoxication, treatment includes the following: freeing of the airways, perhaps combined with respiratory support; tracheobronchial lavage and aspiration, followed by antibiotic treatment; liberal parenteral thiamine administration; cramp, hypoglycaemia and muscle damage may require special measures; in the acute stage, cardiac arrhythmia usually normalizes without special antiarrhythmic treatment.

Alcohol Withdrawal Delirium↗
PubMedDate not supplied

[Phospholipids and free ethanolamine in the brain and liver of albino rats in alcoholic intoxication].

An experimental alcohol intoxication was accompanied by an increase in content of total phospholipids and phosphatide acid in rat brain with simultaneous decrease in content of free ethanolamine. The phenomenon demonstrate the activation of phosphatidogenesis. In the liver tissue an opposite alterations were observed; the lipolytic reactions were activated.

Alcoholic Intoxication↗
PubMed1992

[Aldosterone and electrolyte content in blood and myocardium of rats after single physical load in acute alcoholic intoxication].

It is shown that acute alcoholic intoxication causes essential changes of aldosterone content and balance of electrolytes in blood plasma of Wistar rat males. The SPL test revealed the inadequate reaction in the mineral-corticoid function of the adrenal glands in the rats with acute alcoholic intoxication. The method of the free choice of the load by the experimental rats is the most optimal way to assess. The rats with acute alcoholic intoxication displayed smaller tolerance to physical load.

Acute Disease↗
PubMed1976

[Features of hepatic lesions in patients with chronic alcoholic intoxication].

The authors studied alcoholic hepatosis and hepatic cirrhosis by laboratory, radioisotope and clinical methods. Most of the routine laboratory techniques, excluding hyperurobilinuria were not very informative in alcoholic hepatosis. Much more frequently it was possible to mark disturbances of the bromsulphaleinic and vofaverdine tests. Of special importance in the evaluation of the acuity and depth of the alcohol intoxication was glutamate and sorbitdehydrogenase. The most informative appeared to be radioisotope hepatography in the phase of alcohol hepatosis and scannography in the formation of liver cirrhosis.

Alanine Transaminase↗
PubMed1990

[Changes in the aminopeptidase activity in the brain neurons of rats subjected long-term to alcoholic intoxication].

A histochemical investigation was made of aminopeptidase activities using L-leucine-beta-naphthylamide and D, L-alanine-beta-naphthylamine as respective substrates in the rat's sensomotor cortex neurons during the period of ethanol withdrawal after a prolonged alcohol intoxication. Alcohol intoxication of the rat continued for 8 months. Different dynamics of aminopeptidase activities was shown depending on the substrate used during ethanol withdrawal. The results are discussed from the point of view of the existence of multiple forms of aminopeptidase in the brain and of their involvement in protein metabolism in pathological states.

Alanine↗
PubMed1979

An outbreak of acute methyl alcohol intoxication.

An outbreak of acute methyl alcohol intoxication occurred in Port Moresby, Papua New Guinea, in March 1977. Twenty-eight young men attended a drinking party and drank methyl alcohol. The amount consumed by each individual ranged from an equivalent of 60--600 ml of pure methanol. Three had prior ethanol ingestion. All 28 became ill 8--36 hours after drinking and were hospitalized. The most commonly observed clinical syndromes were: acute metabolic acidosis, severe visual impairment and acute pancreatitis. Four died within 72 hours after admission to the hospital. All had severe metabolic acidosis and visual impairment and three pancreatitis. Of 24 who recovered, 16 showed no residual complications, six had bi-lateral visual impairment and two had difficulty in speech as well as visual impairment. A three month follow-up examination showed no change in the findings. Coma, seizures and prolonged acidosis were poor prognostic signs. The estimated amount of consumed methanol and the rapidity of the appearance of signs of toxicity following methanol ingestion did not seem to influence the outcome of poisoning. The treatment of acute methyl alcohol intoxication in centres where dialysis is not available is discussed.

Adolescent↗
PubMed1991

Degrees of alcohol intoxication in 117 hospitalized cases.

The correlation among degrees of alcohol intoxication, facial flushing, blood alcohol concentration (BAC) and blood acetaldehyde level was studied in 117 male alcoholic patients who underwent various tests to assess alcohol influence. Blood samples were collected and alcohol and acetaldehyde levels were determined. BACs ranged from 29 to 577 mg/dl in all patients and from 200 to 299 mg/dl in 48 of them. Fifty-one patients could stand erect (mean BAC [+/- SD] = 189 +/- 80 mg/dl), while 48 showed apparently normal reaction to a walking and turning test (mean BAC = 192 +/- 78 mg/dl). Some of the cases having BACs over 300 mg/dl could still stand and walk while others with BACs under 100 mg/dl already showed psychomotor impairment. Facial flushing was recognized in 75% of the subjects. Acetaldehyde concentrations in 27 patients ranged from 24 to 147 micrograms/dl. Appearance of facial flushing was correlated with relatively high concentrations of blood acetaldehyde. Seven out of 10 healthy volunteers given 1.6 to 2.0 g/kg of alcohol as a control could do nothing but sleep after reaching peak BAC (mean = 232 +/- 21 mg/dl). These findings are taken to indicate a great difference in response to alcohol between alcoholics and healthy men. This study is the first to report the occurrence of facial flushing and raised blood acetaldehyde concentration among Japanese alcoholics.

Acetaldehyde↗
PubMed1991

[Ultrastructural morphology of the air-blood barrier and pulmonary surfactant in pulmonary inflammation in experimental alcoholic intoxication].

Combined investigation of ultrastructure of components of air-haematic barrier and surface-active properties of surfactant in 21 guinea pigs' lungs with simulated pneumonia against a background of alcoholic intoxication was carried out. It was established, that alcoholic intoxication aggravates a deficiency of pulmonary surfactant occurred in pneumonia because of its high phagocytosis with alveolar macrophages. The increase of mobilization of alveolar macrophages in alcoholic intoxication may be connected with the rise of surfactant secretion by hyperfunctional pneumocytes of the 2nd type. Stopping of alcoholic intoxication may lead to normalization of qualitative composition of surfactant phospholipids.

Alcoholic Intoxication↗
PubMed1991

[Morphogenesis of pneumonia in alcoholic intoxication].

A single moderate dose of ethanol given to 120 Wistar male rats inhibits general immune defence and may facilitate the development of pneumonia. No morphological changes are found in the surfactant system in acute alcoholic intoxication. In chronic alcoholic intoxication with a pronounced withdrawal syndrome, apart from the decrease of general immune defence, lung surfactant system is damaged due to the direct ethanol effect on type II pneumocytes. These are the leading factors in the pneumonia pathogenesis characterized by a grave course and tendency to the abscess formation.

Alcoholic Intoxication↗