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At least 595 records · Page 33Linked to original sources
PubMed1984

[Quantitative changes in peripheral blood thrombocytes in chronic alcoholics and experimental alcoholic intoxication in animals].

The time course of changes in peripheral-blood platelet count was examined in 129 alcoholics and 22 alcohol-intoxicated rats. The data obtained point to the existence of cause-and-effect relationships between the thrombocytopenia and thrombocytosis observed in various periods of abstinence on the one hand, and blood coagulation disturbances manifesting themselves in the forms of hemorrhages, thromboses and embolism, on the other.

Alcoholism↗
PubMed2004

Antioxidant properties of black tea in alcohol intoxication.

Food ingredients such as alcohol may modify cellular redox state. Ethanol metabolism is accompanied by generation of free radicals that can damage cell components especially when antioxidant mechanisms are no able to neutralize them. However black tea is a source of polyphenol antioxidants that may enhance cellular antioxidant abilities. The aim of this study was to investigate the effect of black tea on antioxidant abilities of the liver, blood serum and brain of 12-months old rats sub-chronically (for 28 days) intoxicated with ethanol. Administration of black tea alone caused increase in the activity and concentration of antioxidant parameters more extensively in the liver and serum than in the brain. Alcohol caused decrease in the liver glutathione peroxidase and reductase and catalase activity but increase in activity of superoxide dismutase. Moreover, decrease in the level of non-enzymatic antioxidants, such as reduced glutathione, vitamin C, A and E and beta-carotene was observed. The activity of serum glutathione peroxidase and reductase decreased while superoxide dismutase activity was not changed. The level of non-enzymatic antioxidants in serum was also decreased. However brain activity/level of all examined antioxidants enzymatic as well as non-enzymatic was decreased after ethanol intoxication. Black tea considerably prevented antioxidant parameters against changes caused by ethanol. These results indicate beneficial antioxidant effect of black tea regarding all examined tissues, but especially the liver.

Alcoholic Intoxication↗
PubMedDate not supplied

[Effect of acute alcoholic intoxication on lipogenesis in the liver of rats].

Thirty minutes after a single ethanol injection (4 g/kg bw, i.p.) the activity of rat liver acetyl-CoA-synthetase and ATP-citralyase was decreased. Cholesterol synthesis estimated by label incorporation from 3H2O was increased whereas the synthesis of fatty acids remained at the control level. The possibility of alternative ways of acetyl-CoA production under the conditions of acute alcoholic intoxication is discussed.

ATP Citrate (pro-S)-Lyase↗
PubMed1995

Homicidal blunt head trauma, diffuse axonal injury, alcoholic intoxication, and cardiorespiratory arrest: a case report of a forensic syndrome of acute brainstem dysfunction.

Sudden death can occur in drunk individuals who are severely beaten about the face. The structural basis for this forensic syndrome is unknown. We herein describe the case of an intoxicated 23-year-old man (blood alcohol 234 mg%, 51 mmol/l) who was involved in an altercation and received blows and kicks to his head. A cardiorespiratory arrest occurred during the assault. He was resuscitated in hospital 23 min later but died 90 h after admission of severe ischemic encephalopathy and bronchopneumonia. Postmortem examination revealed diffuse scalp bruising, no evidence of a skull fracture, multiple small hemispheric contusions, severe cerebral edema secondary to ischemic encephalopathy, and axonal swellings in the corpus callosum, subcortical white matter, midbrain, right rostral inferior cerebellar peduncle, and medulla. This case of near sudden death confirms that blunt head trauma sustained during an assault can cause mild diffuse axonal injury. In addition, it is possible that sudden, alcohol intoxication-associated, craniofacial traumatic death is caused by acute dysfunction of the brainstem cardiorespiratory centers, whose capacity to correct potentially fatal dysrhythmias or apnea, induced by injury to their afferent axons, can be compromised by alcohol ingestion.

Adult↗
PubMed1995

[The self concept and personality structure of alcohol intoxicated drivers: how do they see themselves, and how are they judged by others?].

Assessing the problem of "alcohol in road traffic" it becomes apparent that most offenders have high BACs (in excess of 1.6 per mille) and that they are repeating offenders. It can therefore be assumed that those people are drink-drivers, which means that, when assessing the offence, the offender's personality as a whole has to be taken into consideration. The DUI offenders themselves usually justify the offence by balming it on the circumstances of a given situation. On the basis of this discrepancy, the published study deals with the question of whether there are any differences between the way DUI offenders judge their personality and self concept and the way other people do. This also leads to the questions of whether the number of offences play a role or not. The self image of 60 male DUI offenders was rated by means of the Giessen test and the Frankfurt self concept scales "problem solving", "confidence in behaviour and decision making", as well as "judgement by others". For the outside judgement, 60 male volunteers were asked to judge DUI convicted drivers. It showed that the DUI convicted drivers assessed their personality to be no different than that of the average person. Their self concept was characterised by positive attributes. However, the outside judgement showed them to be less socially responsive, lacking self control, as well as rather dominant, depressive, reserved and rather inhibited in heterosexual relationships. The self judgement changes with an increasing number of offences, as does the outside judgement to an even greater extend. The latter turns into a more negative judgement. Regarding the self concepts, only the outside judgement proved to be more negative. The number of convictions didn't influence the DUI offenders' self estimation.

Adult↗
PubMed1985

[In France, is acute alcoholic intoxication in adults a metabolic emergency?].

Some biological data of 63 acute alcoholic poisoning (without drug ingestion) in adults were studied during a brief hospitalization. Mean arterial blood concentration of lactate was 2,34 mmol/l +/- 0,13, of ethanol was 53 +/- 3,68 mmol/l. No correlation was found between these two variables and we have not registered lactic acidosis. Arterial blood acid base balance was normal for 24 of 38 unconscious patients. The results of other fourteen showed moderate acidosis, either mixed or respiratory either metabolic, without hypoglycemia or ketonuria. No correlation between arterial blood ions H+ concentration (44,72 +/- 1,18 nmol/l (m +/- sem) and concomitant arterial blood ethanol concentration was found. Moreover, no correlation between 46 blood glucose concentrations (without prior glucose perfusion) and alcoholemia was found. Only two 18 hours fasting chronic alcoholics showed hypoglycemia. These results confirm that acute ethanol intoxication is a potential respiratory emergency in adults, and not a metabolic one (this last pattern being true for children). No confusion between acute intoxication and alcoholic ketoacidosis, alcohol induced fasting hypoglycemia or shoshin beriberi must be made.

Adolescent↗
PubMed1990

Isopropyl alcohol intoxication.

Three patients had neurologic signs due to isopropyl alcohol (IPA) intoxication. Over a several-week period, a known alcoholic developed apathy, confusion, ataxia, and hyperreflexia. During this period, there was no ethanol available to him, and he denied use of other intoxicants. He was found stuporous in the hospital after drinking IPA and admitted to IPA abuse during the preceding weeks. Two other men were admitted in a stupor after large ingestions of IPA. Intoxication with IPA has two different presentations: stupor in a known alcoholic and encephalopathy of unknown cause in individuals who hide their addiction. Ethanol, methanol, IPA, and ethylene glycol intoxications are associated with different clinical and laboratory findings.

1-Propanol↗
PubMed2003

Increased salivary cortisol concentrations during chronic alcohol intoxication in a naturalistic clinical sample of men.

BACKGROUND: Cortisol, the primary glucocorticoid in humans, is intimately involved in the regulation of such varied and critical biological processes as emotion, cognition, reward, immune functioning, and energy utilization. A persistent increase in cortisol concentration as a result of chronic intoxication could therefore result in alcohol-related disorders such as sleep disruption, cognitive deficits, diabetes, and mood disturbances. Although moderate levels of acute alcohol ingestion are reported to produce an increase in cortisol levels, it is uncertain whether cortisol remains persistently increased during long-term chronic intoxication. METHODS: Salivary cortisol and breath alcohol concentrations (BAC) were obtained on 73 subjects with primary alcohol dependence on initial presentation for treatment and 22 alcohol-dependent subjects participating in a residential treatment program. RESULTS: Both intoxicated alcohol-dependent subjects (n = 38) and nonintoxicated subjects in acute alcohol withdrawal (n = 30) demonstrated significantly increased salivary cortisol concentrations compared with abstinent subjects (n = 27; p < 0.001). Nonintoxicated subjects in acute withdrawal demonstrated significantly increased salivary cortisol concentrations compared with highly intoxicated subjects (BAC >100 mg/dl) but were similar to subjects with lower levels of intoxication (BAC, 10-100 mg/dl). CONCLUSIONS: Chronic alcohol-dependent subjects experience continuously increased concentrations of cortisol during both intoxication and withdrawal. Increased levels of cortisol during chronic intoxication seem to progressively increase with the onset of withdrawal. This suggests a daily cycle of hypercortisolemia during the active drinking phase, with further increases on the cessation of drinking and the emergence of withdrawal symptoms. Persistently increased levels of cortisol may extract a costly allostatic load, resulting in significant central nervous system and peripheral organ morbidity.

Adult↗