Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Alcoholic Intoxication”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 343 records · Page 19Linked to original sources
PubMed2004

Fast, but error-prone, responses during acute alcohol intoxication: effects of stimulus-response mapping complexity.

BACKGROUND: Although moderate doses of alcohol can impair performance on tasks that require information processing, little is known about the locus of the alcohol effects within the processing stream. This study used a psychological refractory period paradigm to investigate the effect of alcohol on the central, cognitive stage of information processing when task complexity is manipulated by altering stimulus-response compatibility. METHODS: Thirty-four healthy male social drinkers were assigned to one of two groups (n = 17) that performed two tasks. Each trial consisted of a task 1 stimulus (tone) followed by a task 2 stimulus (letter) that was presented after one of four stimulus onset asynchronies (50, 200, 500, or 1100 msec). A baseline test of performance was obtained before the groups received a beverage containing either 0.0 g/kg (placebo) or 0.65 g/kg alcohol. Both groups were retested when blood alcohol concentration (BAC) was increasing and was decreasing. RESULTS: The alcohol group made significantly more errors in task 1 compared with their drug-free baseline measure during the ascending phase of the BAC curve, and error rates increased to a greater extent for the more complex arbitrary stimulus-response mapping condition. Moreover, this increase in errors continued unabated during the descending phase of the BAC curve. Increasing BACs also slowed performance (longer reaction time), but unlike errors, reaction time returned to drug-free baseline levels when BAC was decreasing. CONCLUSIONS: The results provide evidence that an acute dose of alcohol can impair one aspect of the central, cognitive stages of information processing. The possibility that errors in information processing remain during decreasing BACs even after processing speed has returned to drug-free levels has important practical implications relating to the detrimental consequences of acute alcohol intoxication.

Adult↗
PubMed1977

[Effect of alcoholic intoxication on the body's natural resistance to exposure to infectious and toxic agents].

The influence of alcoholic intoxication on the resistance of albino mice to bacterial toxins and staphylococcus cultures was investigated. Five-day administration of 40% ethyl alcohol to the animals was accompanied by a significant increase of their resistance to the intoxication caused by C1. perfringens toxins and staphylococcus. Thirty-day alcoholic intoxication promoted a marked reduction of albino mice resistance to the both toxins used and the staphylococcus cultures.

Alcoholism↗
PubMed1992

Cerebral responses to acute maternal alcohol intoxication in immature fetal sheep.

Previous studies in mature fetal sheep have shown that alcohol depresses cerebral blood flow (CBF), cerebral O2 consumption (CMRO2), and cerebral glucose consumption (CMRglu). This effect earlier in gestation might contribute to the pathogenesis of fetal alcohol syndrome. Physiologic studies of immature fetal sheep have demonstrated lower CBF, CMRO2, and CMRglu as well as a blunted vasodilatory response to hypoxia compared with mature fetal sheep. The purpose of this study was to determine whether immature fetal responses to alcohol are blunted compared with near-term fetal responses. We studied seven immature fetal sheep in utero at 92 +/- 1 d gestation (term = 147 d) 2 d after placement of vascular catheters. Pure ethanol (1 g/kg) was infused i.v. to the mother over 1 h. We measured CBF and myocardial blood flow by radioactive microspheres and calculated CMRO2 and CMRglu using arterial and sagittal sinus O2 and glucose concentrations. At a fetal ethanol concentration of 33 + 8 mmol/L (150 +/- 37 mg/dL), there were no significant changes in CBF, CMRO2, or CMRglu. There was mild hypoglycemia (glucose concentration = 1.05 +/- 0.2 versus 1.33 +/- 0.2 mM baseline) and lactic acidemia (lactate concentration = 1.29 +/- 0.3 versus 1.07 +/- 0.2 mM baseline). Cardiovascular variables were unchanged as was myocardial blood flow. The immature fetal sheep brain shows no significant cerebrovascular and metabolic response to acute alcohol intoxication compared with mature fetal sheep. Mild hypoglycemia and lactic acidemia did develop. The reason for the developmental differences in response to alcohol and their relationship to fetal alcohol syndrome remain to be elucidated.

Alcoholic Intoxication↗
PubMed1987

Effect of alcohol intoxication during pregnancy on foetal and placental weight: experimental studies.

Recent animal studies have shown that alcohol intoxication in utero leads to a decrease in foetal weight and an increase in that of placenta. These findings are not, however, satisfactorily explained. The object of this study was to investigate these two effects, using inhalation of various concentrations of ethanol vapour as a method of intoxication. Three groups of 12 gravid female rats (treated groups) were intoxicated by permanent exposure to an alcohol atmosphere (19, 20 or 21 mg/l.). Three control groups of 12 gravid females were not intoxicated but had their diet reduced to the same energy intake as the treated groups. On day 21 of pregnancy, foetuses and placentas were surgically removed and individually weighed. The body-weight of foetuses was found to be lower in the treated groups than in the respective controls. Additionally the reduction of foetal weight was directly related to the severity of intoxication. Increases in placental weight were observed in the three intoxicated groups. The differences observed between foetal and placental weights may be interpreted as a foeto-protective phenomenon.

Alcoholic Intoxication↗
PubMed1987

Pharmacological treatment of alcohol intoxication, withdrawal and dependence: a critical review.

This review critically examines the literature of the past 10 years relating to the use of drugs in treating alcohol intoxication, withdrawal and dependence. Emphasis is given to those studies that have current and potential future clinical relevance. Although research regarding the pharmacological treatment of alcohol disorders still suffers from methodological flaws and lukewarm acceptance, the recognition of this area as a legitimate and fruitful field of study is increasingly apparent.

Alcohol Deterrents↗
PubMed1999

Ex vivo and in vivo investigations of picroliv from Picrorhiza kurroa in an alcohol intoxication model in rats.

Picroliv, the active constituent isolated from the plant Picrorhiza kurroa, was evaluated as a hepatoprotective agent against ethanol-induced hepatic injury in rats. Alcohol feeding (3.75 g/kg x45 days) produced 20-114% alteration in selected serum (AST, ALT and ALP) and liver markers (lipid, glycogen and protein). Further, it reduced the viability (44-48%) of isolated hepatocytes (ex vivo) as assessed by Trypan blue exclusion and rate of oxygen uptake. Its effect was also seen on specific alcohol-metabolizing enzymes (aldehyde dehydrogenase, 41%; acetaldehyde dehydrogenase, 52%) in rat hepatocytes. The levels of these enzymes were found to be reduced in the cells following alcohol intoxication. Ethyl alcohol also produced cholestasis (41-53%), as indicated by reduction in bile volume, bile salts and bile acids. Picroliv treatment (3-12 mg/kg p.o. x45 days) restored the altered parameters in a dose-dependent manner (36-100%).

Alanine Transaminase↗
PubMed1985

Influence of acute alcohol intoxication on the outcome of severe non-neurologic trauma.

The influence of acute alcohol intoxication on the outcome of severe non-neurologic trauma was investigated in a prospective study. Alcohol was found in the blood in 35 of the 69 patients, with mean level 136 +/- 13 mg/100 ml. The patients were admitted to hospital 29.5 +/- 2 min after the injury and had mean ISS 25 +/- 2. In the patients with alcohol in the blood, the blood pressure and PCO2 on arrival were lower than in the other patients. When the alcohol level exceeded 100 mg/100 ml, the blood pressure and PCO2 were lower than in the sober patients despite significantly shorter time between injury and admission to hospital. The hospital stay and mortality were similar in the alcohol and the control group. The greater hypovolemia in the patients with alcohol in the blood indicates that alcohol may be a negative factor for the traumatized patient if resuscitation is delayed, and it underlines the need for rapid and adequate fluid resuscitation of these patients.

Accidents, Traffic↗
PubMedDate not supplied

[Glutathione reductase activation in acute alcoholic intoxication].

Experiments carried out on rats were aimed to study the effect of acute alcohol intoxication on activity of cytoplasmic and mitochondrial forms of glutathione reductase. It has been found that alcohol activates the enzyme. The in vitro experiments have confirmed the effect. The correlation between the activity of the studied enzyme and the content of various forms of endogenous flavines is observed. It is stated that an increase in the alcohol dehydrogenase activity in tissues of rats under study induces a drastic rise of the number of restored nicotinamide coenzymes and as a result of this the glutathione reductase activity grows.

Alcohol Dehydrogenase↗
PubMedDate not supplied

[Concentrations of protein sulfhydryl and amino groups in the brain during acute and chronic alcoholic intoxication].

The content of sulphydryl and amine groups in water- and salt- soluble proteins of different areas of the rat brain was studied as affected by acute and chronic alcohol intoxication. With a relatively unchanged content of sulphydryl groups, noticeable variations are observed in the level of amine groups, most pronounced in proteins of the intermediate and middle areas of the brain. Under chronic intoxication the greatest changes in the content of the functional groups occur on the fourth day after cessation of the alcohol administration, when changes in the clinical state of the animals are most pronounced. It is supposed that the found shifts are caused by an acetaldehyde reversible blockade of amino groups and by the conformation rearrangement of protein molecules.

Alcohol Deterrents↗
PubMed2000

Enhanced urinary excretion of cysteinyl leukotrienes in patients with acute alcohol intoxication.

BACKGROUND & AIMS: Leukotrienes are proinflammatory mediators. Ethanol inhibits the catabolism of both cysteinyl leukotrienes (leukotriene E(4) [LTE(4)] and N-acetyl-LTE(4)) and leukotriene B(4) (LTB(4)) in hepatocytes. We examined the metabolic derangement of leukotriene inactivation by ethanol in humans in vivo. METHODS: LTE(4), N-acetyl-LTE(4), LTB(4), and 20-hydroxy-LTB(4) were quantified in urine samples from 16 patients with acute alcohol intoxication (mean blood ethanol, 75 mmol/L). In 9 healthy volunteers, urinary LTE(4) was determined before and after ethanol consumption (mean blood ethanol, 14 mmol/L). RESULTS: The excretion of LTE(4) during alcohol intoxication was 286 compared with 36 nmol/mol creatinine in healthy subjects (P < 0.01); the corresponding values for N-acetyl-LTE(4) were 101 and 11 nmol/mol creatinine, respectively (P < 0.001). This excretion of cysteinyl leukotrienes decreased when the blood ethanol concentration returned to normal. LTB(4) and 20-hydroxy-LTB(4) were detectable only in patients with excessive blood ethanol concentrations (mean, 95 mmol/L). In healthy volunteers, LTE(4) excretion increased 3-5 hours after ethanol consumption (mean peak concentration of 1.5 nmol/L compared with 0.5 nmol/L for basal values; P < 0.005). CONCLUSIONS: Ethanol at high concentration induces increased leukotriene excretion into urine. These changes are consistent with inhibition of leukotriene catabolism and inactivation induced by ethanol, as well as with a higher leukotriene formation caused by ethanol-induced endotoxemia.

Acute Disease↗
PubMed2005

Using virtual reality to study alcohol intoxication effects on the neural correlates of simulated driving.

The use of virtual reality in the form of simulated tasks can provide a realistic environment in which to study complex naturalistic behaviors. Many of the behavioral effects of alcohol intoxication are well known, but there is relatively little imaging evidence examining how alcohol exposure might transiently modulate brain function, especially in the context of task performance. In this review, we provide a brief synopsis of previous work using functional magnetic resonance imaging (fMRI) to study the neural correlates of alcohol intoxication. We describe in detail two studies from our published work, the first involving a visual perception paradigm, and the second involving virtual reality through a naturalistic behavior; simulated driving. Participants received single-blind individualized doses of beverage alcohol designed to produce blood alcohol content (BAC) of 0.04 and 0.08 or placebo. Subjects were fMRI scanned after training to asymptote performance. In both studies we found specific circuits that were differentially modulated by alcohol, we revealed both global and local effects of alcohol, and we examined relationships between behavior, brain function, and alcohol blood levels.

Adolescent↗
PubMed2003

Alcohol intoxication induces greater reductions in brain metabolism in male than in female subjects.

BACKGROUND: The mechanisms underlying the gender differences in alcohol drinking behavior and alcohol's effects are poorly understood and may reflect gender differences in brain neurochemistry. Alcohol decreases glucose metabolism in the human brain in a pattern that is consistent with its facilitation of GABAergic neurotransmission. We compared the regional changes in brain glucose metabolism during alcohol intoxication between female and male subjects. METHODS: Ten female and 10 male healthy controls were scanned with positron emission tomography and 2-deoxy-2[18F]fluoro-D-glucose twice: 40 min after placebo (diet soda) or alcohol (0.75 g/kg mixed with diet soda). RESULTS: Alcohol significantly and consistently decreased whole-brain metabolism. The magnitude of these changes was significantly larger in male (-25 +/- 6%) than in female (-14 +/- 11%; p < 0.005) subjects. Half of the female subjects had reductions in metabolism during intoxication that were significantly lower than those in male subjects. This blunted response in the female subjects was not due to differences in alcohol concentration in plasma, because these did not differ between the genders. In contrast, the self-reports for the perception of intoxication were significantly greater in female than in male subjects. The cognitive deterioration during alcohol intoxication, although not significant, tended to be worse in female subjects. CONCLUSIONS: This study shows a markedly blunted sensitivity to the effects of acute alcohol on brain glucose metabolism in female subjects that may reflect gender differences in alcohol's modulation of GABAergic neurotransmission. The greater behavioral effects of alcohol in female subjects despite the blunted metabolic responses could reflect other effects of alcohol, for which the regional metabolic signal may be hidden within the large decrements in metabolism that occur during alcohol intoxication.

Adult↗
PubMedDate not supplied

The effects of alcohol intoxication on aggressive responses in men and women.

A considerable literature, clinical and experimental, has demonstrated the aggression-eliciting effects of alcohol intoxication. However, the focus of the experimental literature has been primarily on men and the studies on women have been inconclusive. This study was conducted to test for possible gender differences in the manifestation of alcohol-induced aggression. Participants were 54 males and 60 females, aged 18-30 years, who competed in a competitive aggression paradigm either sober or intoxicated. As expected, intoxicated men were more aggressive than their sober peers. However, under high provocation, both sober and intoxicated, women manifested aggression comparable to the intoxicated men. This study suggests that women can be as aggressive as men, and that alcohol intoxication does not seem to be as important a determining factor.

Adolescent↗
PubMed1988

Cardiac function at rest and during exercise in early and late alcohol intoxication.

Seven healthy men, aged 21 to 30 years, were investigated by radionuclide cardiography at rest and during submaximal exercise at heavy (early) and during declining (late) alcohol intoxication. Control studies, in which alcohol was substituted by an isocaloric, isovolumic drink, were performed on a different day. The left ventricular ejection fraction at rest decreased from 59 to 56% during early intoxication (serum ethanol 35 +/- 6 mmol/l), whereas no change was observed in the ejection fraction during exercise. No significant change was recorded in stroke volume after alcohol consumption as opposed to a small increase after ingestion of the caloric drink. Plasma noradrenaline concentrations were elevated during exercise and early intoxication. During late intoxication (serum ethanol 21 +/- 5 mmol/l) the left ventricular ejection fraction at rest was increased by 7% compared with the baseline value. At rest the heart rate was increased from 68 +/- 7 to 84 +/- 15 beats/min, whereas cardiac output had reverted to the baseline value. Plasma noradrenaline at late intoxication was increased both at rest and during exercise compared with the baseline values. Apart from tachycardia and a reduction in left ventricular volumes during late intoxication no alcohol induced hemodynamic changes occurred during exercise.

Adult↗