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PubMed2004

Effect of acute alcoholism on hepatic enzymes and oxidation/antioxidation in rats.

BACKGROUND: Around the world more and more people suffer from acute alcoholism. The purpose of this study was to determine hepatic enzymes and oxidation/antioxidation in rats with acute alcoholism. METHODS: Rats were randomly divided into three groups: control, low-dose alcohol, and high-dose alcohol. Each alcohol group (n=12) was intravenously infused with ethanol at a dose of 0.3 or 0.7 g/kg body weight respectively. The control group (n=11) was intravenously infused with normal saline at a dose of 0.5 g/kg body weight. Blood was collected for detection of hepatic enzymes and index of oxidation/antioxidation. RESULTS: The ratio of AST to ALT was 2.44+/-0.46, 2.57+/-0.60 and 3.03+/-0.46 in the three groups, and the difference was significant between the control and high-dose alcohol groups (P</=0.05). No significant changes were observed in the levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), total protein (Tp), albumin (Alb), alkaline phosphatase (ALP), cholinesterase (ChE), total bilirubin (TB), C-reactive protein (CRP) and amylase. The levels of serum nitric oxide (NO) in the 3 groups were 39.2+/-73.25 mol/L, 42.30+/-4.60 mol/L and 47.86+/-4.66 mol/L, and significant difference was seen between the control group and the high-dose alcohol group (P<0.01). No significant difference was found in the levels of serum superoxide dismutase (SOD), glutathione (GSH), malondiethylaldehyde (MDA), and CRP in the 3 groups. CONCLUSION: The ratio of AST to ALT appears to be a useful index for acute alcohol intoxication. NO is involved in the mechanism of acute alcohol intoxication.

Alcoholic Intoxication↗
PubMed1998

Cognitive functioning and the inhibition of alcohol-induced aggression.

OBJECTIVE: A highly replicable research finding is that alcohol intoxication tends to induce aggressive responding. Recent research investigating the role of cognitive function in this relationship has shown that individuals who perform poorly on certain cognitive tasks have difficulty responding to contingencies to inhibit aggression, while high performers do not. High performers, however, do show increased aggression while intoxicated. This study investigated whether subjects with above average cognitive functioning would, when intoxicated, inhibit aggression in order to attain monetary reward. METHOD: Men (N = 43), aged 18-30, selected on the basis of high performance on a neuropsychological test putatively assessing function of dorsolateral prefrontal cortex, the spatial conditional associative learning task, participated in a modified version of the Taylor Aggression Task. Half the subjects were acutely alcohol intoxicated, the other half were sober. Furthermore, half the subjects in each of these groups received contingent monetary reward for choosing lower shocks. Aggression was defined as shock intensity delivered to a sham opponent. RESULTS: Contrary to the hypothesis, intoxicated subjects, even though significantly impaired cognitively relative to their nonintoxicated peers (F = 4.29, 1/41 df, p < .05), appeared to have no difficulty inhibiting their aggression in order to gain monetary reward. That is, there was no difference between intoxicated and nonintoxicated subjects on the dependent variable, shock intensity, when contingent money was available (F = .01, 1/20 df, p = .935). CONCLUSION: This finding provides further evidence that alcohol-induced aggression is not a uniform phenomenon, and it suggests a neuropsychological mechanism that may mediate the relationship. It may be that individuals with above average cognitive abilities retain sufficient residual functioning to inhibit aggressive responding, even when acutely alcohol intoxicated.

Adult↗
PubMed2005

Clinical assessment compared with breathalyser readings in the emergency room: concordance of ICD-10 Y90 and Y91 codes.

OBJECTIVES: The purpose of this study was to analyse the validity of clinical assessment of alcohol intoxication (ICD-10 Y91) compared with estimated blood alcohol concentration (BAC) using a breath analyser (ICD-10 Y90) among patients in the emergency room (ER). METHODS: Representative samples of ER patients reporting within six hours of injury (n = 4798) from 12 countries comprising the WHO Collaborative Study on Alcohol and Injuries were breath analysed and assessed blindly for alcohol intoxication at the time of ER admission. Data were analysed using Kendall's Tau-B to measure concordance of clinical assessment and BAC, and meta analysis to determine heterogeneity of effect size. RESULTS: Raw agreement between the two measures was 86% (Tau-B 0.68), but was lower among those reporting drinking in the six hours prior to injury (raw agreement 39%; Tau-B 0.32). No difference was found by gender or for timing of clinical assessment in relation to breath analysis. Patients positive for tolerance or dependence were more likely to be assessed as intoxicated at low levels of BAC. Estimates were homogeneous across countries only for females and for those negative for alcohol dependence. CONCLUSIONS: Clinical assessment is moderately concordant with level of BAC, but in those patients who have actually been drinking within the last six hours the concordance was much less, possibly because, in part, of a tendency on the part of clinicians to assign some level of intoxication to anyone who appeared to have been drinking.

Alcohol Drinking↗
PubMed1985

Has mortality related to alcohol decreased in Sweden?

In Sweden sales of alcohol dropped 17% from 1976 to 1982. Similarly, comparison of data from 1979 and 1982 shows that the mortality from cirrhosis of the liver declined appreciably, by 28% in men and 29% in women. During 1979-82 mortality from pancreatitis also declined noticeably, by 30% in men and 36% in women. By contrast, no decrease occurred in mortality from alcoholic psychosis, alcoholism, or alcohol intoxication. The decrease in mortality from cirrhosis of the liver and pancreatitis is probably explained by a decrease in the consumption of alcohol among an important subgroup of high consumers of alcohol. The lack of a decrease in mortality from alcoholic psychosis, alcoholism, and alcohol intoxication may be because such diagnoses are often made in socially deteriorated, more dependent alcoholic subjects who have not been able to reduce their consumption.

Alcoholic Intoxication↗
PubMedDate not supplied

[Potentialities of histological examinations of the spleen in the diagnosis of alcoholic and narcotic intoxication].

Qualitative changes observed in the spleen in chronic narcotic and alcoholic intoxication are described. The below signs are recommended for use in the diagnosis of chronic exogenous intoxication: an increased thickness and sclerosis of the splenic connective structures and myelosis of the red pulp. The diagnostic criteria of chronic intoxication with intravenous opiates are the below changes in the spleen: hyperplasia of the splenic follicles, germinative foci in the follicles' stases and folds in vessels, edema of the vascular wall, hyperemia of follicular arteries and diapedetic hemorrhages. Hypoplasia of the follicles and venous hyperemia of the spleen should be regarded as signs of chronic alcoholic intoxication. The data obtained within the case study can be used by forensic medical experts in the diagnosis of narcotic and alcoholic intoxication.

Alcoholic Intoxication↗
PubMed2005

Alcohol-induced motor impairment caused by increased extrasynaptic GABA(A) receptor activity.

Neuronal mechanisms underlying alcohol intoxication are unclear. We find that alcohol impairs motor coordination by enhancing tonic inhibition mediated by a specific subtype of extrasynaptic GABA(A) receptor (GABAR), alpha6beta3delta, expressed exclusively in cerebellar granule cells. In recombinant studies, we characterize a naturally occurring single-nucleotide polymorphism that causes a single amino acid change (R100Q) in alpha6 (encoded in rats by the Gabra6 gene). We show that this change selectively increases alcohol sensitivity of alpha6beta3delta GABARs. Behavioral and electrophysiological comparisons of Gabra6(100R/100R) and Gabra6(100Q/100Q) rats strongly suggest that alcohol impairs motor coordination by enhancing granule cell tonic inhibition. These findings identify extrasynaptic GABARs as critical targets underlying low-dose alcohol intoxication and demonstrate that subtle changes in tonic inhibition in one class of neurons can alter behavior.

Action Potentials↗
PubMed2002

Differential effects of alcohol consumption on eukaryotic elongation factors in heart, skeletal muscle, and liver.

BACKGROUND: Acute and chronic alcohol administration diminishes rates of protein synthesis in a variety of tissues including skeletal muscle, heart, and liver, through a diminished translational efficiency rather than a reduction in the number of ribosomes. METHODS: The purpose of the present study was to examine the effect of chronic alcohol exposure (8, 12, or 16 weeks) on elongation factors (eEF) as a potential mechanism for controlling mRNA translation in psoas, soleus, heart, and liver. The cellular content of eEF1A and eEF2 and the phosphorylation state of eEF2 in each tissue was measured using immunoblot techniques. RESULTS: The protein content of eEF1A was reduced in psoas, heart, and liver (but not soleus) from rats fed a diet containing alcohol for 16 weeks, but not for 8 or 12 weeks, compared with time-matched pair-fed controls. eEF2 content was only reduced in myocardium after feeding rats an alcohol-containing diet for 16 weeks. In other tissues, no change in eEF2 content was observed. The decreases in eEF protein content were not associated with a concomitant reduction in the mRNA abundance for eEF1A or eEF2. The phosphorylation state of eEF2 was not affected by chronic alcohol consumption in the skeletal muscle or heart. In contrast, the level of eEF2 phosphorylation in the liver was reduced after 8, 12, and 16 weeks of feeding rats an alcohol-containing diet. In contrast, acute alcohol intoxication failed to modulate the content of eEF1A or eEF2 in any of the tissues examined. The phosphorylation state of eEF2 was reduced in psoas following acute alcohol intoxication. CONCLUSIONS: A decreased eEF1A protein content could account, in part, for the inhibition of translational efficiency following chronic (16 weeks) alcohol feeding but not the response to acute alcohol intoxication.

Alcohol Drinking↗
PubMed1988

Alcohol antagonism of hypercortisolism induced by naloxone.

The reversal of acute alcohol intoxication by naloxone is controversial. Naloxone increases cortisol secretion but there are no reports of this effect during acute alcohol intoxication. This study examines the effect of 20 mg naloxone on alcohol-induced intoxication using a balanced placebo design to investigate the role of cortisol, participant expectancy of treatment, and possible pharmacokinetic interactions during intoxication. Our results show differences in the time course of subjective self-evaluation of drunkenness in the presence of naloxone. Also, changes are observed in naloxone pharmacokinetic parameters with the ingestion of alcohol, specifically a decrease in plasma clearance. Whereas the cortisol response induced by naloxone was greater in the subgroup of participants with positive expectancy, in the presence of alcohol the naloxone effect on cortisol response was not observed. These observations may help explain the observed reversal of alcohol-induced coma by naloxone in a subgroup of patients.

Adult↗
PubMed2004

Predictors of problem drinking among older adolescent emergency department patients.

This study investigated consumption patterns, alcohol-related problems and predictors of problematic drinking among older adolescents. Two-hundred eighty older adolescents (148 males, mean +/- SD age = 18.5 [1.8] years) treated in two Emergency Departments (ED) completed the Alcohol Use Disorders Inventory Test (AUDIT) to identify problem drinkers. Logistic regression was used to determine predictors of problem drinker status. Higher rates of problem drinking were found among participants who were treated for physical assaults or for acute alcohol intoxication than were found among participants treated for medical illness. Being alcohol-positive in the ED, increasing frequency of drunkenness, and being treated for physical assault were predictive of problematic drinking after controlling for demographic variables. In conclusion, older adolescents who present for treatment of an assault-related injury or acute alcohol intoxication, who are alcohol-positive in the ED, and who report getting intoxicated once a month or more are likely to have a severe drinking problem.

Adolescent↗
PubMed2001

Comparison of the effects of sleep deprivation, alcohol and obstructive sleep apnoea (OSA) on simulated steering performance.

Patients with obstructive sleep apnoea (OSA) are reported to have an increased risk of road traffic accidents. This study examines the nature of the impairment during simulated steering in patients with OSA, compared to normal subjects following either sleep deprivation or alcohol ingestion. Twenty-six patients with OSA and 12 normal subjects, either deprived of one night's sleep or following alcohol ingestion [mean (SD) alcohol blood level 71.6 mg dl(-1) (19.6)], performed a simulated steering task for a total of 90 min. Performance was measured using the tendency to wander (SD), deterioration across the task, number of 'off-road' events and the reaction time to peripheral events. Control data for OSA, sleep deprivation and alcohol were obtained following treatment with nasal continuous positive airway pressure (nCPAP), after a normal night of sleep, and following no alcohol, respectively. Patients with untreated OSA, and sleep-deprived or alcohol-intoxicated normal subjects performed significantly less well, compared to their respective controls (P<0.01 for all tests), with untreated OSA lying between that of alcohol intoxication and sleep deprivation. Alcohol impaired steering error equally throughout the whole drive, whilst sleep deprivation caused progressive deterioration through the drive, but not initially. Untreated OSA was more like sleep deprivation than alcohol, although there was a wide spread of data. This suggests that the driving impairment in patients with OSA is more compatible with sleep deprivation or fragmentation as the cause, rather than abnormal cognitive or motor skills.

Adult↗
PubMedDate not supplied

[Glucose consumption by the rat brain in ethanol intoxication and the abstinence syndrome].

The effect of acute and chronic alcohol intoxication and of the syndrome of ethanol withdrawal on the consumption of glucose by the brain of rats was studied by means of intravascular ethanol infusion. Infusion of ethanol into the internal carotid artery had no effect on glucose consumption by the brain, while its infusion into the femoral vein reduced consumption twofold. The effect was completely removed by the inhibitor of alcohol dehydrogenase pyrazole. Chronic intoxication also caused a twofold decrease of glucose utilization by the brain of rats. Infusion of ethanol into the internal carotid artery of rats who were in a state of alcoholic intoxication led to increase of glucose consumption by the brain to the control level. Infusion of ethanol into the femoral vein in this case had no effect on glucose consumption by the rat brain. Utilization of glucose by the brain diminished to an equal degree in rats suffering from the syndrome of ethanol withdrawal and in animals who were in a state of alcoholic intoxication. Infusion of ethanol, both intraarterial and intravenous, had no effect on glucose consumption by the brain. Activation and inhibition of the function of external respiration were encountered in equal concentrations of ethanol in blood flowing from the brain, whatever the method of its infusion.

Alcoholic Intoxication↗
PubMed1999

Traumatic brain injury: influence of blood alcohol level on post-acute cognitive function.

Alcohol intoxication frequently contributes to the occurrence of traumatic brain injury. Few studies, however, have examined whether acute pre-injury alcohol intoxication or premorbid history of alcohol abuse exacerbate cognitive impairments that commonly result from traumatic brain injury. This study examined the influence of blood alcohol level at time of hospital admission on cognitive functioning during the post-acute stage of recovery from traumatic brain injury. After controlling for pre-injury history of alcohol abuse, hospital admission blood alcohol level was predictive of poorer delayed verbal memory, greater decrement in verbal memory over time, and poorer visuospatial functioning. Moreover, there were non-significant trends for higher blood alcohol levels to predict poorer performance on measures of immediate verbal memory and perseveration.

Adolescent↗
PubMed1996

The combined effect of alcohol and physical exercise on serum testosterone, luteinizing hormone, and cortisol in males.

The combined effect of alcohol and physical exercise on the serum levels of testosterone, luteinizing hormone, and cortisol was studied in healthy male volunteers by performing an exhaustive ergometer exercise (1) followed by alcohol intoxication (induced by 1.5 g of alcohol/kg body weight), (2) during alcohol intoxication (induced by 0.8 g of alcohol/kg body weight), and (3) during hangover (13 hr after a dose of 1.5 g of alcohol/kg body weight). Physical stress immediately before alcohol administration prolonged the depressant effect of alcohol on testosterone secretion. This seemed to be mainly a consequence of direct inhibition at the testicular level, even though the role of luteinizing hormone as a contributory regulatory factor cannot be totally ruled out. Cortisol response to exercise was not modified by alcohol under any of the experimental conditions.

Adult↗
PubMed1984

Naloxone-ethanol interaction in experimental and clinical situations.

The effect of naloxone on ethanol-induced impairment of psychomotor performance was studied in a series of three placebo-controlled, double-blind trials. In all trials, two successive intravenous injections of naloxone (0.4 and 2.0 mg) were given at an interval of 0.5-1.5 hours. Cross-over trials with healthy volunteers (n = 17) were performed in laboratory. In these conditions, naloxone alone had no effect on performance. Ethanol alone (1.0 and 1.5 g/kg) dose-dependently induced nystagmus and impaired coordination, reactions, hand cooperation, body balance, flicker discrimination and extraocular muscle balance. When naloxone was given after ethanol, the first injection reduced slightly but significantly ethanol-induced (1.5 g/kg) nystagmus, while the second injection did not enhance this counteraction any more. Other alcohol effects were not significantly antagonized by naloxone. The clinical part of the study, consisting of parallel groups of either naloxone (n = 11) or saline (n = 7) -treated alcohol-intoxicated (mean blood alcohol concentration 2.9 mg/ml) out-patients, most of them alcoholics, showed that no counteraction of alcohol inebriation (measured by clinical inebriation tests) was associated with the treatment with naloxone in the clinical situation either. Our results suggest that naloxone has no clinical significance in antagonizing ethanol intoxication. The inebriating effects of ethanol are not importantly mediated via central opioid mechanisms.

Adult↗
PubMedDate not supplied

Effects of some hypotensive drugs on the clearance of I125 hippurate in rats after acute and subacute ethanol intoxication.

The influence of dihydralazine, propranolol, clonidine, furosemide and reserpine on the clearance of I125 hippurate in rats in alcohol intoxication was investigated. It was found that both in acute and subacute ethanol intoxication the renal blood flow was impeded. Reserpine and propranolol did not significantly change the half time of I125 hippurate in blood both in animals treated and not treated with alcohol. Furosemide prolonged the clearance of hippurate and increased kidney ischemia in alcohol intoxication. Dihydralazine and clonidine increased the effective renal blood flow in normal animals but not in acute and subacute ethanol intoxication.

Alcoholic Intoxication↗