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PubMedDate not supplied

Leptin levels of alcohol abstainers and detoxification patients are not different.

AIMS: Leptin is a cytokine-type peptide hormone, recently implicated as a putative state marker of alcohol use and in craving. Our goal was to evaluate the potential of leptin as a state and trait marker and to rule out the role of current alcohol intoxication on leptin levels. METHODS: Eighteen alcohol withdrawal patients (16 males, 2 females) whose blood contained 202 mg/dl (median) of ethanol at hospitalization, who had a median age of 43.5 years and had consumed 1075 g of ethanol (median) in the last 7 days were included in the study. Leptin was determined in samples at day 1 (when still intoxicated) and day 7 of withdrawal. Expected leptin levels were calculated with a formula. For comparison, 27 blood samples of 18 abstinent persons, matched for gender, age and body mass index were used. Furthermore, mean cell volume, gamma-glutamyl transferase (GGT), blood glucose, cholesterol, triglycerides and body composition (bioimpedance device) were determined. For statistical analysis, SPSS 11 was used. RESULTS: Expected leptin levels were 1.71 ng/ml (median), leptin measured at day 1 was 2.65 ng/ml (median) and 2.85 ng/ml on day 7 for the alcohol withdrawal patients and 2.2 ng/ml (median) for the abstainers. These concentrations were not significantly different. Significant correlations were found between leptin day 1 and expected leptin levels, percentage fat body mass, cigarettes smoked per day, GGT and blood alcohol concentration. CONCLUSIONS: Our preliminary data do not support the hypothesis of leptin as a state or trait marker and suggest only a minor influence of acute intoxication on leptin levels in alcohol detoxification patients.

Adult↗
PubMed1982

Cholinergic activity in hippocampus in chronic alcoholism.

Evidence indicates that hippocampus and cholinergic mechanisms play a role in memory function. Animal studies have indicated an effect of prolonged ethanol treatment on cholinergic parameters. It is well known that chronic alcoholics often have a disturbed memory function. In this postmortem study the cholinergic activity in the hippocampus was studied in 20 chronic alcoholics and 14 controls. Of the alcoholics, 13 were classified as 'intoxicated alcoholics' and 7 as 'sober alcoholics', i.e., without ethanol in blood and urine at the time of death. To study both pre- and postsynaptic effects, the enzyme choline acetyltransferase (ChAT, presynaptic marker) as well as muscarine- and nicotine-like receptor binding sites were measured. There was a lower, although not significant, activity in ChAT in the hippocampus of the chronic alcoholics as compared to the controls. The lowest ChAT activity was found in the group of 'sober alcoholics', however it was not statistically significant. In the chronic alcoholics there was a trend towards lower numbers of muscarine-like binding sites reaching significance for the oldest group of alcoholics (59 - 68 years; -30%; p less than 0.01) in comparison to controls. The combination of the normal aging process with degenerative nerve cell changes and alcohol abuse might lead to the more pronounced decrease in muscarinic binding sites found for the older alcoholics.

Adult↗
PubMedDate not supplied

[Homogeneity of the erythrocyte volume distribution during chronic alcoholism macrocytosis (author's transl)].

The increase in volume of human erythrocytes during chronic alcoholic intoxication and its decrease after alcoholic deprivation was studied with a multichannel analyzer. When fractions of the population of red cells were separated by differential centrifugation the macrocytosis was found to be uniformly distributed. The presence of macrocytes was not related to changes of plasma osmolality or hyperhydration of red cells. A central origin was evoked, however, the role of the folic acid deficiency could not explain the macrocytosis, the mechanism of which remains to be elucidated.

Adult↗
PubMedDate not supplied

[The effect of a diet with different contents of linoleic acid on the development of alcoholic liver diseases].

White rats received rations with varying content of linoleic acid (3.17 and 90 g/kg of food) during 30 days. The control rats that received food with low content of linoleic acid showed a higher content of triglycerides in the liver. Elevation of linoleic acid level in the ration of animals with chronic alcoholic intoxication diminishes the symptoms of alcoholic hepatosis: hepatocyte vacuolization and the content of neutral lipids in them are lowered, serum enzyme (alanine-aminotransferase, gamma-glutamyltransferase) activity decreases as well as the signs of essential fatty acid deficiency disappear.

Animals↗
PubMedDate not supplied

[Lateralization of visuo-spatial function during masking in healthy subjects and in patients with chronic alcoholism].

In healthy subjects and patients with chronic alcoholism, the ability to construct in mind geometric figures in conditions of masking was studied by means of recording the number of correct decisions, the reaction time and evoked cortical electrical activity. It has been found that solution of visual-spatial task of mentally constructing geometric figures is accomplished better if a figure-standard can be formed from the presented fragments. During solution of the visual-spatial task in norm the reaction time is shorter if the information comes "directly" to the right hemisphere. Such interhemispheric differences are not observed at chronic alcoholic intoxication. In patients with chronic alcoholism the late components of EPs N200 and P300 developed with a longer latency and lesser amplitude than in healthy subjects. The greatest depression of cortical activity is observed in the right hemisphere.

Adult↗
PubMed1979

[Homogeneity of the erythrocyte volume distribution during chronic alcoholism macrocytosis (author's transl)].

The increase in volume of human erythrocytes during chronic alcoholic intoxication and its decrease after alcoholic deprivation was studied with a multichannel analyzer. When fractions of the population of red cells were separated by differential centrifugation the macrocytosis was found to be uniformly distributed. The presence of macrocytes was not related to changes of plasma osmolality or hyperhydration of red cells. A central origin was evoked, however, the role of the folic acid deficiency could not explain the macrocytosis, the mechanism of which remains to be elucidated.

Adult↗
PubMed1994

Patterns of substance abuse and intoxication among murderers.

A series of 100 murderers was examined to discern patterns of substance abuse and intoxication in relation to homicidal events. More than half of the study subjects were found to be actively abusing drugs at the time of their crime, and almost half were intoxicated. Alcohol was the drug most often abused. Demographic and other discriminating factors were utilized to examine the hypothesis that murderers do not constitute a homogeneous population and that subgroups differ in their abuse patterns. Cluster analytic techniques were applied to the study population. Utilizing a set of 13 proximate causal factors, a typology of seven distinct homicide profiles was created. Two of the seven profiles exhibited extremely high abuse and intoxication rates, three others intermediate rates, and two profiles very low rates. Moreover, different substances were prime offenders in different profiles. These findings demonstrate that substance abuse is an important etiological contributor in some types of murderer but not in all types.

Adolescent↗
PubMed2004

Nursing from an ethanol-intoxicated dam induces short- and long-term disruptions in motor performance and enhances later self-administration of the drug.

RATIONALE: During interactions with an ethanol-intoxicated dam, preweanling rats encode ethanol-related chemosensory information. These experiences have been observed to enhance subsequent recognition of ethanol's chemosensory properties and to modulate learning about ethanol. OBJECTIVE: The present study tested the effects of ethanol-related nursing experiences on motor function in later infancy and adolescence and on ethanol intake during adolescence. METHODS: Wistar-derived rats were reared by dams intragastrically administered with ethanol (2.5 g/kg) or with water during postnatal days (PDs) 3, 5, 7, 9, 11, and 13. Later in infancy or in adolescence, these rats were tested on a motor coordination task (Accelerod) while either sober or acutely intoxicated with ethanol (1 g/kg). During adolescence, animals had simultaneous access to varying ethanol concentrations (3, 4, 5, or 6% v/v) and water. RESULTS: Both infants and adolescents that had been reared by ethanol-intoxicated dams exhibited dramatic behavioral impairments in the Accelerod task when compared with the offspring of water control dams. Ethanol intoxication disrupted motor performance in both age groups, but this effect was independent of prior maternal treatment. When tested for voluntary ethanol intake as adolescents, those with prior nursing experiences with an intoxicated dam ingested more ethanol than adolescents reared by sober dams. CONCLUSIONS: Early experiences with alcohol comprising interactions with an alcohol-intoxicated dam result in motor impairment and enhanced ethanol intake later in life.

Alcoholic Intoxication↗
PubMed2005

Breath alcohol concentrations in Japanese outpatients following paclitaxel and docetaxel infusion.

Patients receiving paclitaxel or docetaxel also receive a significant amount of ethanol, as both products contain ethanol as solvent. Patients in our clinics have occasionally exhibited signs of alcohol intoxication immediately after paclitaxel infusion. In 2002, the Japanese government lowered the minimum ethanol concentration for the definition of drunk driving, with the threshold breath alcohol concentration (BRAC) of 0.15 mg/l. The aim of this study was to measure BRAC in Japanese outpatients treated with paclitaxel or docetaxel and to assess intoxication according to this standard. Fifty-two Japanese patients were enrolled from October 2003 to February 2004. Patient characteristics were as follows: male/female, 13/39: median age, 71 (range: 34-78); breast/lung/ovarian cancer 24/16/12; and paclitaxel/docetaxel treatment: 36/16, respectively. The mean total doses of paclitaxel or docetaxel were 178 mg (range: 107-300) and 53 mg (30-100), respectively. Breath samples were measured three times immediately following the infusion of paclitaxel or docetaxel via ethyl alcohol detector and the mean value was recorded. BRAC was detected in 20 patients (56%) with paclitaxel and in none of the docetaxel patients. BRAC was measured again 30 min after the initial measurement in BRAC-detected cases with the patients' permission. In four of six BRAC-remeasured patients, BRAC became undetectable after 30 min. There was no correlation between the total doses of paclitaxel and BRAC or between the infusion rates of paclitaxel and BRAC. In conclusion, clinicians should recognize the potential for alcohol intoxication with paclitaxel administration. Patients should be instructed to avoid driving on the day of paclitaxel administration.

Adult↗
PubMed2005

Ataxia and c-Fos expression in mice drinking ethanol in a limited access session.

BACKGROUND: Although previous murine studies have demonstrated ethanol self-administration resulting in blood ethanol concentrations (BECs) believed to be pharmacologically relevant, to our knowledge, no study reported to date has demonstrated intoxication via ataxia after self-administration. Thus, the goal of this study was to demonstrate ataxia and to examine changes in c-Fos expression in mice after self-administration of intoxicating doses of ethanol. METHODS: Male C57BL/6J mice were trained to drink a 10% ethanol solution during daily 30-min limited access sessions. Mice were exposed to increasing concentrations of ethanol until a 10% ethanol solution was reached. BEC and ataxia, measured as foot slips off of a balance beam, were examined after the limited access self-administration session. In a separate experiment, various brain structures from mice drinking water or ethanol were examined for changes in c-Fos expression two hr after the limited access session. RESULTS: Mice drank between 1.5 and 2 g/kg of 10% ethanol during the daily 30-min session. BECs for these mice 15 min after the limited access session ranged between 0.52 and 2.13 mg/ml. A significant increase in foot slips off a balance beam was seen immediately after ethanol consumption during the limited access session. Among mice drinking ethanol, an increase in c-Fos expression was seen in the Edinger-Westphal nucleus, and a decrease in c-Fos expression was seen in the cingulate cortex, ventral tegmental area, lateral and medial septum, CA1 region of the hippocampus, and basolateral amygdala. CONCLUSIONS: After this procedure in mice, BECs are achieved that are in a range considered pharmacologically relevant and intoxicating. Significant ataxia was observed after ethanol self-administration. Brain regions showing changes in c-Fos expression after voluntary intoxication were similar to those previously reported, suggesting that these brain regions are involved in regulating behavioral effects of alcohol intoxication.

Alcohol Drinking↗
PubMed1988

Lack of effect of the benzodiazepine antagonist flumazenil (Ro 15-1788) on the performance of healthy subjects during experimentally induced ethanol intoxication.

Flumazenil is a specific benzodiazepine antagonist. This study was designed to determine whether it also reverses CNS depression due to acute alcohol intoxication. Intoxication was experimentally induced in 6 healthy volunteers by intravenous infusion of ethanol. Individual constant ethanol plasma concentrations in the range 1.47 +/- 0.04 g.l-1 to 1.71 +/- 0.03 g.l-1 were maintained over 6 h. Two doses of flumazenil (0.1 or 0.2 mg.kg-1) and placebo were administered intravenously in a randomized, double-blind, two-way cross-over fashion. A battery of psychometric tests and subjective ratings of mood and performance were performed at baseline and at regular intervals during the study. Before the administration of flumazenil the characteristic symptoms and signs of ethanol intoxication were present in all subjects. Performance (measured by visual analogue scales), reaction time, digit symbol substitution test, and a tracing test, were markedly impaired by ethanol. After the injection of flumazenil three volunteers reported some subjective improvement in performance. However, in none of the subjects was there a difference between either dose of flumazenil and placebo in terms of an improvement in the objective psychometric variables.

Adult↗
PubMed1984

Alcohol-influenced changes in activation peaking during paired-associate verbal learning.

Activation response patterning, termed activation peaking, was examined to understand the effects of alcohol intoxication on complex information processing. A total of 23 men social drinkers were divided into alcohol and placebo groups: Ns = 10 and 13, respectively. The alcohol group was administered enough alcohol to obtain blood alcohol levels of at least 10 mg/dl. Heart rate and skin conductance was measured before and during paired-associate learning. Learning consisted of a random presentation of eight letter-word pairs followed by the presentation of letters only, with subjects required to remember the associated word. Results showed a clear pattern of peripheral activation related to verbal learning behavior in the alcohol group, with no differences between the groups in verbal learning performance.

Adult↗
PubMedDate not supplied

[Histochemical changes in the hypothalamus, hypophysis, and adrenal glands observed in ethanol poisoning].

A comprehensive morphological-and-histochemical study of neuroendocrinal internals in cases of ethanol poisonings was undertaken. Actual forensic medical materials were used (62 cadavers) to make morphometry examinations of the hypothesis and adrenal glands. Besides, the distribution of alcohol dehydrogenase and acetaldehyde dehydrogenase was investigated in the mediatory differential brain sections, i.e. cerebellum, locus coeruleus, dorsal raphe nucleus, hypothalamus and adrenal glands. A differential distribution of ethanol-oxidizing enzymes as well as their changes in ethanol lethal poisoning were established; additionally, a variety of morphological signs were defined, which enable the differential diagnosis of a death reason in acute alcoholic intoxication.

Adrenal Glands↗
PubMed1983

Lysosome injury by perfusion of the isolated rat liver with ethanol or a molasses distillate (cachaça).

An isolated rat liver perfusion model was used to study the effects of acute exposure of the organ to either ethanol or a molasses distillate (cachaça). When ethanol (72 mM) or a molasses distillate (68 mM ethanol) was added to the perfusion fluid, lysosomal injury was indicated by the increased release of tartrate-inhibited acid phosphatase activity at the end of a 3 h period of perfusion. Other cellular compartments were not significantly damaged in these acute experiments, as judged by the release of aspartate and alanine aminotransferases, lactate dehydrogenase and alkaline phosphatase. The behavior of both ethanol itself and the alcoholic beverage was similar as far as enzyme release is concerned but only the molasses distillate caused significant acidosis (a decrease in perfusate pH) at the end of a 3 h period of perfusion. These data may be of importance for a better understanding of the hepatic damage caused by alcohol abuse and useful for laboratory investigation of alcohol intoxication.

Alcoholic Intoxication↗
PubMed1984

The influence of ethanol intoxication on outcome of injured motorcyclists.

Previous reports have failed to demonstrate a statistically significant adverse effect of acute ethanol intoxication in the well-resuscitated trauma patient. In the present study the prevalence of acute alcohol intoxication and its effect on outcome was analyzed in a homogenous population of young, previously healthy motorcycle accident victims (N = 134). The incidence of intoxication was 25%. The intoxicated cyclists were at fault for the accident 50% more often than the nonintoxicated cyclists and were found to wear helmets one third as frequently. Furthermore, the protective effect of helmet use as seen in the nonintoxicated group was lost in the intoxicated group, who sustained head injuries twice as frequently. Only patients with critical head injuries died and, although the ISS levels of those dying were similar in the two groups, the mortality following the critical head injury was twice as high among intoxicated patients (80 vs. 43%). Overall, the intoxicated group had a fourfold increased mortality rate. Thus, although intoxicated motorcyclists comprised 25% of the total population, they represent a mere 9% of the helmet-wearing population, and, in contrast, 39% of the severely head-injured victims and a majority (57%) of the mortality rate.

Accidents, Traffic↗
PubMed1985

The effects of alcohol on prose memory.

The present study examined the effects of acute alcoholic intoxication on prose memory. Intoxicated and sober subjects listened to six narrative passages at different presentation rates. Immediately after listening to a tape-recorded version of each story, subjects orally recalled it. The results demonstrated that sober subjects recalled more than intoxicated subjects, but subjects from both groups favored the main ideas in their recalls. However, at the fastest presentation rate, intoxicated subjects showed some diminished sensitivity to the semantic structure of prose. It was suggested that alcohol induced deficits in prose memory may result from a general slowing in the rate with which text is encoded into working memory.

Adolescent↗
PubMed1985

Alcohol and strokes in young adults.

Current drinking, alcoholic binges, and a history of alcohol intoxication differentiated young stroke patients from older stroke patients and young medical control subjects. Acute heavy alcohol consumption may be an important element in the development of strokes among young adults.

Adult↗
PubMed1990

[Prevention of acute renal failure in rhabdomyolysis caused by alcohol and drug intoxication].

Authors report a case of rhabdomyolysis occurring in a chronic alcoholic patient where they suspect in the development of rhabdomyolysis beside the effect of alcohol also a role of drug intoxication and muscle compression. They found sustained myoglobinaemia and myoglobinuria, while in this case beside the hypocalcemia during the initial phase of rhabdomyolysis normal parathyroid hormone level was found. Therefore in alcoholic intoxicated patients the measurement of creatine kinase is indicated. Beside total lactate dehydrogenase the determination of isoenzymes is in some cases helpful. In the presented case despite extensive rhabdomyolysis, acute renal failure was prevented by early volumen replacement therapy and use mannitol-sodium bicarbonate infusions. Authors discuss the possibility of the role of calcium blocking agent nifedipine in the prevention of rhabdomyolysis and acute renal failure.

Acute Kidney Injury↗