Effects Of Acute Alcohol Intoxication Research Articles

Acute Alcohol Intoxication Suppresses the Interleukin 23 Response to Klebsiella pneumoniae Infection

Bacterial pneumonia is a widely recognized infection in the alcohol-abusing patient. Interleukin 23 (IL-23) is a recently described cytokine critical for IL-17 induction and host survival during Klebsiella pneumoniae infection, a pulmonary pathogen commonly seen in alcoholics. We investigated the effect of acute alcohol intoxication on the IL-23 response to this infection. Male C57BL/6 mice were given an intraperitoneal injection of ethanol (3.0 g/kg) or phosphate-buffered saline (PBS) 30 minutes before infection. Alveolar macrophages (AM) were cultured with bacteria in ethanol (0, 50, and 100 mM) to determine alcohol's effect on AM IL-23 expression, the bioactivity of which was determined by splenocyte IL-17 inducing activity. The role of IL-10 in alcohol-mediated suppression of AM IL-23 p19 mRNA expression was assessed using wild-type (WT) and IL-10 knock-out (KO) mice. Efficacy of AM pretreatment with interferon gamma (IFN-gamma) on IL-23 expression before ethanol exposure and infection was evaluated. In vivo, acute intoxication suppresses the lung and bronchoalveolar lavage cell IL-23 response to pathogen. This effect was confirmed in vitro as ethanol dose-dependently inhibits AM IL-23 during infection. Acute intoxication increases lung and BAL cell IL-10 mRNA expression 2 hours after in vivo infection and, in vitro, recombinant IL-10 inhibits AM IL-23 expression. However, alcohol impairs IL-23 similarly in AM harvested from both WT and IL-10 KO mice. Interferon gamma pretreatment strongly inhibits AM IL-23 production in both the presence and absence of alcohol. Acute alcohol intoxication inhibits the pulmonary IL-23 response to K. pneumoniae infection both in vivo and in vitro, an effect independent of IL-10 induction. Interferon gamma priming antagonizes IL-23 and is, therefore, not likely to be a useful adjuvant therapy in restoring IL-23/IL-17 responses during infection and intoxication.

Yings and Yangs of Acute Ethanol Intoxication in Experimental Traumatic Brain Injury

Abstract:Although the deleterious effects of acute alcohol intoxication on traumatic brain injury (TBI) are well known, neuroprotective features of lower doses of ethanol (EtOH) before head trauma have been reported during recent years. Inhibition of N-methyl-D-aspartate receptor (NMDA)-mediated exc

A Failure to Replicate Alcohol-Induced Laboratory Aggression among College Men without Evidence of Personality Disturbance

The effect of acute alcohol intoxication on laboratory-induced aggression among men has been fairly well established. The present study hypothesized that alcohol effects on Point Subtraction Aggression Paradigm (PSAP) responding would not be replicated among "low-risk' college men distinguished by their absence of personality disorder features. Participants were assigned to either Alcohol (n=18), Placebo (n=7), or Time (n=8) comparison groups with each completing 25-min. sessions during the baseline, ascent, peak (70 mg%), and descent (40 mg%) phases of absorption and elimination process. Participants assigned to the Alcohol condition received a .80 ml/kg dose of 95% ethanol mixed with soda in a 1:5 ethanol/soda ratio. As hypothesized, alcohol was associated with stable Point Subtraction Aggression Paradigm responding across the course of absorption, peak, and elimination for all three groups. Aggression Paradigm responding was least variable among the men administered alcohol. The present procedure served to identify a subset of "low-risk" college men whose Point Subtraction Aggression Paradigm responding was not adversely affected by alcohol. The extent to which aggressive personality dispositions contribute to alcohol-induced laboratory aggression remains to be identified. Low-risk college drinkers warrant systematic examination to specify what factors attenuate their reactions to alcohol and other situational provocations.

Alcohol intoxication increases allopregnanolone levels in male adolescent humans.

Teenage drinking is a cause of growing concern in industrialized countries, where almost 35% of alcohol drinkers are under 16 years old. Increased anxiety, irritability and depression among adolescents may induce them to seek the anxiolytic and rewarding properties of alcohol. Allopregnanolone is rewarding in rodents, and therefore may contribute to the effects of alcohol. In this paper, we studied the effects of acute alcohol intoxication on the plasma levels of allopregnanolone in male adolescents. Blood samples were drawn from male adolescents who arrived at the Emergency Department of the Hospital. Two groups were studied: one study group was formed by adolescents who arrived with evident behavioral symptoms of acute alcohol intoxication (AAI) and the other by those arriving for mild trauma (contusions, sprains) after no consumption of alcohol (Controls). Our results demonstrate that AAI significantly increases serum allopregnanolone levels in male adolescents. Because alcohol and allopregnanolone positively modulate gamma-aminobutyric acid type A (GABAA) receptors, allopregnanolone may play a major role in the anxiolytic and rewarding effects of alcohol, either directly or by influencing the sensitivity of GABAA receptors to alcohol.

Alcohol Intoxication Increases Allopregnanolone Levels in Female Adolescent Humans

Teenage drinking is a cause of growing concern in industrialized countries, where almost 35% of alcohol drinkers are under 16 years old. Increased anxiety, irritability, and depression among adolescents may induce them to seek the anxiolytic and rewarding properties of alcohol. We studied the effects of acute alcohol intoxication (AAI) on the plasma levels of progesterone and allopregnanolone in female adolescents. Blood samples were drawn from female adolescents who arrived at the emergency department. One study group was formed by those who arrived with evident behavioral symptoms of AAI and the other by those arriving for mild trauma (contusions, sprains) after no consumption of alcohol (controls). Our results demonstrate that AAI significantly increases serum progesterone and allopregnanolone levels in both follicular and luteal phases of the ovarian cycle. Since alcohol and allopregnanolone positively modulate gamma-aminobutyric acid type A (GABA(A)) receptors, allopregnanolone may play a major role in the anxiolytic and rewarding effects of alcohol, either directly or by influencing the sensitivity of GABA(A)-receptors to alcohol.

Effects of acute alcohol intoxication on pituitary-gonadal axis hormones, pituitary-adrenal axis hormones, beta-endorphin and prolactin in human adults of both sexes.

- The effects of acute alcohol intoxication (AAI) on the pituitary-gonadal axis hormones, and the possible contribution of pituitary-adrenal axis hormones, beta-endorphin and prolactin to alcohol-induced dysfunction of pituitary-gonadal axis hormones were studied in adult men and women. Blood samples were drawn from adults of both sexes who arrived at the emergency department with evident behavioural symptoms of drunkenness (AAI) or from adult volunteers with nil consumption of alcohol (controls). Our results demonstrated that AAI produces a high increase in plasma prolactin, corticotropin (adrenocorticotropic hormone, ACTH), and cortisol in adults of both sexes, a decrease in luteinizing hormone levels only in men, an increase in dehydroepiandrosterone-sulphate (DHEAS) and a contradictory behaviour of testosterone according to gender, with increased plasma testosterone in women and a decrease in men. ACTH and prolactin correlated positively with cortisol, DHEAS and testosterone in women, which suggests that prolactin and ACTH could contribute to stimulated adrenal androgen production. In contrast, the decrease in testosterone and increase in beta-endorphin in men suggests that AAI could have an inhibitory effect on testicular testosterone, perhaps mediated by beta-endorphin. Our results suggest that the effect of alcohol on pituitary-gonadal axis hormones in humans could depend on the gender and degree of sexual maturity of the individual.

Alcohol and suicidal behavior

Alcohol dependence and alcohol intoxication are important risk factors for suicidal behavior. However, the mechanism for the relationship remains unclear. This review presents a conceptual framework relating alcohol to suicidal behavior. Distal risk factors create a statistical potential for suicide. Alcohol dependence, as well as associated comorbid psychopathology and negative life events, act as distal risk factors for suicidal behavior. Proximal risk factors determine the timing of suicidal behavior by translating the statistical potential of distal risk factors into action. The acute effects of alcohol intoxication act as important proximal risk factors for suicidal behavior among the alcoholic and nonalcoholic alike. Mechanisms responsible for alcohol's ability to increase the proximal risk for suicidal behavior include alcohol's ability to: (1) increase psychological distress, (2) increase aggressiveness, (3) propel suicidal ideation into action through suicide-specific alcohol expectancies, and (4) constrict cognition which impairs the generation and implementation of alternative coping strategies. Moreover, the proximal risk factors associated with acute intoxication are consistent with Baumeister's (1990) escape theory of suicide. Suggestions for additional research are discussed, including the possibility that a nonlinear cusp catastrophe model characterizes the relationship between alcohol intoxication and suicidal behavior.

Effects of acute alcohol intoxication on growth axis in human adolescents of both sexes

We previously reported the deleterious effects of acute alcohol intoxication (AAI) on pituitary-gonadal and pituitary-adrenal axes hormones in human adolescents. In the present paper we studied the effects of AAI on the growth axis hormones, and the possible contribution of the insulin-glucose axis to the alcohol-induced dysfunction of the growth axis in human adolescents. Blood samples were drawn from adolescents that arrived at the emergency department with evident behavioural symptoms of drunkenness (AAI) or with nil consumption of alcohol (controls [C]). AAI produced in the adolescents of both sexes in our series: a decrease in growth hormone (GH) levels, without significant alteration of either insulin-like growth factor-I (IGF-I) or insulin-like growth factor binding protein-3 (IGFBP3); an increase in plasma glucose and a decrease in insulin in the female adolescents but not in the males. Males and females undergo a significant period of bone growth during adolescence. Growth axis hormones play an important role in the pubertal spurt. Thus, ethanol consumption during adolescence could have long-lasting deleterious effects on this aspect of development. In industrialised countries, around 35% of alcohol drinkers are under 16 years old, therefore the result of this study should be made known to adolescents and the appropriate authorities.

Effects of acute alcohol intoxication on pituitary-gonadal axis hormones, pituitary-adrenal axis hormones, β-endorphin and prolactin in human adolescents of both sexes

Teenage drinking continues to be a major problem in industrialized countries, where almost 35% of alcohol drinkers are under 16 years old. In the present paper we studied the effects of acute alcohol intoxication (AAI) on the pituitary-gonadal (PG) axis hormones, and the possible contribution of pituitary-adrenal (PA) axis hormones, β-endorphin (BEND), and prolactin (PRL) to the alcohol-induced dysfunction of PG axis hormones. Blood samples were drawn from adolescents that arrived at the emergency department with evident behavioral symptoms of drunkenness (AAI) or with nil consumption of alcohol (controls [C]). Our results demonstrated that AAI produces in adolescents a high increase in plasma PRL, ACTH, and cortisol (F), and a contradictory behavior of testosterone (T) according to gender: plasma T was increased in females and decreased in males. ACTH and PRL correlated positively with F, dehydroepiandrosterone-sulphate (DHEAS) and T in females, which suggests that PRL and ACTH could synergistically stimulate adrenal androgen production. In contrast, the decrease in T and increase in BEND in males suggests that AAI could have an inhibitory effect on testicular T, perhaps mediated by BEND. The hormones studied are involved in the development of secondary sexual characteristics and the growth axis during adolescence. The deleterious effects of alcohol abuse should be made known to adolescents and the appropriate authorities.

Alcohol effects on movement-related potentials: a measure of impulsivity?

To assess the effects of acute alcohol intoxication on lateralized readiness potential (LRP), a central measure of movement-related brain activity, and the potential association of such effects with personality measures. Male volunteers (N = 12) alternated responding hands during a "go/no go" verbal recognition task across all four sessions of the balanced placebo design in which beverage content (either juice only or a vodka and juice mixture that raised the average blood alcohol concentration to 0.045%) was crossed with instructions as to beverage content. Whereas the instructions had no effect on behavioral (response accuracy and reaction time) and physiological (LRP) measures, alcohol decreased reaction times adjusted for psychometer speed. As expected, large LRPs were recorded on "go" trials and were not affected by the beverage. However, the "no go" words that did not require and did not evoke motor responses, also evoked significant LRPs under alcohol but not placebo. Since only trials with correct responses and correct abstentions from responses were included in the averages, the motor preparation was not completed and was terminated before the motor response on "no go" trials. Similarly, there was a decrease in spectral power of the movement-related mu-rhythm on "no go" trials under alcohol. Alcohol may result in disinhibition such that the "response execution" process is activated based on very preliminary stimulus evaluation. This alcohol-induced brain activity signaling premature motor preparation exhibited correlation trends with personality traits related to impulsivity, hyperactivity and antisocial tendencies, thus concurring with other evidence that indicates commonalities between alcoholism and impulsivity, disinhibition and antisocial behaviors. The LRP on "no go" trials could potentially be used as a psychological index of the impulsiveness induced by alcohol intoxication.

Effects of Alcohol on Picture Drawing During the Verification Phase of the Creative Process

This study tested effects of acute alcohol intoxication on elaboration and revision in the verification phase of Wallas' (1926/1970) four stage model of creativity. Forty-two male and female participants were randomly assigned to three groups of equal size--a control group, a placebo group, and an alcohol group. The alcohol dose was I ml 100% alcohol/kg body weight. Participants were instructed to read a poem and to draw a picture using the poem. These pictures were judged by 2 separate panels of judges. Panel A was comprised of 3 professional artists. Panel B was comprised of 3 college art instructors. No group differences were apparent in ratings given by Panel A, but Panel B gave the work of the alcohol group low handicraft ratings. Results were interpreted as an indication that a moderate dose of alcohol inhibits certain relevant abilities during the verification phase of the creative process.

Ontogenetic differences in the expression of olfactory-conditioned aversions resulting from a state of acute alcohol intoxication in the rat

Three experiments examined the effects of acute alcohol intoxication on olfactory conditioning in infant (16 days old) and adult rats (60–65 days old). In both age groups, alcohol administration (2 g.kg, IG) prior to conditioning procedures failed to affect subsequent expression of methyl-conditioned aversions in a two-way odor locational test. Nevertheless, whenever this same alcohol dose was administered prior to testing procedures, the expression of the olfactory conditioning was substantially impaired in infants but unaffected in adults. The factorial design allowed rejection of the possibility that ontogenetic differences in alcohol-induced state-dependent retention might explain this developmental difference (Experiment 1). A subsequent experiment (Exp. 2a) revealed major age-related differences in terms of peak blood alcohol levels (BALs) that resulted from the 2 g/kg alcohol dose previously employed. As revealed by gas chromatography, infants exhibited significantly higher BALs than adults at time of conditioning and/or testing. Therefore, in Experiment 2b, the alcohol dose administered in adults was increased until BALs were comparable to those attained in infants given 2 g/kg. This was accomplished with a 2.5 g/kg alcohol dose, employed in Experiment 2c to evaluate responsiveness of adults in conditioning circumstances identical to those of Experiment 1. Yet even with this dose the adults' expression of the conditioned olfactory aversion was unaffected by the alcohol at the time of testing. Experiment 3 analyzed the effects of alcohol intoxication on infantile and adult motor responses elicited by methyl and a novel odor (lemon), which might conceivably have affected performance in the two-way odor locational tests used to assess olfactory conditioning. The results failed to support possibility that the previously observed ontogenetic differences in the expression of olfactory-conditioned aversions were due to alcohol's effect on sensorimotor responsiveness. In accordance with prior studies, the present results seem to indicate age-related sensitivity to alcohol's effects on cognitive processes.

Effect of acute alcohol intoxication on the opioid system in humans

We investigated the possible relation between the endogenous opioid system and acute alcoholic intoxication in 21 subjects, of whom 13 were drinkers who came to the emergency service with evident symptoms of drunkenness, and 8 were nondrinkers who consumed 1 g alcohol per kg body weight over a short period. Different patterns of changes were found in the two groups for plasma concentrations of β-endorphin and adrenocorticotropic hormone. In drinkers, plasma levels of both substances increased, whereas in nondrinkers both concentrations decreased, the declines being especially notable 15, 30, and 45 min after ingestion. We found no differences between the two groups in plasma cortisol concentrations. The different levels of these substances may reflect differences in drinking behavior between the two groups.

SYNAPTIC MEMBRANE RESPONSES TO ACUTE AND CHRONIC ALCOHOL INTOXICATION IN HIGH ALCOHOL SENSITIVE (HAS) AND LOW ALCOHOL SENSITIVE (LAS) SELECTIVELY BRED RATS

HAS (high alcohol sensitive) and LAS (low alcohol sensitive) lines of rats have been selectively bred based on their differences in ethanol-induced sleep time. In the present study, the two lines were compared to examine another central effect of acute alcohol intoxication: namely, hypothermia. As the disturbances in membrane microorganization have been associated with the nervous system's sensitivity and tolerance to ethanol, the synaptic plasma membrane fluidity and acute sensitivity to ethanol were also evaluated by fluorescence polarization of DPH probes in the HAS and LAS rats. The two lines did not differ in the magnitude of their hypothermic response after acute injection of ethanol (3 g/kg body wt, i.p.). Although membranes in the HAS line were slightly more rigid than in the LAS line, the level of membrane disordering after acute ethanol addition was identical for the two lines in the region examined with the DPH probe. Following the chronic intoxication of the rats, the two lines developed tolerance to the hypnotic and hypothermic effects of ethanol. In the same way, a membrane resistance (i.e. tolerance) to the disordering effect of acute ethanol addition developed in the region probed with DPH. In general, the LAS line showed a more pronounced level of tolerance than the HAS line at both the functional and membrane level. These results suggest that different measures used to assess the depressant action of ethanol, such as sleep time, hypothermia or membrane disordering, may not be related and could indicate different genetic origins.(ABSTRACT TRUNCATED AT 250 WORDS)

The Effect of Acute Alcohol Intoxication and Chronic Alcohol Abuse on Outcome From Trauma

To determine the effect of acute alcohol intoxication and chronic alcohol abuse on morbidity and mortality from trauma. Prospective cohort study. Blunt or penetrating trauma patients at least 18 years of age admitted to one trauma center or dying at the injury scene. Mortality, complications (infection, pneumonia, respiratory failure, or multiple organ failure), and length of hospital stay. Acute intoxication had no effect on risk of dying--at the injury scene, within the first 24 hours of hospitalization, after the first 24 hours, or overall. Acute intoxication also did not increase the risk of complications and was associated with shorter lengths of stay. Patients with both biochemical and behavioral evidence of chronic alcohol abuse had a twofold increased risk of complications, particularly pneumonia and any infection, compared with those with no evidence of chronic alcohol abuse. Chronic, but not acute, alcohol abuse adversely affects outcome from trauma. Attention to the problem of chronic alcohol abuse in trauma patients is necessary, and screening trauma patients for chronic alcohol abuse appears to be warranted.

The effect of acute alcohol intoxication and chronic alcohol abuse on outcome from trauma

The effect of acute alcohol intoxication and chronic alcohol abuse on outcome from trauma

Effects of acute alcohol intoxication on gluconeogenesis and its hormonal responsiveness in isolated, perfused rat liver

Rats were acutely administered ethanol as a primed constant infusion in order to produce sustained blood ethanol levels of 8–12 or 55–65 mM. At the end of ethanol infusion the livers were either freeze-clamped in vivo or isolated and perfused for metabolic studies. The rate ofgluconeogenesis and its responsiveness to phenylephrine (10μM), prostaglandin F 2α (5μM) and glucagon (10 nM), as well as the redox state of the cytosolic NAD +-NADH system were assessed in livers isolated from acutely ethanol-treated rats, and subsequently perfused without ethanol. For liver clamped in vivo, high- but not low-ethanol treatment decreased the ATP content by 31% and slightly increased ADP and AMP content, resulting in a decreased energy charge (11%). Glutamate and aspartate content was also increased in high-dose ethanol-infused rats with no changes in malate and 2-oxoglutarate content. Gluconeogenesis with saturating concentrations of lactate (4 mM) + pyruvate (0.4 mM) was delayed in reaching a plateau in the livers of high-dose ethanol-treated rats and its response to all three stimulators was impaired. Low-dose ethanol treatment only decreased the liver response to phenylephrine. While the perfused livers of low-dose ethanol-treated rats displayed no changes in adenine nucleotide content, the livers of high-dose ethanol-treated rats had a decreased ATP (35%) and an increased AMP (77%) content, paralleled by a fall in the total adenine nucleotides (14%) and energy charge (14%). No differences were observed between the saline- and ethanol-treated rats with respect to malate-aspartate shuttle intermediate concentration in perfused livers. Also, the livers of high-, but not low-dose ethanol-treated rats had a more negative value of NAD +-NADH redox state as compared to the livers of control rats. The data suggest that acute ethanol intoxication produces changes in liver metabolism and its responsiveness to hormones/agonists that are demonstrable for at least 2 hr after isolation and perfusion of the liver.

The effect of acute alcohol intoxication on psychometric testing and 5‐HT‐induced platelet aggregation in normal subjects; modulatory role of evening primrose oil

AbstractGroups of university students were exposed acutely to alcohol (100 ml vodka) and their performance in the Bexley Maudsley Automated Psychological Screening Tests (BMAPS) was assessed. Blood samples were also taken to assess platelet aggregation to 5‐HT challenge. After 1 week administration of Evening Primrose Oil (EPO) or placebo under double‐blind conditions the students were re‐assessed. No mean difference was found in the psychometric testing of any of the groups either before or after the administration of EPO; however 5‐HT‐induced platelet aggregation was significantly potentiated in those groups exposed to alcohol, and was further increased in the group receiving EPO. These results suggest that platelet aggregation in response to 5‐HT is more sensitive than psychometric tests commonly used to assess alcoholism in detecting changes due to acute alcohol intoxication.

The effect of acute alcohol intoxication on psychometric testing and 5‐HT‐induced platelet aggregation in normal subjects: Modulatory role of evening primrose oil

AbstractGroups of university students were exposed acutely to alcohol (100 ml vodka) and their performance in the Bexley Maudsley Automated Psychological Screening Tests (BMAPS) was assessed. Blood samples were also taken to assess platelet aggregation to 5‐HT challenge. After 1 week's administration of evening primrose oil (EPO) or placebo under double‐blind conditions the students were re‐assessed. No mean difference was found in the psycho‐metric testing of any of the groups either before or after the administration of EPO. However 5‐HT‐induced platelet aggregation was significantly potentiated in those groups exposed to alcohol, and was further increased in the group receiving EPO. These results suggest that platelet aggregation in response to 5‐HT is more sensitive than psychometric tests commonly used to assess alcoholism in detecting changes due to acute alcohol intoxication.

The effects of acute alcohol intoxication on biophysical activities: A case report

A computer-assisted biophysical assessment was performed in a woman with chronic alcoholism at 37 weeks' gestation. She was first seen in a state of acute alcohol intoxication (322 mg/dl). Although fetal breathing movement incidence was normal (30%), fetal tachypnea (67 breaths per minute) and decreased fetal body movements (0.11%) were seen. Because these findings differ from those previously reported with regard to normal pregnancies exposed to lower levels of alcohol, their implications are discussed.