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PubMedDate not supplied

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.

Acute Disease↗
PubMed1997

Effects of alcohol intoxication on the perceived consequences of risk taking.

In 2 laboratory studies, the authors tested the hypothesis that intoxicated risk taking results from alcohol's effects on negative outcome expectancies. Young adults (N = 107) consumed alcohol or no alcohol and made ratings of the likelihood that negative and positive consequences would result from a variety of risky activities. Consistent with study hypotheses, participants rated negative consequences as less likely when they were intoxicated than when sober. Results were replicated in a second study (N = 88), which further showed that alcohol, rather than expectancy set, contributed to these reduced perceptions of risk. Findings provide the first experimental evidence that alcohol intoxication may contribute to risk-taking behavior be altering expectations about negative consequences.

Adult↗
PubMed1990

[The lymphatic system of the liver in alcoholic intoxication].

Liver of men and test animals (dogs, white rats) has been studied by means of a complex of injection, histological and electron microscopical methods (179 organs). At alcoholic intoxication all elements of the lymphatic bed (capillaries, postcapillaries, lymphangions) demonstrate certain adaptive-compensatory or pathological changes. Their manifestation degree depends on duration of alcoholization (in the experiment--up to 7 months). The greatest changes are noted in the hepatic lymphatic bed of adolescents and of the first mature age. In the test animals the functional rearrangement is demonstrated as certain changes of lymph outflow via the thoracic duct, which was wider than in the control during the whole period of the experiment. A high resistivity of the lymphatic bed, activation of its function, absence of any parallelism between the morphological and functional rearrangements in the lymphatic bed have been revealed. Certain parallelism is noted in development of the morphological rearrangements between the lymphatic and circulatory links of the hepatic vascular bed and cell elements of the organ.

Adolescent↗
PubMed1976

[Acute lethal alcohol intoxication (author's transl)].

In 14,744 autopsy cases from an 18-year period 92 cases (of which 7 were ruled out because of decomposition were observed in which death was supposed to be due to direct acute alcoholic intoxication. In the police reports 81 persons were designated as chronic alcoholics or abusers of spirits. The blood alcohol level ranged between 2.04 and 4.92 o/oo. The cases studied were divided into two groups, one with low and the other with high lethal alcohol level. Fatty liver and cirrhosis were found with identical frequency in the two groups, whereas cardiac hypertrophy of obscure origin occurred markedly more often in the group with low lethal blood alcohol level. On the basis the possible mechanism of death in the cases with cardiac hypertrophy is discussed. Finally, the relation between the blood and urine alcohol concentrations observed in 72 cases is discussed. On the assumption that the water phase of the blood was 75 per cent of the total blood, death occurred in the persons without cardiac hypertrophy with fairly identical frequency either in the phase of absorption or the phase of elimination, whereas in the persons with cardiac hypertrophy death most often occurred in the phase of absorption. These statements should, however, be taken with some reservation, partly because the water phase of the blood may vary considerably post mortem (60-90 per cent) and partly because the urine alcohol concentration depends on serval variable factors.

Adult↗
PubMed1993

[Neurologic emergencies in acute alcoholic intoxication].

Neurologic complications of acute alcohol intake are less well known to the general practitioner than those punctuating the course of chronic alcohol dependency. The state of ebriety is a poor incentive to precise neurologic analysis and follow-up. Nevertheless, only such surveillance in acute intoxication can distinguish a specific neurological complication, a complication following a fall or prolonged immobilisation, or rapid decompensation of alcoholic encephalopathy. Among the specific complications, myopathies and strokes are described here because of their rarity compared to the more common epilepsy and withdrawal syndromes. The neurologic semiology of ebriety is reviewed, including recent pathophysiological acquisitions specifying the mechanism of functional disorders in regions susceptible to alcohol such as the cerebellum and the reticular formation.

Alcoholic Intoxication↗
PubMed1991

Transient hypoparathyroidism during acute alcohol intoxication.

BACKGROUND: Persons with chronic alcoholism frequently have hypocalcemia, hypomagnesemia, and osteoporosis. The short-term effects of alcohol ingestion on calcium and magnesium metabolism are poorly understood, however. METHODS: We measured serum calcium, magnesium, and phosphate concentrations in 17 normal men and 7 normal women before and at intervals up to 16 hours after the ingestion of 1.2 to 1.5 g of alcohol per kilogram of body weight over a 3-hour period (doses sufficient to cause acute intoxication). Urinary excretion of calcium, magnesium, and phosphate and serum calciotropic hormone levels were measured in 16 of these subjects. As a control, the same measurements were made after the ingestion of fruit juice instead of alcohol. RESULTS: The mean (+/- SE) peak blood alcohol level in the men was 37.5 +/- 1.6 mmol per liter, and in the women it was 38.0 +/- 3.2 mmol per liter. In the men the mean serum parathyroid hormone concentration decreased from 16.1 +/- 2.1 to 6.8 +/- 0.9 ng per liter at the end of the three-hour drinking period. The value at this time was 30 percent of that at the end of the three-hour session during which the men drank fruit juice (P = 0.004). The serum concentration of ionized calcium reached a nadir eight hours after the beginning of alcohol administration (decreasing from 1.18 +/- 0.01 to 1.15 +/- 0.01 mmol per liter; P less than 0.001 as compared with values during the fruit-juice study), and urinary excretion of calcium increased from 0.34 +/- 0.08 to 0.36 +/- 0.08 mmol per hour (P less than 0.01 as compared with values during the fruit-juice study). Serum parathyroid hormone levels exceeded base-line values during the last 4 hours of the 16-hour study period; this increase was accompanied by a decrease in the urinary excretion of calcium. Both serum levels of magnesium (in the first 6 hours) and urinary levels (in the first 12 hours) increased after the ingestion of alcohol. In the women, serum parathyroid hormone levels decreased from 29.2 +/- 2.8 to 17.3 +/- 2.6 ng per liter two hours after the administration of alcohol was begun (P less than 0.001) and increased above base-line values during the last four hours of the study period. The serum concentration of ionized calcium decreased from 1.20 +/- 0.01 to 1.16 +/- 0.01 mmol per liter, reaching a nadir 8 to 12 hours after alcohol administration was begun (P less than 0.001). CONCLUSIONS: Short-term alcohol administration causes transitory hypoparathyroidism. This decline in the secretion of parathyroid hormone accounts at least in part for the transient hypocalcemia, hypercalciuria, and hypermagnesuria that follow alcohol ingestion.

Adult↗
PubMed1989

[Morphofunctional characteristics of autonomic disorders in patients with chronic alcohol intoxication].

Clinico-physiological and biochemical methods were used in 136 patients with chronic alcoholism and morphological investigations of the cingulum and hypothalamic region in 40 alcoholized rabbits with the purpose of evaluating vegetative disorders. The severity of anatomo-clinical changes depended on the stage of the neurotoxis process and duration of alcohol abuse. As alcohol intoxication advanced functional disorders were followed by organic.

Adult↗
PubMed1980

Mood change with alcohol intoxication.

The effects of increasing blood alcohol concentration (BAC) on a set of six mood variables were investigated in 10 men and 10 women subjects. The Profile of Mood States (POMS) was used to assess mood states, and blood alcohol levels were determined by breathalyser readings. Results indicated a reduction in tension and an increase in confusion for subjects in general, as BACs increased, while levels of tension were consistently lower for women. Important interaction effects were observed, with men becoming more depressed and angry, and women less so, with increasing BACs.

Adolescent↗
PubMed1990

[Acoustically evoked brain stem potentials in acute alcoholic intoxication].

Under the acute influence of alcohol with blood alcohol concentrations (BAK) ranging between 0.62 to 2.04%, the IPL prolongations of our subjects were within standard deviations compared with normal data. Depending on the BAK, these minor IPL alterations hint at a special vulnerability in the pontomesodiencephal area. The increase in BAK significantly correlates with the reduction of body temperature. The BAEP proves to be suitable for defining undear states of coma different origin.

Adult↗
PubMed1989

Acute alcohol intoxication paired with aversive reinforcement: ethanol odor as a conditioned reinforcer in rat pups.

Previous research has suggested that infant rats process ethanol sensory properties during acute alcohol intoxication. The present study was designed in order to examine if alcohol odor could act as an aversive conditioned stimulus after the organism experiences the state of intoxication paired with nociceptive stimulation (footshock). In a first experiment 11-day-old pups received intragastric alcohol administration (1.5 g/kg). At different postabsorptive intervals footshock was presented (0-30, 30-60, 60-90, or 90-120 min). An explicitly unpaired control group which experienced footshock prior to the state of intoxication was also employed. All animals were subsequently tested in terms of alcohol intake and ethanol locational odor preferences. Both assessments indicated that pups which were exposed to the unconditioned peripheral stimulus 30-60 min after receiving ethanol expressed strong alcohol aversions. In a second experiment pups were exposed to footshock during this postabsorptive interval. Twenty four hours later, pups experienced ambient ethanol odor paired with soft or rough texture surfaces. Differential texture aversions were registered in experimental animals when compared with controls which suffered the state of intoxication explicitly unpaired with footshock, or unpaired presentations of ethanol odor and the tactile stimuli under consideration. These results appear to support the hypothesis concerning orosensory processing during an acute state of intoxication. Additionally it seems that the hedonic value of sensory attributes of this drug varies as a function of associative processes occurring during such a state.

Alcohol Drinking↗