Alcohol
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Prolonged alcohol consumption is associated with a variety of neuropsychiatric conditions, including the dense amnesic disorder known as Korsakoff's syndrome. Korsakoff's syndrome is frequently diagnosed in alcoholics after an episode of acute thiamin deficiency. The accepted view within the medical literature is that the etiology of this disorder lies in thiamin deficiency or Wernicke's encephalopathy. ⋯ The etiology of alcohol-related cognitive impairments such as Korsakoff's syndrome is still poorly understood but several lines of evidence suggest multiple causal factors interact to produce deficits in performance. Animal models that manipulate only a single putative etiological factor are unlikely to elucidate the multiple influences that lead to Korsakoff's syndrome. A study of the natural history of alcohol-related brain damage is needed that will allow an assessment of individual risk factors and their interactions.
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Recent studies suggest substantial interactions between opioids and ethanol (EtOH). Both in vivo and in vitro experiments indicate that EtOH can regulate opioid systems and that opioids can modify EtOH consumption. In the present studies, we examined if EtOH consumption altered opioid receptors and the potency of opioid analgesics. ⋯ Saturation binding studies indicated no changes in the density or affinity of brain and spinal cord delta-opioid ([3H]DPDPE, [3H]DSLET, [3H]DeltorphinII) and mu-opioid ([3H]DAMGO) receptors. Similarly, there was no significant effect of EtOH on delta-opioid receptor mRNA in either brain or spinal cord preparations. Taken together, these data suggest that EtOH consumption decreases the analgesic potency of opioids in mice through a mechanism that is unrelated to pharmacokinetics or opioid receptor changes in brain and cord.
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Randomized Controlled Trial Clinical Trial
Acute alcohol tolerance in cognitive and psychomotor performance: influence of the alcohol dose and prior alcohol experience.
Using tests for cognitive performance (the Pauli test) and psychomotor coordination (the Pursuit Rotor test), the interaction between the drinking history of the subjects, the alcohol dose, and acute alcohol tolerance were examined in light and moderate alcohol consumers (N = 10). Both groups of subjects were tested with doses of alcohol corresponding to 0.5 and 1.0 g/kg. Dose order was random and tests were carried out at an interval of 1 week. ⋯ However, in the moderate alcohol consumers, acute tolerance was only observed for the higher of the doses and only for the duration measure. Given the difference in drinking history between the two groups of subjects, the implication would be that when the dose of alcohol exceeds the subjects' prior experience, acute tolerance seems inevitable. The present results clearly demonstrate the complexity of the acute tolerance phenomenon, and emphasize the fact that the results are dependent on the subjects' prior experience with alcohol as well as the dose of alcohol ingested, and consequently suggest the interaction between acute and chronic alcohol tolerance.
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Hypothermia and ethanol are often closely linked and in hypothermic accidents ethanol is often a contributing factor. To study the effects of ethanol on the circulation in hypothermic conditions, cardiac catheterization was carried out on 18 anaesthetized beagle dogs. They were divided into two groups. ⋯ Changes in negative dP/dt coincided with the changes in the time constant of exponential isovolumic pressure fall. Ethanol did not influence relaxation. All the parameters we checked recovered to normal during rewarming.
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Clinical Trial
Plasma concentrations of beta-endorphin, adrenocorticotropic hormone, and cortisol in drinking and abstinent chronic alcoholics.
Previous studies of the relationship between the endogenous opioid system and alcohol consumption have reported contradictory results. To shed light on this connection, we compared plasma concentrations of beta-endorphin, adrenocorticotropic hormone, and cortisol in 70 alcoholic persons after different periods of abstinence and a group of 80 control subjects. ⋯ On the other hand, lowered circulating concentrations of beta-endorphin may be a cause, rather than an effect, of alcoholism. Plasma levels of adrenocorticotropic hormone and cortisol did not differ in alcoholics and controls (19.29 +/- 1.66 vs. 13.27 +/- 1.85 pg/ml for ACTH, 20.37 +/- 0.78 vs. 17.22 +/- 0.64 ng/ml for cortisol), and thus appear to have no relation with chronic alcohol consumption.