[Disorders of sexual function associated with chronic alcoholic intoxication (psychoendocrinologic aspects: a lecture].
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Chemokines are involved in the inhibition of HIV-1 infection and in the pathogenesis of tissue injury in a number of conditions, including endotoxemia and alcoholic liver disease. CC chemotactic peptides (MIP-1alpha, MCP-1 and RANTES) are produced by a wide variety of cell types in response to immunological stimuli, bacterial endotoxin and gp120 from HIV-1 and HIV-2. This work tests the hypothesis that prior exposure to endotoxin and/or ethanol in vivo inhibits the production of CC-chemokines following a secondary challenge with HIV-1 gp120 in vitro. Male Sprague-Dawley rats received in intravenous infusion of ethanol to maintain blood ethanol level at 170 mg/dl for 3 hr. Escherichia coli LPS (1 mg/Kg) was given intravenously 5 min after the ethanol bolus was injected. Control groups received similar volumes of saline. Three hr after LPS treatment, Kupffer cells were obtained and treated with HIV-1 gp120 (5 microg/10(6) cells/24 hr). At the end of the incubation period, cells were obtained for RT-PCR analysis of CC-chemokine mRNA expression. Chemokine release in culture supernatants was measured by ELISA. Results show that in vivo ethanol was associated with downregulation of MIP-1alpha and MCP-1 mRNA expression and protein release in primary cultures of Kupffer cells. However, ethanol alone primed isolated Kupffer cells for enhanced RANTES mRNA and protein release in the presence or absence of HIV-1 gp120. These results demonstrate that acute ethanol intoxication and endotoxemia may selectively act as a desensitizing agent in response to a secondary challenge with bacterial or viral products.
Repeated ip injection of ethyl alcohol in a relatively high dose depressed the immune response, to a greater degree in Swiss mice than in C57BL/6 mice, as shown by a diminution in granuloma size and in the hypersensitivity reaction to tuberculin compared with untreated controls. The control of bacillary multiplication in the popliteal lymph node was more efficient in alcohol-treated Swiss mice than in the corresponding controls, but was less efficient in alcohol-treated C57BL/6 animals than in their controls. Alcohol treatment caused no reduction in the number of circulating lymphocytes, and no modification of the distribution of B and T lymphocytes in the spleen, or of the stimulation of T lymphocytes in the presence of mitogens.
The data available in literature concerning the induction of lipid peroxidation (LP) with chronic alcohol administration are systematized. LP can be considered as one of the main processes leading to cellular membrane damage. The cytotoxic activity is attributed not only to the free radicals but also to the final products of the lipid hydroperoxide decomposition, such as malonic dialdehyde and 4-hydroxyalkenals. Data about antioxidative defence enzymes (glutathione peroxidase and transferase, catalase superoxide dismutase) and less investigated protein factors which inhibit LP are summarized; particular attention is paid to changes in their activity during chronic alcoholization. Molecular mechanisms underlying the LP stimulation in the liver tissue against a background of ethanol ingestion are analyzed. New data are presented on the role of peroxisomes in the development of alcohol cardiomyopathy.
AIMS: To investigate whether, compared with middle-aged men (aged 30-50), older men (age > or =60) (i) perform more poorly on a driving simulator and (ii) are more sensitive to the effects of ethanol in terms of blood alcohol concentration (BAC) and driving performance, but more aware of their driving difficulties, and therefore exercise better driving judgement. METHODS: 14 Healthy middle-aged men (mean age 36 years) were compared with 14 healthy older men (mean age 69 years) on an interactive driving simulator, while sober and while legally intoxicated (BAC >80 mg/dl). RESULTS: Older age was associated with poorer driving performance on the simulator. While sober, older men exhibited more improper braking, slower driving, greater speed variability, fewer appropriate full stops and more crashes, and spent more time executing left turns (across oncoming traffic); all values < or =0.02. BACs > or =80 mg/dl were associated with impaired driving, with more inappropriate braking, fewer appropriate full stops and more time executing left turns (all values > or =0.02) and trends towards more speed variability, more low speed collisions and more wrong turns (values <0.1). However, similar ethanol consumption did not produce higher peak BAC or more driving impairments in older drivers. While there were no differences between age groups in terms of awareness of intoxication or driving difficulties, older men were unwilling to drive while legally intoxicated because of fear of physical injury, whereas middle-aged men were more likely to avoid driving when intoxicated due to fear of legal ramifications. CONCLUSION: While both age and legal intoxication affected driving performance, older men were no more sensitive to ethanol in terms of peak BACs, driving performance or awareness/judgement than middle-aged men.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
BACKGROUND: Research on the aetiology of sudden cardiac death among young men in Russia strongly suggests an association with binge drinking. However, the possibility remains that such deaths are misclassified as being attributable to cardiovascular disease when they are really caused by acute alcohol poisoning. OBJECTIVE: To describe postmortem levels of blood alcohol in Russian men dying from various causes and so determine whether deaths from alcohol poisoning are being misclassified as cardiovascular deaths. SETTING: Ishevsk, capital of the Udmurt Republic, situated in the Ural region of the Russian Federation. METHODS: The study was part of a larger one on adult mortality. The study sample was 309 deaths among men aged 20-55 dying between August 1998 and March 1999 from other than neoplasms, infectious diseases or unspecified causes and on whom necropsy records could be obtained. Information on cause of death was extracted from death certificates and data on postmortem blood alcohol concentration (BAC) from forensic records. Blood alcohol concentrations were adjusted where necessary to allow for delay in necropsy. RESULTS: Medium or greater levels of intoxication occurred in a quarter of those recorded as dying from cardiovascular disease but in over half of those dying from external causes. BAC levels consistent with at least strong intoxication were seen in 13.5% of deaths from cardiovascular disease and 27.1% from external causes. No cardiovascular deaths had BAC at levels usually thought to be fatal while this level was seen in 26% of deaths from accidental poisoning. CONCLUSION: Evidence of recent consumption of alcohol is common among Russian men dying under the age of 55, with severe intoxication common where death is from external causes. However, the high death rates from cardiovascular disease in Russia cannot be explained by misclassification of deaths attributable to acute alcohol poisoning. This study thus resolves one of the outstanding controversies in the story of alcohol and cardiovascular disease in the former Soviet Union.
In the experimental conditions used, cysteine administered per os together with ethanol reduces the blood alcohol levels, but does not modify significantly the rate of alcohol oxidation. No effect of cysteine administration is however observed when ethanol is injected intraperitoneally. Cysteine addition in vitro enhances ethanol consumption by liver slices and reduces at the same time 14CO2 production from [2-14C] ethanol. This effect is only observed with a high cysteine/ethanol molar ratio. The changes in the blood alcohol level resulting from cysteine administration do not appear to result from such an interaction with ethanol oxidation, but seem to be due to a delayed ethanol absorption from the gastrointestinal tract.
Hormone levels were examined in the venous blood in 54 men suffering from stage 2 alcoholism and in 30 normal subjects, using a radioimmunochemical assay. The alcoholics were found to have a statistically significant increase in prolactin and a decrease in testosterone. A definite ratio in the secretion of these hormones differing from that in the control group was elucidated. This ratio (prolactin-testosterone index) is proposed as a diagnostic test of alcoholism.
Intoxications with ethylene glycol, methanol, and isopropanol are among the most common ingestions, in the treatment of which a nephrologist plays an important role. These three substances have the ideal characteristics for intervention by hemodialysis, and the three parent compounds and their metabolites are readily dialyzable. Two of the three substances, ethylene glycol and methanol, are metabolized to more toxic substances, so that an early treatment strategy that removes the parent compound or blocks its metabolism can prevent the development of many of the adverse events that are often seen in these ingestions. Fomepizole, an inhibitor of alcohol dehydrogenase, slows the metabolism of these substances and is now approved by the US Food and Drug Administration for use in ethylene glycol intoxication. The present review addresses recent advances in the diagnosis and treatment of intoxication with ethylene glycol, methanol and isopropanol.
Explore the source record for details and available documents.
Explore the source record for details and available documents.