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Total and ionized calcium decreased with increasing blood alcohol concentration in both alcoholics and nonalcoholics. Alcohol consumption caused no significant differences between alcoholics and nonalcoholics in plasma protein and ionized calcium but caused higher plasma phosphate levels in alcoholics.
All cases of criminal homicide in northern Sweden between 1970-81 were studied, 71 cases altogether (64 offenders). Homicide was a rare event and more infrequent compared with Sweden as a whole. The offenders were predominantly males, ages 20 to 40. Half of the victims were females. Mutual intoxication was a feature in 44% of the cases and in 34% both participants were sober. The majority of the victims were related by blood or marriage to the offender. Sharp instruments, blunt instruments and use of firearms were, in this order, the most common methods of killing. Almost one-third of the offenders had no former conviction, minor trespasses excluded. Sixty-three percent of the offenders had previously been subjected to psychiatric care, 31% were considered mentally diseased at the trial and another 22% had also a coexisting abuse or personality disorder. Three-quarters of the offenders were transferred to closed psychiatric care. Alcohol abuse and alcoholism were prevalent among 30% of the offenders and another 27% were also mentally diseased or had a personality disorder. The shares of mentally diseased and abusers/alcoholics outnumbered the prevalence of these conditions in the general population as well as in many international studies. Ten subjects committed suicide before trial; these persons were relatively more often sober at the act and fewer were alcoholics. Eight had previously received psychiatric treatment. They were more prone to kill a member of their nuclear family. Only two subjects had a previous criminal record; both concerned convictions of manslaughter. Nineteen offenders were sober at the act; 15 of these were mentally diseased. The sober offenders hardly ever attacked a person outside their family. Their motives were frequently premeditated. The killings were usually by quick, certain methods, such as firearms. No sober offender attacked an intoxicated person. The sober offenders usually had no criminal records and the homicides were often considered as murder. Five of the sober offenders committed suicide while the others were surrendered for closed psychiatric care in all but one case. Of the preventive measures, restrictions in the trade of alcohol are possibly the only factors that can reduce the homicide rate to any observable degree.
Alcohol dehydrogenase activity (ADH; KP 1.1.1.1.) in blood serum of rats and rabbits is 1 and 2 orders of magnitude higher than in humans. In chronic alcoholics, blood ADN is activated with an increase in alcoholism standing. Twelve hours after acute alcoholic intoxication alcoholics and heavy drinkers manifest a significant reduction in blood ADH activity. Acute alcoholic intoxication does not influence blood ADH in men who do not abuse alcohol. Chronic exposure of rabbits to ethanol leads to a decrease in ADH activity in the liver and to its rise in the blood. ADH activation is observed only in those animals which demonstrate the signs of fatty and protein liver dystrophy. It is concluded that chronic exposure to ethanol does not induce ADH synthesis in the liver. The blood ADH content ascends as a results of an increase in ADH transport from hepatocytes to the bloodstream.
Auditory brain stem evoked responses were in unrestrained rats during periods of acute and chronic alcohol intoxication, alcohol withdrawal, and recovery. Acute alcohol administration altered the auditory brain stem potentials by a prolongation of both peak latency and central conduction time, beginning with early peaks. Similar but lesser effects affecting only the latter peaks were observed during chronic alcohol intoxication. By contrast, alcohol withdrawal resulted in a decrease in the peak latencies of auditory brain stem potentials and a facilitation of central conduction time. Recovery of the auditory brain stem potentials to the normal form required at least three to four weeks. The present study provides the first quantitative data, to our knowledge, on manifestations of alcohol tolerance and withdrawal.
Alcohol's suppressive effects on polymorphonuclear leukocyte (PMN) production and function increases host susceptibility to a wide variety of infections and impairs the ability of these effector cells to seek and destroy invading pathogens. Granulocyte colony-stimulating factor (G-CSF), an important regulator of PMN production and function, is known to be increased in the plasma during infectious episodes. In previous studies we found acute alcohol intoxication to suppress the tumor necrosis factor-alpha (TNF alpha) response to in vivo challenges with bacteria or lipopolysaccharide. The present study was initiated to determine the impact of alcohol intoxication on the plasma G-CSF response to gram-negative infection. For this purpose, rats received an intravenous challenge of Escherichia coli (10(6) CFU) 30 min after an intraperitoneal injection of ethanol (5.5 g/kg) or an equivalent volume of saline (control). Ethanol-intoxicated rats had a greater 48 hr mortality to live E. coli injection than did unintoxicated animals (45% vs. 8%). Despite an increased bacterial burden in both the lung and liver at 24 hr after initiating E. coli infection in alcohol-intoxicated animals, PMN tissue recruitment, indexed as myeloperoxidase activity, did not differ between control and alcohol-treated rats. Moreover, alcohol suppressed blood PMN phagocytic capacity to a greater extent in animals given alcohol than controls at 5 and 24 hr after initiating infection. In control animals after intravenous E. coli injection, bioactive G-CSF increased in plasma and peaked near 300 ng/ml at 8 hr. In rats pretreated with alcohol, the plasma G-CSF response was markedly suppressed in response to intravenous E. coli (p < 0.05). In a second experiment, neutralization of the E. coli-induced plasma TNF alpha response by pretreatment with anti-TNF alpha antibody similarly inhibited the plasma G-CSF response. These results support the postulate that alcohol-induced inhibition of TNF alpha directly contributes to the adverse effects of alcohol on PMN function by suppressing the normal autocrine amplification pathway responsible for G-CSF production.
Alcohol was given to rats in a dose of 1 ml of 35-per-cent ethanol per 100 g body weight daily for 20, 40, 60, 90, and 120 days. Each period of the alcoholic intoxication was characterized by specific changes in the neurons, glia, and capillaries. Characteristic of initial periods of the alcoholic intoxication were reactive changes in the neurons: an important place in these changes belonged to compensatory-adaptive processes. The longer the period of the alcoholic intoxication, the greater the scope of the morphological changes, up to dystrophic lesions and grave forms of cell damage. A certain relationship between vascular changes and neuronal damages were noted.
Alcohol is used in most cultures despite knowledge of the physical, psychological and social problems associated with its abuse. Behavioural impairment is a function of several factors, including blood alcohol concentration (BAC) and the rate of alcohol metabolism by alcohol dehydrogenase and the microsomal ethanol-oxidizing system. Their availability and activity depend upon alcohol use history, ethnicity, other drug use and gender. Adverse social consequences related to alcohol intoxication include impaired driving, acts of aggression and violence towards self and others, and various types of accidents. About 40% of all fatal traffic accidents in Canada and the US in 1986-1987 were alcohol-related. Similar statistics have been reported in the UK and Europe (e.g. Sweden). The risk of a fatal car accident increases exponentially with a driver's BAC, prompting recommendations to lower the legal BAC limit for driving and piloting aircraft. Risks of falls, drownings, and fires and burns may also be increased by alcohol intoxication. At least 22% of work-related accidents may have involved alcohol use. These data are probably conservative estimates as under-reporting of alcohol use is likely. Alcohol facilitates aggressive behaviours, but it is difficult to separate the pharmacological effect from psychosocial effects or some other common factor (e.g. low CSF levels of the serotonin metabolite 5-H1AA have been reported in alcoholics, suicide attempters, violent offenders). In addition, alcohol interacts with other drugs to increase or decrease their behavioural and therapeutic effects. An acutely high BAC inhibits the metabolism of other CNS depressants (e.g. benzodiazepines), but long-term alcohol use increases the metabolism of most drugs. A potential amethystic agent, to block or reverse alcohol's effects, has been identified in preclinical studies (Ro15-4513, an imidazobenzodiazepine). Some clinical studies indicated that naloxone, lithium, ibuprofen, zimeldine and catecholamine agonists may reduce ethanol-induced behavioural or cognitive effects but the results have not been consistently replicated. More research is needed to determine the potential clinical use of amethystic agents and other pharmacotherapies in the prevention and treatment of problem behaviours associated with alcohol abuse and intoxication.
Alcohol abuse has long been suspected clinically to cause paroxysmal atrial tachyarrhythmias. However, such a relationship has never been conclusively proven, partly due to the lack of experimental evidence. Although atrial fibrillation (AF) is the most common atrial arrhythmia attributed to acute alcoholic ingestion, atrial flutter has occasionally been noted. We analyzed the possible role of alcohol in initiation and/or maintenance of a variety of atrial tachyarrhythmias in a closed-chest porcine model. Nine pigs underwent nine endocardial right atrial stimulation protocols (RASP) at baseline and 17 RASPs after increasing doses of ethanol (first infusion 1,230 mg/kg, second infusion 870 mg/kg) by means of one multipolar catheter advanced under heavy sedation from the femoral vein. Each RASP included 1, 2, and 3 extrastimuli, and rapid pacing at 5 times diastolic threshold. Venous ethanol concentrations were measured (HPGC method) every 10 minutes and at the time of arrhythmia induction. Atrial tachyarrhythmias were induced in 4 of 9 baseline RASPs, and lasted for a mean of 21 seconds, and in 16 of 17 RASPs after alcohol lasting for a mean of 357 seconds. Only fibrillation was observed at the baseline RASP. The atrial tachyarrhythmias induced after alcohol were AF in 11 RASPs and atrial flutter in 5 RASPs (in 5 animals). The mean venous ethanol concentration at the time of the longest arrhythmia induced for each RASP were 200 +/- 89 mg/dL for RASP inducing fibrillation and 292 +/- 40 mg/dL for RASP inducing flutter (P < 0.05). Flutter tended to be sustained (> 1 minute in duration) more often than fibrillation (4 of 5 flutter vs 2 of 11 fibrillation P < 0.05). In three experiments, atrial flutter persisted for > 10 minutes and was terminated by overdrive atrial pacing. We concluded: (1) in this closed-chest porcine model, an ethanol infusion facilitates a variety of atrial arrhythmias related to the ethanol concentration; (2) flutter tended to be sustained, and its termination by overdrive pacing suggests the possibility of an alcohol induced reentrant mechanism; and (3) the higher concentration required for atrial flutter, exceeding that usually seen in humans, may help to explain the rarity of atrial flutter in clinical alcohol intoxication.
Alcohol intoxication is the principal drug addiction in many countries of the world. It affects all age groups, both sexes and almost all social groups. Mortality associated with acute alcohol poisoning on its own is exceptional, but it can be an important factor if it coexists with recreational drugs. It is directly responsible for more than half of traffic accidents. Diagnosis is easy by means of anamnesis and clinical examination, and can be confirmed by determining the level of ethanol in the bloodstream. Supportive care is the best therapy in order to protect the patient from secondary complications. Methanol, or alcohol fuel, is used as a solvent, and can also be found as an adulterant of alcoholic drinks. Poisoning by oral means is the most frequent. Oxidized in the liver through dehydrogenase enzyme alcohol, toxicity is due to its metabolites, formaldehyde and formic acid. The clinical picture basically consists of cephalea, nausea, vomiting, hypotension and depression of the central nervous system. The optic nerve is especially sensitive, with total and irreversible blindness as a possible result. Ethylenglicol is used as a solvent and as an antifreeze; toxicity is due to an accumulation of its metabolites. The clinical picture includes symptoms that are held in common with methylalcohol intoxication. Kidney failure due to tubular necrosis and the deposit of oxalate crystals can occur.
80 alcoholic men and women registered for counseling at different Swedish outpatient units volunteered to complete semantic differential scales related to emotional expected effects of alcohol intoxication. Analyses indicated that alcoholics expect large doses of alcohol to increase pleasure, dominance, and arousal. These results were discussed in comparison with the results from previous related studies with nonalcoholic samples.
Alcohol is more often unpleasant and causes tissue damage more rapidly in women than men. The present study was designed to find out whether acetaldehyde, the primary metabolite of alcohol, could play a crucial role in these actions. Special emphasis was focused on the appropriate determination of blood acetaldehyde and hormonal factors. Occurrence of elevated blood acetaldehyde levels during alcohol oxidation was established in both normally cycling women and ones taking oral contraceptives, but not in men. An association between elevated acetaldehyde levels and high estrogen phases was observed in both groups of women. Estrogen-related acetaldehyde elevation is suggested to be the key factor explaining the gender differences of the adverse effects of alcohol.
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The conclusion is made about the permanent growth of the percentage of lethal cases connected with alcoholism, particularly in 1993. Among persons dying from alcoholism the percentage of young people and women is increased. Several unusual cases are described.
Ethanol blood levels are the result of alcohol absorption and the process of its distribution, metabolism and excretion. Kinetics are complex and not yet well known. They can be influenced by acquired factors (type of alcohol ingested, association with fasting or eating, induction or inhibition of ethanol metabolism) or by genetically determined differences in the activity of alcohol and of acetaldehyde dehydrogenase. The presence of ethanol in the organism leads to various consequences. On the one hand, hydropic changes on membranes modify their function and thus that of membrane proteins (particularly receptors); on the other, ethanol can affect neurotransmitter metabolism. Such modification of the major neurotransmitter systems (cholinergic, aminergic and GABA) in some cerebral regions explains the pharmacologic consequences of acute alcohol ingestion. In chronic alcohol dependence, adaptation phenomena occur, in both the membranes (increased rigidity) and the neurotransmitter systems. They are reflected by the hyperexcitability (catecholaminergic hyperactivity and GABA hypoactivity) observed after disappearance of the tranquilizing effect of ethanol and are clinically expressed by the withdrawal syndrome.