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Ocular manifestations and complications of acute methyl alcohol intoxication.

The ocular manifestations of acute methyl alcohol intoxication were studied in 24 men during an outbreak in Port Moresby, Papua New Guinea. The visual acuity, pupillary reactions to light, fundal appearances and visual fields were recorded in all patients within 72 hours of ingestion of methanol and again three months later. Three groups were identified. Nine patients had no ocular abnormality (Group 1). Seven patients had only transient ocular abnormalities (Group 2). Eight patients had permanent ocular abnormalities (Group 3). Transient abnormalities included peripapillary oedema, optic disc hyperaemia, diminished pupillary reactions to light, and central scotomata. Permanent ocular abnormalities included optic disc pallor, attenuation of arterioles, sheathing of arterioles, diminished pupillary reaction to light, diminished visual acuity, central scotomata, and other nerve fibre bundle defects. Complete blindness occurred in two patients, while severe visula deficit resulted in four others. The incidence of permanent ocular abnormalities was found to correlate with the incidence of metabolic acidosis (P less than 0.01), and with the stated volume of methanol consumed (P less than 0.05). An inverse correlation was found between stated volume of methanol consumed and onset of blurred vision. The difficulties in management and rehabilitation of these patients are discussed.

Adaptation, Ocular↗

[The irrefutable benefits of courses for alcohol intoxicated drivers].

The benefit of courses for alcohol conspicuous drivers, as it is shown by Winkler et al. in a careful and clear manner, still is to be considered as not refuted so far. The participants in courses (experimental group), who according to their situation were supposed to have a substantial higher rate of recidivism, had an actual recidivism-rate, which was significantly lower than the rate of the control group. Interpreting the present scientific literature correctly, Hundhausen's (1989) five main arguments against the results of Winkler et al., which all his further conclusions depend on, are not right.

Accidents, Traffic↗

The respiratory aspect of the treatment of brain injury associated with acute alcohol intoxication--results of an animal experiment.

The effects of spontaneous respiration and mechanical ventilation were examined by investigating the interaction between elevated intracranial pressure and alcohol intoxication. Ethanol (200 ml 48%) was infused in 11 young pigs with elevated cerebral pressure during mechanical ventilation (group 1), 7 young pigs with elevated cerebral pressure during spontaneous respiration (group 2), and 4 young pigs without elevated cerebral pressure during spontaneous respiration (group 3). While the behavior of intracranial pressure during mechanical ventilation in the animals from group 1 was inhomogeneous with a tendency to rise (29-34 mmHg), cerebral pressure (28-55 mmHg) increased drastically in the animals from group 2. This increase was associated with a sharp rise of Pa,CO2 (37.6-73.3 mmHg) and a decrease of Pa,O2 (74 mmHg to 13 mmHg). None of the animals in group 2 survived. Pa,CO2 also rose in alcoholized animals without elevated cerebral pressure (group 3) (41.9-63.9 mmHg); intracranial pressure, however, remained within the normal range. All animals in group 3 survived. Our findings indicate that elevated intracranial pressure and alcohol intoxication have a cumulative or potentiating effect on depression of the respiratory center. Respiratory depression can be prevented by mechanical ventilation and, therefore, a further rise of intracranial pressure generally avoided.

Alcoholic Intoxication↗

[Cardioprotective effect of GABA derivatives in acute alcohol intoxication].

Cardioprotective properties of GABA analogs under conditions of acute alcoholic intoxication have been studied using the following functional tests: volume loads, tests for adrenoreactivity, and maximum isometric load. The experiments showed that a 32% aqueous ethanol solution intraperitoneally injected in a dose of 8 g/kg produces a cardiotoxic action, which is manifested by a decrease in the inotropic reserve in load tests. Citrocard (50 mg/kg), phenibut (50 mg/kg), and piracetam (200 mg/kg) prevent the alcohol-induced myocardium injury, as shown by the heart contractility retained on a higher level in the test group than in the control group.

Acute Disease↗

[Interorgan relationships in alcoholic intoxication].

It is suggested, on the basis of 315 necropsies of patients who died of drunkenness and alcoholism and examination of 300 rats with acute and chronic alcoholic intoxication, to distinguish an "alcoholic disease" as a separate nosological entity. The stages of this disease are drunkenness, alcoholism and alcoholic abstinence syndrome. Multiple organ pathology is characteristic for the disease with obligatory microangiopathy, alcoholic encephalo-, cardiomyo- and hepatopathy. The development of the disease follows a principle of vitium cordis at which the changes in certain organs result in the progression of pathological lesions in other organs. The course of the disease is characterized by periods of remission and exacerbation provoked either by a regular alcohol consumption or by an alcoholic abstinence syndrome. Toxic effects of alcohol, acetaldehyde and catecholamines are main factors in the pathogenesis of lesions in various organs.

Alcoholic Intoxication↗

[Content of hydroperoxides in lipids, superoxide dismutase and glucose-6-phosphate dehydrogenase activity of erythrocytes in alcoholic intoxication].

Content of lipid hydroperoxides was studied in erythrocytes of rats after single and chronic administration of alcohol within 7, 15, 30 and 60 days at a dose of 6 g/kg. Simultaneously, activity of superoxide dismutase as well as activity and kinetic patterns of glucose-6-phosphate dehydrogenase were studied. Phase alterations in content of peroxides and in the enzymatic activity were shown to depend on duration of alcohol intoxication. Inhibition of the enzymatic activity of the mixed type was the cause of a decrease in the glucose-6-phosphate dehydrogenase activity in erythrocytes.

Alcoholic Intoxication↗

Comparative effects of thiopental and propofol on atrial vulnerability: electrophysiological study in a porcine model including acute alcoholic intoxication.

BACKGROUND: Atrial tachyarrhythmias (AT) frequently complicate the perioperative period. Alcohol intoxication is a recognized causative factor for dysrrhythmias. We studied the effects of propofol and thiopental on atrial electrophysiology and vulnerability to AT in a closed-chest porcine model in which AT are facilitated by ethanol. METHODS: Thirty-eight pigs were randomly assigned to thiopental (T-group, n=19) or propofol (P-group n=19). All animals were assigned to undergo a right atrial electrical stimulation protocol (RASP) at baseline. Thirty pigs were assigned to undergo additional RASP during ethanol infusion, while the remaining eight were assigned to undergo additional RASP during saline infusion (control group). We analysed effective refractory period (ERP), and intra-atrial conduction interval (ICI) (between atrial sites 4 cm apart), at several cycle lengths (CL). RESULTS: There were no significant differences at baseline. During ethanol infusion, propofol produced a greater rate-dependent decrease in excitability, manifested by a longer minimum paced CL with 1:1 atrial capture: 145 (11) vs 164 (27) ms in the T- and P-group, respectively (P=0.01). Propofol was associated with a greater rate-related slowing in conduction: difference between ICI at CL of 300 ms and ICI at minimum CL: 30 ms in P-group and 22 ms in T-group (P<0.03). In the P-group we observed a longer duration of induced arrhythmias (145 (131) vs 74 (91) s, P<0.03) and a higher proportion with atrial flutter (AFl) (76 vs 19%, P<0.001). CONCLUSIONS: Propofol in this model was more arrhythmogenic than thiopental, as manifested by a longer duration of induced arrhythmias, particularly AFI.

Alcoholic Intoxication↗

[Homicidal alcoholic intoxation versus manual neck compression].

A case of homicide involving a 49-year-old man is reported. In the course of a booze-up he was forced to excessive consumption of alcohol and was pushed back into a sofa by repeated grasping his neck which finally left him dead. The postmortem examination revealed a small abrasion in the right mandibular region, a contusion of the subcutaneous tissue above the left clavicle, a haemorrhage in the deep muscles of the neck at the right side of the cervical spine, a fatty tissue haemorrhage between the left cornus of hyoid and thyroid cartilage as well as petechiae of the eyelids and conjunctivae. The blood alcohol concentration amounted to 4.00@1000, the urine alcohol concentration to 5.26@1000. Thus, a manual strangulation of the neck versus a lethal alcohol intoxication had to be taken into consideration as cause of death. The morphological findings of the postmortem examination and the pathophysiological concepts of the underlying mechanisms of death in manual strangulation versus lethal alcohol intoxication are discussed with regard to their significance for the juridical assessment.

Alcoholic Intoxication↗

[Effect of alcoholic intoxication on the lymphatic bed of the heart].

Cardiac lymphatic bed was studied in 120 male corpses at the age of 17--55 years, normal and of those died from alcohol intoxication and from cardiac ischemia. The methods of intratissue injection of coloured masses, impregnation after V. V. Kuprianov, histological and histochemical investigations were applied. Data in figures were obtained by means of a grid for cyto-, histo- and stereometric investigations and by a scanning integrant microspectrophotometer sim-2. Statistical data were obtained by a computer "Mir". It was demonstrated that the cardiac lymphatic system responds in a definite way to alcohol intoxication. Four forms of structural state in the lymphatic bed elements were revealed, specific density of its different components was calculated. A certain connection was noted to occur between morphological changes under the effect of toxic doses of alcohol; there was also a reaction of compensatory-adaptive elements of lymphodynamics. A number of pathological changes in cardiac tissues resulting in heart insufficiency were presented. Peculiarities in poisoning phases were demonstrated morphologically.

Adult↗

[Ultrastructure of the cerebral cortex of the rat during noise stress and alcoholic intoxication].

Ultrastructure of the rat sensomotor and acoustic cortex has been studied at a separate and joined effect of noise and alcoholic intoxication during 7 and 35 days. Certain changes in vessels, neural and glial cells specific for separate effect of noise and alcohol have been revealed. Combined application of noise and alcohol results in a more profound disorders in the cerebral vessels, with predominance of changes specific for alcoholic intoxication. Simultaneous decrease of the ultrastructural changes, peculiar for the separate effect of noise is explained as a decreasing functional loading on the cortical cells resulted from blocking synapses with alcohol.

Alcoholism↗

[Role of phospholipids in changes in lysosomal membrane stability in conditions of chronic alcoholic intoxication].

Pronounced destabilization of liver lysosomal membranes has been revealed in rats in conditions of 30-day-long alcohol intoxication. Noticeable fractional changes in phospholipid composition of lysosomal membranes have been found. Significant increase in lysophosphatidylethanolamine and lysophosphatidylcholine levels have been observed. Type A2 phospholipase activity was found in lysosomal fractions, with the enzyme activity Ca2+-dependent, optimal at pH 8 and increasing many-fold following alcohol intoxication. The changes in lysosomal membrane phospholipids appear to be related to phospholipase A2 activation.

Alcoholism↗

Effect of cold water immersion and its combination with alcohol intoxication on urine flow rate of man.

Urine flow rate was determined for man before and after immersion in either thermoneutral (33 degrees C) or cold (10 degrees C) water. The effect of alcohol intoxication of a level of approximately 80 mg dL-1 was also evaluated for the cold water immersion. Immersion and cold were additive in their effect, resulting in a mean urine flow rate of 4.25 mL min-1, approximately 3.5 times the preimmersion level. Alcohol intoxication in conjunction with cold water immersion caused a further large increase in urine flow to 8.03 mL min-1. These results permit better evaluation of the importance of volume diuresis as it relates to the reduction of insulative performance of dry-type immersion suits for cold water survival, and to the possible enhancement of "rewarming shock" during therapy for hypothermia victims. The increased urine production observed when alcohol treatment was added to cold immersion provides information for speculation on mechanisms of volume diuresis.

Adult↗

Disruption of maternal behavior by alcohol intoxication in the lactating rat: a behavioral and metabolic analysis.

BACKGROUND: Preweanling rats exhibit clear behavioral signs of distress after interacting with an alcohol-intoxicated dam. Interestingly, behavioral reactivity of infants to the experience of alcohol in the nursing context decreases as a function of repeated alcohol administrations to the mother. In this study, maternal activities were examined when dams were exposed to repeated administrations of a subnarcoleptic alcohol dose. Maternal changes in alcohol metabolism were also analyzed as a function of repeated exposures to the drug. METHODS: During postpartum days 3, 5, 7, 9, 11, and 13, nursing dams received an intragastric administration of either 2.5 g/kg of alcohol or water. Maternal behaviors were evaluated (experiment 1). Blood alcohol levels (BALs) of the dams were determined on postpartum day 16 after all mothers received either an intragastric (experiment 2) or an intraperitoneal (experiment 3) dose of alcohol. The doses used (2.5 g/kg intragastrically and 1.5 g/kg intraperitoneally) were chosen because they promote similar peak BALs in dams naive to alcohol. RESULTS: Maternal behaviors were strongly affected by the state of intoxication. Nevertheless, these disruptions clearly subsided with progression of alcohol-related experiences (experiment 1). Chromatographic analysis of alcohol metabolism indicated the development of tolerance in dams that had prior experience with alcohol (experiment 2). Changes in BALs as a function of prior experience with alcohol seemed related to first-pass alcohol metabolism rather than hepatic oxidative processes of the drug (experiments 2 and 3). CONCLUSIONS: When the dam first experiences a moderate state of alcohol intoxication, maternal behaviors are uniformly disrupted. Subsequent exposures to alcohol lead to maternal metabolic tolerance. In conjunction with previous studies, these data indicate that infantile reactivity to alcohol is dependent on how the members of the dam/pup dyad express or perceive ethanol's postabsorptive effects.

Alcoholic Intoxication↗

[Alcohol intoxication via the lung in rats].

1. The technique of chronic alcohol intoxication by inhalation of alcohol vapor was developed in rats. 2. The blood alcohol level value of rats staying in an alcohol-containing atmosphere increases (from 0 to 4 mg/l) in terms of the atmospheric alcohol level (from 0 to 20 mg/l). 3. The mean blood alcohol level of a group of animals maintained during 20 days in an atmosphere containing 15 mg/l of air, increases regularly during 7 days, and then decreases slowly. 4. Animals that are staying in an atmosphere with a regularly increasing alcohol level can breathe an air containing 20 mg/l of alcohol. This dose is early lethal when used in other animals from the beginning of treatment, what confirms the metabolic tolerance. 5. Withdrawal signs characterized by a central nervous system hyperexcitability are shown by animals which had a high blood alcohol level during 4 or 5 days, when they are back into the ambient atmosphere.

Animals↗

[Diagnostic implication of blood and urine morphine content in alcohol intoxication].

A total of 198 cases of acute parenteral poisoning with opiates are characterized. The range of concentrations of opiates metabolites in the blood and urine, main causes of death due to opiate poisoning in alcohol intoxication are analysed. Opiates toxicity was assessed with the logit-regression method and dose-effect curves valid for analysis of relationships between probability of death and opiate metabolites concentration in blood and urine. Correlation between probability of death and detection of morphine and ethanol in biological media of the victims is considered. Concentrations of morphine in blood and urine definitely indicating opiates poisoning in alcohol intoxication as a cause of death are determined.

Alcoholic Intoxication↗

[Chondrodysplasia punctata and maternal alcohol intoxication. Apropos of 7 cases].

The authors report 7 cases of chondrodysplasia punctata in whom maternal alcohol intoxication was found. Most often, it consisted of chronic and confirmed alcoholism, except for the last case, in which an acute intoxication had occurred at about the 4th or 5th week of pregnancy. Clinically, the appearance of the children was evocative of fetal alcohol syndrome, except in the last case when, in contrast, the facial dysmorphy was very typical of chondrodysplasia punctata. The skeletal anomalies preferentially involve the lower limbs, sometimes the sacrum, and in one single case, the dorsal spine. Upper limbs are always spared. The maternal hepatic lesions may be responsible for the skeletal impairment, due to their repercussion on the metabolism of vitamin K. This skeletal impairment would then be close to that induced by treatments with warfarin during pregnancy. Whatever, it is absolutely necessary to X-ray the lower limbs in cases with fetal alcohol syndrome, in order to not overlook associated bone lesions.

Adult↗