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At least 235 records · Page 13Linked to original sources
PubMed1999

Effect of alcohol intoxication on hemodynamic physiology and outcome in patients with traumatic cardiac tamponade.

BACKGROUND: Alcohol intoxication has a detrimental effect on hypovolemic shock. Our aim, was to study its effects on "pure" cardiac tamponade (i.e., without hypovolemia) in patients with penetrating chest injuries. METHODS: Thirty-five intoxicated and 15 nonintoxicated patients (blood alcohol > and < 17 mmol/L) were studied. Initial vital signs (trauma scores), special investigations (hematologic profiles, blood gases, glucose, lactate, and catecholamines), clinical progress (24- and 72-hour acute physiology and chronic health evaluation II scores) and outcome were compared. RESULTS: Intoxicated patients were older (p = 0.02) and more tachypneic on admission (p = 0.006), but no other differences were noted. Mortality was proportional to the degree of shock and was greater in patients who had "front-room" thoracotomies (p < 0.001). Despite the higher percentage of intoxicated patients who were "lifeless" or "in extremis" on admission, they fared no worse than nonintoxicated patients. CONCLUSION: Alcohol intoxication does not have an adverse affect on traumatic cardiac tamponade.

APACHE↗
PubMedDate not supplied

[Correction with formate of metabolic disorders in alcoholic intoxication].

Formate was studied for its effect on the content of acetaldehyde, activity of the total aldehyde dehydrogenase, content of substrates of glycolysis and tricarbonic-cycle and pool of free amino acids of rat tissues during alcohol intoxication. The introduction of formate during the acute alcohol intoxication lowers the acetaldehyde content in the blood; the ethanol load being prolonged--it increases the activity of aldehyde dehydrogenase and normalizes the content of pyruvate, glutamate and malate in the liver and glutamate and oxaloacetate in the brain, that evidences for the correction of metabolic disturbances in the organism.

Acetaldehyde↗
PubMed1975

A mechanism for decreased resistance to infection by gram-negative organisms during acute alcoholic intoxication.

The propensity of alcoholics to develop infections with gram-negative bacteria is well known. However, the known effects of ethanol on host-defense mechanisms do not explain this tendency satisfactorily. Since the principal defense mechanism against gram-negative bacteria is their destruction by complement in the presence of specific antibody, we investigated the effect of acute ethanol intoxication on serum complement concentrations and correlated these with serum bactericidal activity against a gram-negative organism. Serial measurements of total hemolytic complement (CH5O) and C'3, ethanol concentration, and serum bactericidal capacity were performed on the serum of 7 dogs infused with a 10 per cent ethanol solution. All animals showed a substantial decrease in total hemolytic complement activity which was inversely related to the increase in serum ethanol concentration. A decrease in serum bactericidal activity correlated with the decrease in CH50. Control animals showed no variation in either CH50 or serum bactericidal activity. Immunoprecipitation studies, using antibody to dog C'3, indicated that serum concentrations of this protein were not altered by infusing the animals with ethanol. Incubation of serum in vitro with both ethanol and acetaldehyde had no effect on CH50. We conclude that the effect of ethanol on serum complement is an in vivo phenomenon probably relating to decrease in the synthesis of one or more of the components of complement other than C'3, although the formation of an anticomplementary substance cannot be excluded. These findings are presented as a possible explanation for the development of infections with gram-negative bacteria in ethanol-intoxicated subjects.

Acetaldehyde↗
PubMed1981

Does alcohol intoxication precipitate aneurysmal subarachnoid haemorrhage?

Seventy-five consecutive patients aged 15 to 55 years with aneurysmal subarachnoid haemorrhage verified by CSF examination and cerebral angiography or at necropsy were studied. In 19 cases (25%; four women and 15 men) the bleeding was preceded within 24 hours by a bout of alcohol drinking. Alcohol-related cases composed 33% and 14% of the patients in the age groups 15-40 and 41-55 years, respectively. Alcohol intoxication preceding the subarachnoid haemorrhage was two to four times as common in male and three to five times as common in female patients as alcohol intoxication in the general Finnish population of the same age and sex. Occasional alcohol intoxication seems to carry an increased risk of aneurysmal subarachnoid haemorrhage.

Adolescent↗
PubMed1992

[Multiple cerebral embolism in acute alcoholic intoxication. A pathological case].

A 37 year-old man sustained 2 ischemic strokes during acute alcohol intoxication. One month after the onset of strokes, a spontaneous atrial flutter occurred. Autopsy revealed an embolic rostral occlusion of the basilar artery. Cardiac verification did not show myocardiopathy or coronary disease. The relations between acute alcoholic intoxication and paroxystic cardiac rhythm disorders are discussed.

Adult↗
PubMed1998

In vivo association between alcohol intoxication, aggression, and serotonin transporter availability in nonhuman primates.

OBJECTIVE: Studies on brain serotonin metabolism in human and nonhuman primates have indicated that dysfunction of serotonin transmission may play a role in the biological vulnerability to dependence on alcohol. Among young men, low sensitivity to alcohol intoxication predicts subsequent alcohol abuse and dependence. METHOD: The authors used single photon emission computed tomography and the radioligand [(I)123]beta-CIT ([(I)123]methyl 3beta-(4-iodophenyl) tropane-2-carboxylate) to measure the availability of serotonin transporters in 11 male rhesus monkeys, and the monkeys were genotyped for a functional polymorphism of the serotonin transporter gene. The 11 monkeys had experienced parental separation after birth; their behavior and 5-hydroxyindoleacetic acid (5-HIAA) concentrations in CSF had been assessed regularly. RESULTS: In the 5-year-old monkeys, there was a significant negative correlation between beta-CIT binding to serotonin transporters in the brainstem and 5-HIAA concentrations in CSF. Animals with greater beta-CIT binding and low CSF 5-HIAA concentrations displayed greater aggressiveness and were less sensitive to alcohol-induced intoxication. The genetic constitution of the serotonin transporter promoter gene did not significantly contribute to the availability of brainstem serotonin transporters as measured by beta-CIT binding. CONCLUSIONS: In adult nonhuman primates who underwent early developmental stress, variables indicating a low serotonin turnover rate were associated with behavior patterns similar to those predisposing to early-onset alcoholism among humans.

Adult↗
PubMed1989

[Morphofunctional changes of the neurosecretory system and microcirculatory bed of the hypothalamus in patients with chronic alcoholic intoxication of varying degree].

Microcirculation was studied in the hypothalamus in acute alcohol intoxication. Blood flow was sharply decelerated with capillaries paretically dilated, overfilled with blood. Stasis, sludge formation and venue microthrombosis were directly related to the alcohol concentration in blood and urine. In neurosecretion areas the hemorrhagic sites were detected with neurosecretory cells activity sharply reduced. Chronical alcohol administration increased the number of functionally inactivated capillaries. These with luminal vesiculation were also found as were lymphoid cell infiltrates in venule walls. The number of capillaries inactivated in the neurosecretory system paralleled the number of dark cells that reflected the inhibition effects.

Adult↗
PubMedDate not supplied

[Histomorphometric characteristic of human brain in acute alcoholic intoxication].

Different brain sections were studied in 20 subjects, who died of ethanol intoxication and in 14 subjects who died of injuries of the heart and main vessels, in order to detect histological changes in the brain and for the purpose of defining spatial and quantitative ratios between cerebral tissue structures in alcoholic intoxication. Different histological, stereometric and morphometric tools were made use of. It was demonstrated that, in alcoholic intoxication, there occur severe disorders of the circulation with affection of vessels in the brain; there are also dystrophic and necrotic changes in neurocytes, glial cells and white substance. The square of neurons shrinks due to death of some of them in the cortex of hemispheres, thalamus and cerebellum. As for the medulla, they are more resistant, there, to ethanol. The diameter of capillaries in the studied brain sections diminishes due to a reduced tonus of cerebral arteries; the quantity of such vessels increases within a standard area, which is conditioned by the compensatory opening of reserve capillaries. All this can be important in dealing with issues of thanatogenesis and of forensic medical diagnosis in death of alcoholic intoxication.

Acute Disease↗
PubMed2002

[Development of a porcine experimental model of alcoholic intoxication].

Despite important epidemiologic suggestions that alcohol causes a variety of cardiovascular abnormalitíes, and particularly cardiac arrhythmias, the demonstration of this causal effect in animal models is still lacking. Previous open-chest models, heavily instrumented and using epicardial stimulation have failed to demonstrate such causal effect. We developed a porcine, closed-chest model with sedation, a rigorous control of venous alcohol concentration and endocardial electrical stimulation, in a multidisciplinary framework. In this model, we observed that the infusion of alcohol facilitated atrial tachyarrhythmias. This model is available to study a variety of alcohol effects "in vivo", in a controlled fashion.

Adolescent↗
PubMedDate not supplied

Efficacy of metadoxine in the management of acute alcohol intoxication.

This randomized, open-label study evaluated the efficacy of 300 mg metadoxine (given intravenously) added to standard treatment compared with standard treatment alone in managing the physical and psychological signs of acute alcohol intoxication. Fifty-two acutely intoxicated patients were randomly assigned to one of two groups and followed during a 2-h period. Changes in clinical symptoms, degree of intoxication, and blood alcohol level were monitored. More patients receiving metadoxine in addition to standard therapy significantly improved by at least one degree of intoxication (one clinical category) compared with those receiving standard treatment alone (76.9% versus 42.3%, respectively). Metadoxine-treated patients also exhibited a significantly greater decrease in blood alcohol concentration compared with those receiving standard treatment alone (-105.4 +/- 61.5 mg/dl versus -60.1 +/- 38.6 mg/dl, respectively). Metadoxine improved the clinical signs of acute alcohol intoxication and accelerated alcohol clearance from the blood, thus supporting existing data. In contrast to previous data, these effects were concurrent but independent. No adverse effects were observed with metadoxine therapy.

Adult↗
PubMed1995

Alcohol intoxication in young children.

This article presents two cases of severe ethyl alcohol intoxication in pediatric patients, with one of these cases resulting in the death of a child. A review of the current literature is provided along with a comparison of our regional poison control centers and the national intoxication statistics regarding pediatric alcohol ingestion. Medical evaluation is recommended for all symptomatic children; hourly observations x 6 h are recommended for asymptomatic children.

Alcoholic Intoxication↗
PubMedDate not supplied

[The use of vitamins A and E for the correction of immunologic disorders in chronic alcoholic intoxication].

In experiments on BALB/c mice it has been shown that in chronic alcoholic intoxication the immune response to sheep red blood cells is drastically suppressed. Oral administration of vitamin A or E oil solution in doses 3000 and 5 IU/day, respectively, during 3 days, led to correction of the immune response to sheep red blood cells disordered as a result of alcoholic intoxication.

Alcoholism↗
PubMedDate not supplied

[Concentration of lipids and apolipoproteins A-1 and E in blood plasma of men with acute alcohol intoxication].

Content of lipids and apolipoproteins A-1 and E was studied in blood plasma of men with acute alcohol intoxication as well as within 10-12 hrs after their treatment in a special clinic. Acute alcohol intoxication caused a distinct increase of triglycerides as well as of cholesterol in high and very low density lipoproteins simultaneously with decrease in content of cholesterol in low density lipoproteins. At the same time, content of apolipoprotein A-1 was increased and of apo E--unaltered. Within 12 hrs after treatment of the men concentrations of triglycerides and cholesterol of very low density lipoproteins became quite normal but the other patterns studied did not alter. Alcohol appears to affect the distribution of cholesterol between individual lipoprotein fractions in blood. This process depended distinctly on alteration of apo A-1 concentration in blood plasma.

Adult↗
PubMedDate not supplied

[The ultrastructural indices of the morphofunctional state of the heart in acute and chronic alcoholic intoxication].

Morphofunctional myocardial characteristics in subjects who died of acute and chronic alcoholic intoxication were studied at ultrastructural level. The resulting new data enhance the level of diagnosis concerning the cause of death, the grounds of thanatogenesis. Possibilities for using the results of investigation in scientific and practical work are shown.

Adult↗
PubMed1995

Provocation, acute alcohol intoxication, cognitive performance, and aggression.

This study investigated the relationships between provocation, acute alcohol intoxication, impaired frontal-lobe function, and aggressive behavior. The authors ranked 114 men according to their performance on two neuropsychological tests associated with frontal-lobe function. Forty-eight men (24 with scores in the upper and 24 with scores in the lower performance quartiles) participated in the full study. Half completed and aggression task while intoxicated, the remainder while sober. Aggression was defined as shock intensity delivered to a sham opponent. Shock intensity significantly increased as a main effect of provocation, alcohol intoxication, and lower cognitive performance. Furthermore, provocation interacted significantly with test performance such that individuals in the lower cognitive performance quartile responded to increased provocation with heightened aggression.

Adolescent↗
PubMed1993

[Acute alcoholic intoxication and drugs].

Acute alcohol ingestion can induce drug interactions, either pharmacokinetic or pharmacodynamic. Metabolically, they especially result from interference in the enzymatic systems which catalyse ethanol oxidation, the blocking of alcohol dehydrogenase, blocking of the microsomal oxidation system of ethanol with accumulation of the xenobiotic and risk of overdose, and blocking of acetaldehyde dehydrogenase with an antabuse effect. Pharmacodynamically, the main interactions result from the action of drugs having a sedative effect, such as tranquilizers but also antidepressants, neuroleptics, analgesics, H1 antihistamines, central antihypertensive drugs (CNS depressant?), etc. This sedative effect is increased by ethanol, which can be dangerous in at-risk situations.

Alcoholic Intoxication↗
PubMed2002

Immediate S-100B and neuron-specific enolase plasma measurements for rapid evaluation of primary brain damage in alcohol-intoxicated, minor head-injured patients.

The neuroproteins S-100B and neuron-specific enolase (NSE) released into the circulation are suggested to be reliable markers for primary brain damage. However, safe identification of relevant post-traumatic complications after minor head injury (MHI) is often hampered by acute intoxication of the patients. The objective of this study was to determine the diagnostic validity of immediate plasma measurements of S-100B and NSE in comparison with neurological examinations and cerebral computed tomography (CCT) findings in alcohol-intoxicated MHI patients. One hundered thrity-nine MHI individuals were enrolled in this prospective study during Munich's Oktoberfest 2000. Plasma levels of S-100B and NSE as well as serum alcohol and glucose values were determined by fully automated assays immediately after admission. The results were compared with Glasgow Coma Scale score, a brief neurological examination, and the CCT findings. Without being influenced by alcohol, median S-100B levels of the CCT+ group were significantly increased compared with those of the CCT- group (P < 0.001). NSE, alcohol, and glucose levels showed no significant group differences. As calculated by the ROC analysis, a cutoff value of 0.21 ng/mL with an area under the curve of 0.864 clearly differentiates between CCT+ and CCT- patients at a sensitivity of 100%, a specificity of 50.0%, and a positive likelihood ratio of 2.0. Although acute alcohol intoxication did not confound plasma measurements of S-100B and NSE, only S-100B levels below the cutoff level of 0.21 ng/mL seem to indicate absence of primary brain damage. Thus, in addition to routine neurological examinations, S-100B measurements immediately after admission might help to reduce CCT scans in alcohol-intoxicated patients early after MHI.

Adult↗