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At least 37 records · Page 2Linked to original sources
PubMed1978

[Adaptive changes in brain metabolism during chronic alcoholic intoxication].

Chronically alcoholized intoxication (1.5--2 months) induces adaptation of cerebral neurones to changing equilibrium states of biochemical processes by altering the activity of enzymes of GABA metabolism, reduction of alanine and aspartate transaminase activity and increase of LDH and succinate dehydrogenase activity. In the cerebellum and cerebral hemispheres during alcohol abstinacy the activity of GABA-T, succinate dehydrogenase and aspartate transaminase was reduced while that of LDH and alanine transaminase was increased. The administration of fusarinic acid (100 mg/kg i. p.) to control animals induced a sharp increase of GAD activity in both structures of the brain. The stimulatory effects of fusarinic acid were not observed when it was administered to animals receiving alcohol chronically. Motor activity or rats was markedly reduced during chronical alcoholism and the first days of alcohol abstinacy (24--48 h), as well as following injection fusarinic acid and homopantothenic acid. The increase of locomotion and the vertical component of motor activity was observed only following one week or one month after alcohol abstinacy.

4-Aminobutyrate Transaminase↗
PubMedDate not supplied

[Effect of chronic alcoholic intoxication on liver alcohol dehydrogenase activity in progeny].

Effect of chronic alcoholic poisoning on the activity of alcohol dehydrogenase (ADH) in the liver of rats was studied during ontogenesis. The activity of the enzyme was detectable for the first time in the fetal liver days 17-18 of the ontogenesis and reached the level seen in adult rats day 25 after the birth. ADH activity was dramatically increased in the liver of fetuses and progeny of females alcoholized before and during the entire pregnancy period as well as of females alcoholized before and during mating. Alcoholization of females before and over the first 15-16 days of pregnancy did not modulate the activity of liver ADH in the fetuses and progeny despite the fact that this activity in the mothers liver was 2.5 times as high as that in control.

Alcohol Oxidoreductases↗
PubMed1992

[Acute alcoholic intoxication--risk of complications].

Alcohol intoxication is the commonest cause of unconsciousness among patients admitted to hospital. Studies have shown that, of all acute admissions to medical wards, approximately 20 per cent are patients who are intoxicated or have alcohol-related damage. A study cited in the article showed patients in deep stupor generally to have a blood alcohol concentration above 70 mmol/l, and to be at increased risk of respiratory complications and aspiration of regurgitated stomach content. In cases of severe alcohol intoxication, treatment includes the following: freeing of the airways, perhaps combined with respiratory support; tracheobronchial lavage and aspiration, followed by antibiotic treatment; liberal parenteral thiamine administration; cramp, hypoglycaemia and muscle damage may require special measures; in the acute stage, cardiac arrhythmia usually normalizes without special antiarrhythmic treatment.

Alcohol Withdrawal Delirium↗
PubMedDate not supplied

[Study of the restoration and balance of thiamine in the tissues of albino mice in alcoholic intoxication].

Acute inhalative alcoholic intoxication has been studied for its effect on the influx and level of free and bound thiamine in tissues of white mice. It is established that acute inhalative ethanol intoxication increases 35S-thiamine incorporation in tissues and decreases the level of endogenic free and bound thiamine. The results obtained permit a conclusion on intensification of the thiamine renewal in tissues with its sufficient influx from outside as affected by the ethanol narcosis.

Alcoholic Intoxication↗
PubMedDate not supplied

[Phospholipids and free ethanolamine in the brain and liver of albino rats in alcoholic intoxication].

An experimental alcohol intoxication was accompanied by an increase in content of total phospholipids and phosphatide acid in rat brain with simultaneous decrease in content of free ethanolamine. The phenomenon demonstrate the activation of phosphatidogenesis. In the liver tissue an opposite alterations were observed; the lipolytic reactions were activated.

Alcoholic Intoxication↗
PubMedDate not supplied

[Arginase activity in various tissues of rats in alcohol intoxication].

Effects of acute and chronic alcohol intoxication on activities of arginase, alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (AcDH) were studied in rat liver, brain and kidney tissues. Alcohol intoxication altered both ureotelic (liver) and non-ureothelic (brain, kidney) arginase activity. The arginase activity in all the tissues studied was increased in chronic alcohol intoxication. Elevation in the arginase activity in liver tissue indicates that the urea cycle is activated as well as that hyperproduction of glutamic acid in brain may occur. Specific inhibitory effects of ethanol and acetaldehyde might be responsible for alterations of the arginase activity in all the tissues studied in acute alcohol intoxication. In vitro acetaldehyde at 5 X 10(-6) M concentration inhibited the arginase activity in partially purified preparations of brain and kidney tissues by 40-50% and of liver tissue--by 10-15%; 10% ethanol inhibited the liver enzyme by 90% and affected only slightly the activity of brain arginase.

Alcohol Dehydrogenase↗
PubMed1983

Acute isopropyl alcohol intoxication. Diagnosis and management.

Alcohol intoxication (methyl, ethyl, isopropyl, and ethylene glycol) is treated frequently in emergency room and intensive care units. Although high morbidity and mortality rates exist, effective therapies for methyl alcohol and ethylene glycol (ethyl alcohol blocking and hemodialysis) and ethyl and isopropyl alcohol (hemodialysis) are available. Prompt and accurate clinical and laboratory differentiation is needed to optimize these therapies. This review presents clinical, pharmacologic, and management data, contrasts important aspects in differential diagnosis, and suggests an appropriate approach to management of isopropyl alcohol intoxication.

1-Propanol↗
PubMed1990

The blood alcohol concentration at post-mortem in 175 fatal cases of alcohol intoxication.

The mean blood alcohol concentration (BAC) in 175 fatal cases of acute alcohol intoxication was found to be 355 mg/100 ml. This figure is less than that quoted in many standard textbooks on forensic medicine. The BAC in fatal cases of acute alcohol intoxication complicated by aspiration was lower than in those cases where there was no evidence of aspiration at autopsy. In those individuals with a previous history of alcohol abuse the BAC causing death was found to be significantly higher than in those without a history of prolonged heavy alcohol consumption suggesting that a degree of tolerance to the effects of alcohol may be induced.

Adult↗
PubMed1988

[Characteristics of the clinical picture and course of chronic alcoholic intoxication in patients with various types of neuroendocrine changes].

Clinical and hormonal indices of androgenic activity were compared in 118 males chronically intoxicated with alcohol. The population was divided into two groups with respect to their clinical and hormonal androgenic indices: 76 patients with (Group 1), and 46 patients without (Group 2) androgenic insufficiency. Distinct signs and syndromes of alcohol addiction were shown to correlate with the extent of cross-regulation impairment within hypothalamo-hypophyseo-gonadal system. This was particularly derived from comparison of clinical picture of chronic alcohol intoxication and hormone activity in the groups. Conventional therapy failed to restore the neuroendocrine indices that was apparently due to inhibition of cross-regulation links in the hypothalamo-hypophyseo-gonadal system at several stages of alcohol addiction.

Adult↗
PubMed1984

[Arrhythmia in relation to acute alcoholic intoxication in the absence of obvious cardiopathy].

Following acute intoxication with alcohol, 8 patients developed 16 episodes of arrhythmia, including 15 supraventricular tachycardias and one torsade de pointe. Seven of the 8 patients were chronically abusing of alcoholic drinks. None of the patients had clinically obvious cardiac pathology nor echocardiographic evidence of myocardiopathy. In 7 of them, however, baseline electrocardiograms disclosed disorders of intra-atrial conduction. The role of the different factors which might determine the occurrence of arrhythmia (notably alcohol, the autonomic nervous system, associated metabolic abnormalities and absorption of medicines) is discussed.

Adult↗
PubMed1982

Alcohol intoxication: a risk factor for primary subarachnoid hemorrhage.

We studied 172 consecutively presenting patients (88 men and 84 women; aged 15 to 55) with primary subarachnoid hemorrhage (SAH) verified by hemorrhagic CSF or at autopsy. In 37 (22%) of the patients, the onset of symptoms was preceded within 24 hours by alcohol intoxication. Alcohol intoxication preceding SAH was two to three times as common in men and two to thirteen times as common in women as alcohol intoxication in the general Finnish population of the same age and sex. Thirty-two (19%) of the patients were heavy drinkers. Heavy drinking was twice as common in men and seven times as common in women as heavy drinking in the general Finnish population of the same age and sex. Both occasional ethanol intoxication and regular heavy drinking seem to carry an increased risk of SAH.

Adolescent↗
PubMed1983

Acute alcohol intoxication, mood states and alcohol metabolism in women and men.

The course of alcohol absorption and elimination was investigated in seven women and nine men administered a moderate (0.66 ml/kg) dose of 95% ethanol. Women were tested during the postmenstrual phase (Day 6-7), when levels of estrogen and progesterone were estimated to be relatively low. Data reflecting alterations in physical sensations, perceived levels of intoxication, and positive and negative mood states were also collected. Women reached significantly higher peak blood alcohol concentrations (BAC's) than men (p less than 0.01). However, differences in peak BAC's between men and women could be explained by differences in body water content between the sexes. When the raw data on BAC's were corrected for differences in body water content between men and women, no difference in the amount of alcohol metabolized, or in the length of time necessary to metabolize that amount of alcohol, could be found between the sexes. Although women attained higher blood and, presumably, brain levels of ethanol, men did not differ from women in perceived levels of intoxication, physical sensations and mood states. Acute alcohol intoxication appeared to elevate positive mood states during the ascending limb of the BAC curve, but was associated with increased negative affect during the descending limb.

Adult↗
PubMed1986

Hyperamylasemia following methyl alcohol intoxication. Source and significance.

Methyl alcohol intoxication has been reported to cause hyperamylasemia and pancreatitis. We describe a patient with severe, nonfatal methyl alcohol intoxication who had a rise in serum amylase activity with the level peaked on the second hospital day at tenfold the upper limit of normal. However, isoamylase analysis showed that this striking hyperamylasemia was due to salivary-type amylase. Furthermore, the serum lipase activity remained entirely normal during the peak amylase elevation. Thus, in cases of methyl alcohol intoxication, as in other clinical situations, hyperamylasemia, even when striking, should not be equated with pancreatitis. More specific laboratory tests for pancreatitis should be used before embarking on extensive investigations of the pancreas.

Acute Disease↗