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Results for “Alcoholic Intoxication”

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PubMedDate not supplied

Hypoparathyroidism in chronic alcohol intoxication: a preliminary report.

It is well known that osteoporosis is more common in chronic alcoholists than in age-matched controls. Possible aetiological factors could be: malabsorption of calcium and vitamin D, liver disease, abnormal parathyroid function. With this study, the authors investigated parathyroid hormone (PTH) behaviour in thirteen selected patients with alcohol abuse, free from any clinical or humoral sign of hepatopathy, and in ten healthy subjects as a control group. In alcohol abusers a significant reduction of plasmatic PTH, compared to normal calcium levels were found. A possible direct interaction effect between ethyl alcohol and PTH may be suggested, even if further studies are required.

Adult↗
PubMed1999

Hepatoprotective activity of leaves of Cassia occidentalis against paracetamol and ethyl alcohol intoxication in rats.

Cassia occidentalis L. (Caesalpiniaceae), commonly known as 'Kasondi', is used in Unani medicine for liver ailments and is an important ingredient of several polyherbal formulations marketed for liver diseases. The hepatoprotective effect of aqueous-ethanolic extract (50%, v/v) of leaves of kasondi was studied on rat liver damage induced by paracetamol and ethyl alcohol by monitoring serum transaminase (aspartate amino transferase and serum alanine amino transferase), alkaline posphatase, serum cholesterol, serum total lipids and histopathological alterations. The extract of leaves of the plant produced significant hepatoprotection.

Acetaminophen↗
PubMedDate not supplied

[The effect of chronic alcoholic intoxication on the bioelectrical activity of the human brain].

Results from examinations of 110 spirit-abused men are presented. Changes in the EEG are found indicating the formation of an excitation focus that affect the reticular formation and induces an increase of the ascending activating effects on the cortex. Degree of these changes correlates with heaviness of the alcoholic disease. Results from the research permit a conclusion on diagnostic valuableness of the EEG examination with an aminazine test in case of alcoholism.

Adult↗
PubMedDate not supplied

[Effect of chronic alcoholic intoxication on the body of rats].

Experiments involving chronic introduction of ethanol (36 per cent of caloric value) as a part of a specially devised liquid ration demonstrated the trainability of rats to sharply decrease, their antistress resistance to significantly decline, especially in rats kept on a low-protein diet. A general tendency toward a reduced activity of acetylcholinesterase in different sectors of the brain was revealed both in animals receiving alcohol against the background of a normal protein allowance and in those kept on a low-protein diet (when compared with the enzyme activity in animals maintained on a ration with a normal of protein).

Acetylcholine↗
PubMed1992

[The effect of naloxone on the activation, inducible by chronic alcoholic intoxication, of the membrane-bound form of enkephalin convertase in the midbrain and hypothalamus of rats].

The activity of membrane-bound and soluble enkephalin convertase was determined with dansyl-Phe-Leu-Arg as substrate in midbrain, including hypothalamus, of Wistar rats, who were given ethanol (20% solution i.g., 9-15 g/kg per day during 4 days) or naloxone (2 mg/kg i.p. twice a day during 4 days) or their combination. It was shown that activation of membrane-bound enzyme, observed after alcohol treatment of rats, didn't develop by combined ethanol-naloxone administration. It's supposed that alcohol-stimulating effect on this enzyme realizes throughout the hyperstimulation of opioid receptors by enkephalins and, possible, by other opioid-active compounds.

Alcoholism↗
PubMed2005

Chronic alcohol intoxication in rats leads to a strong but transient increase in NGF levels in distinct brain regions.

Nerve growth factor (NGF), a member of the neurotrophin family, is an essential mediator of neuronal activity and synaptic plasticity of basal forebrain cholinergic neurons. In this study NGF-protein levels were determined in areas of the basal forebrain cholinergic system, its projection areas as well as the striatum and the cerebellum after long-term exposure (6 and 9 months) to ethanol and a phase of withdrawal in male Sprague-Dawley rats. 6-month alcohol treatment led to an increase of NGF to 650-850% of controls in the basal forebrain and the septum and to a 210-485% increase in the cholinergic projection areas (anterior cortex, hippocampus and olfactory bulb). After 9 months exposure to ethanol, a decrease of NGF by 16% in the frontal cortex was observed compared to controls. In the other brain regions no differences in NGF expression were detectable at this time-point. These results support the idea of an endogenous neuroprotective mechanism acting through a transient NGF induction followed by a decrease in NGF-levels during the course of further neuronal degeneration.

Acetylcholine↗
PubMed1979

Impeded cerebellar development and reduced serum thyroxine levels associated with fetal alcohol intoxication.

Pregnant albino rats were placed on a complete liquid diet (Ensure) containing either 9% ethanol or an isocaloric amount of sucrose between the third and twentieth day of gestation. The pups born to these rats were sacrificed either day 11 or day 14 postnatum and morphometrical, histological and biochemical analyses were done on their cerebellums and cerebrums. Pups that were exposed to ethanol in utero had significantly smaller body weights, cerebrums and cerebellums than pair-fed controls. The cerebellar mass was reduced by 10% and the cerebral weight by 3% in the pups exposed to alcohol when body weights were normalized to that of pair-fed controls. Cerebellar aspartyl aminotransferase (EC 2.6.1.1) activity was reduced at day 11 and 14 in ethanol treated pups compared with controls. Serum T4 levels were also reduced in the ethanol treated group. Histological analyses revealed that the external granule cell (EGC) layer of ethanol treated pups was significantly thicker at 11 and 14 days postnatum than that of pair-fed control pups. Cerebellar ornithine decarboxylase (ODC, EC 4.1.1.17) activity was higher at day 11 in the ethanol treated pups than in controls. The reduced mass, AAT activity, T4 serum levels and the increased thickness of the ECG layer indicate a delayed or impeded maturation of cerebellum in ethanol treated pups. These data are considered from the viewpoint that ethanol, other drugs such as methadone and prenatal stress (malnutrition) may cause delayed cerebellar maturation by reducing serum T4 levels in the early postnatal period (day 5-14).

Alcohol Drinking↗
PubMed1995

[Revoking the right to drive--a blunt weapon against alcohol intoxicated drivers, hit-and-run drivers and speed limit and red light offenders?].

The differences of the driving ban are determined by the text of law and the type of offence (drink driving, hit-and-run driving) or minor infringement. "Levelling down" is inappropriate. Character defects can be compensated by re-training programmes for drivers, years of sound driving experience and economic difficulties (unemployment). In these cases--especially if it is a first offence--the best way out of the dilemma is an exemption from the driving ban. Despite years of good reputation the exemption from the driving ban is out of the question if alcohol abuse is reinforced by violence.

Accidents, Traffic↗
PubMedDate not supplied

[Effect of chronic alcoholic intoxication on the circadian rhythm of the hypothalamic neurosecretory centers in rats].

Experiments were conducted on male rats; by means of quantitative cytochemical analysis and karyometry circadian rhythm of the hypothalamo-hypophysial neurosecretory system function was studied. In the evening (9--10 p.m.) the intensity of the synthesis, transport, and neurosecretion showed a significant elevation in comparison with the day (3--4 p.m.). Neurosecretory process was suppressed and the circadian rhythm of the hypothalamic neurosecretory system activity was disturbed in rats given a 5% ethanol solution as the only source of fluid for 2 months. As suggested, damage of an important biorhythm synchronizer (the neurosecretory centers of the hypothalamus) could play an important role in the pathogenesis of chronic alcoholism.

Alcoholism↗
PubMedDate not supplied

[Enzyme activity changes in chronic alcoholic intoxication and the simultaneous administration of pyridoxine].

After prolonged application of ethanol the liver and brain of rats show an appreciable increase in lactate dehydrogenase activity, noticeable lowering of cytoplasmic aspartate and alanine aminotransferase activity, elevation of liver arginine succinate lyase activity with unchanged activities of other enzymes of the ornithine cycle (ornithine carbamoyltransferase and arginase), reduction of glutamate and malate dehydrogenase and mitochondrial aspartate aminotransferase activity in brain tissue. Concurrent application of ethanol and pyridoxine normalizes the effect of ethanol on liver arginine succinate lyase and on brain tissue lactate and malate dehydrogenase, mitochondrial and cytoplasmic aspartate aminotransferase and alanine aminotransferase.

Alcoholism↗
PubMed1982

[Effect of the administration of nucleotide coenzymes on the lipogenic enzyme changes caused by chronic alcohol intoxication].

Lipogenic enzymes glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, isocitrate dehydrogenase NADP+ soluble and malic enzyme have been determined in the hepatic soluble fraction of rats chronically treated with ethanol and a lipid rich diet. The treatment based on protectives and lipotropic substances administered as nucleotides: UDP-glucose, CDP-choline, S-adenosyl methionine and Coenzyme A, elicits a significant restoration on the activities of G6PDH, 6PGDH and ICDH. These results show that the treatment, on promoting lipid mobilization, could increase the rate of hepatic lipogenesis. The malic enzyme enhanced activities, when ethanol and lipid diet were simultaneously administered, may be interpreted as a requirement for NADPH by the microsomic drug oxidation system.

Alcohol Oxidoreductases↗
PubMedDate not supplied

[Phospholipid composition, lipid peroxidation, and activity of enzymes of hepatocyte organoids in alcoholic intoxication].

During chronic ethanol intoxication phase alterations in phospholipid composition and in intensity of oxidation were observed in liver microsomes and mitochondria. The oxidative reactions were most pronounced within the first 15 and 30 days as shown by an increase in activity of malate- and isocitrate dehydrogenases from the mitochondrial fraction. Administration of ethanol within 15 days was accompanied by an increase in content of phospholipids and their separate fractions both in microsomes and in mitochondria. In microsomes content of lipid peroxides was distinctly increased but content of free phospholipid fractions was most distinctly lowered within 90 days.

Alcoholism↗
PubMed1995

[Determining the duration of suspended license for alcohol intoxicated drivers].

Public safety on the road and the need of each individual to participate in road traffic call for drink drivers to be dealt with legally. They should be dealt with in a preventive, successful and individual manner. The insuperable difficulties encountered by a criminal judge when having to determine the type, extent and duration of the offence as well as determining the motivation for improvement, would justify the judge not having to determine the period of suspension as well. This could be achieved by introducing a minimum period of suspension for all offenders. For those interested in reacquiring their driving licence, directives should be imposed so that appropriate and individual steps can be taken right at the beginning of their suspension, in order that their suitability for road traffic can be restored. In that case Sunder's question asked at the beginning could be answered as follows: "The authority to withdraw driving licences should not be withdrawn from the judge."

Adolescent↗