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PubMedDate not supplied

[Amide groups of brain and spinal proteins in acute and chronic alcohol intoxication].

Acute and chronic alcohol intoxication causes a considerable deamidation of central nervous system proteins which is most pronounced in the spinal cord. There occurs rearrangement in the amide bonds lability and in the ratio of easy-hydrolyzable and strongly bound amide groups. The metabolic response to the single administration of ethanol is disturbed. Alcohol intoxication causes changes in the amount of amide groups in the central nervous system proteins under conditions of physical exercises and fatigue development.

Alcoholism↗
PubMed2004

Impact of alcohol intoxication and withdrawal syndrome on social phobia and panic disorder in alcoholic inpatients.

PURPOSE: To investigate the impact of alcohol intoxication and withdrawal on the course of social phobia and panic disorder. METHOD: A group of 41 alcoholic inpatients undergoing detoxification therapy were interviewed using the SCID-I (DSM-IV) and questions to detect fluctuations in the course of social phobia and panic disorder as a function of the different phases in alcohol dependence (intoxication, withdrawal, and lucid interval). RESULTS: Only 1 (2.4%) patient presented panic disorder throughout life, and 9 (21.9%) had panic attacks during alcohol intoxication or during the withdrawal syndrome. Sixteen (39%) alcoholic patients showed social phobia with onset prior to drug use. However, drinking eventually became unable to alleviate social phobia symptoms or worsened such symptoms in 31.2% of social-phobic patients. While patients with social phobia reported a significant improvement in psychiatric symptoms during alcohol intoxication, patients experiencing panic attacks worsened significantly during intoxication. In the withdrawal phase, patients with social phobia tended to have more and more intense phobic symptoms. CONCLUSION: Our findings indicate that the impact of alcohol intoxication is different for social phobia as compared to panic disorder, at first decreasing the social-phobic symptoms but later aggravating them. In panic disorder, the impact of intoxication by alcohol is more harmful, at least in the short term.

Adult↗
PubMed2002

Impact of alcohol intoxication on hemodynamic, metabolic, and cytokine responses to hemorrhagic shock.

BACKGROUND: Alcohol intoxication is associated with a high incidence of traumatic injury, particularly in the young healthy population. The impact of alcohol intoxication on the immediate pathophysiologic response to injury has not been closely examined. We hypothesized that acute alcohol intoxication would aggravate the immediate outcome from hemorrhagic shock by impairing homeostatic counterregulation to blood loss. METHODS: Chronically catheterized male Sprague-Dawley rats were randomized to receive an intragastric infusion of ethyl alcohol (1.75 g/kg followed by 250-300 mg/kg/h) or isocaloric dextrose (3-mL bolus + 0.375 mL/h) for 15 hours. Before initiating fixed-pressure hemorrhage followed by fluid resuscitation, an additional intragastric bolus of ethyl alcohol (1.75 g/kg) was administered. Hemodynamic, metabolic, cytokine, and acid-base parameters were assessed during the hemorrhage period and at completion of resuscitation. Lungs were obtained for cytokine determinations. RESULTS: Basal mean arterial pressure was significantly lower in alcohol-intoxicated (blood-alcohol concentration, 135 +/- 12 mg/dL) animals than in controls during baseline (20%) and after the initial fluid resuscitation period (30%). Hemorrhage decreased arterial HCO3 and Pco2, and increased Po2 without significant alteration in arterial blood pH. Alcohol intoxication blunted the decrease in Pco2 and increase in Po2 and decreased blood pH during baseline and throughout the course of the hemorrhage period. Hemorrhage produced marked and progressive elevations in plasma glucose and lactate levels in controls, and this was inhibited by alcohol intoxication. Hemorrhage elevated plasma tumor necrosis factor-alpha (TNF-alpha) (686 +/- 252 pg/mL) and interleukin (IL)-10 (178 +/- 25 pg/mL), and did not alter IL-6 and IL-1 levels. Alcohol blunted the hemorrhage-induced rise in plasma TNF-alpha (142 +/- 48 pg/mL) and enhanced the hemorrhage-induced increase in IL-10 (678 +/- 187 pg/mL). Hemorrhage produced a two- to threefold increase in lung content of TNF-alpha, IL-1alpha, and IL-6 without significantly altering lung IL-10. Alcohol exacerbated the hemorrhage-induced increase in lung TNF-alpha, and did not alter the IL-1alpha, IL-6, and IL-10 lung responses. CONCLUSION: These results indicate marked alterations in the hemodynamic and metabolic responses to hemorrhagic shock by alcohol intoxication. Furthermore, our findings suggest that alcohol modulates the early proinflammatory responses to hemorrhagic shock. Taken together, these alterations in metabolic and inflammatory responses to hemorrhage are likely to impair immediate outcome and predispose to tissue injury.

Alanine Transaminase↗
PubMed2001

Nursing experiences with an alcohol-intoxicated rat dam counteract appetitive conditioned responses toward alcohol.

BACKGROUND: Infant rats detect small amounts of alcohol (175 mg%) that are present in maternal milk whenever the dam is moderately intoxicated with alcohol. Interaction with an alcohol-intoxicated mother during the first 2 weeks of life facilitates the preweanling's subsequent discrimination of alcohol's orosensory attributes and produces conditioned aversion to alcohol. The present study further analyzed the hedonic content of infantile alcohol memories established in the nursing context by testing the interaction between experiences with an alcohol-intoxicated dam and learning procedures aimed at establishing an appetitive conditioned response toward alcohol. METHODS: Experiment 1 was to determine appropriate parameters to establish a reliable conditioned preference for alcohol in 16-day-old infants. For conditioning, intraorally infused sucrose solution (appetitive reinforcer) was paired with alcohol's orosensory cues derived from an acute state of alcohol intoxication (3 g/kg). Two control groups included an unpaired condition and a group given sucrose after water intubation. Infants then were evaluated in an alcohol intake test. Relative to control animals, a reliable conditioned preference for alcohol was registered in paired pups. In experiment 2, these conditioning procedures were applied to infant rats which, before conditioning, suckled from dams subjected to a 2.5 g/kg alcohol dose (intragastric) or from water-treated females during postpartum days 3, 5, 7, 9, 11, and 13. RESULTS: Experiment 2 showed that maternal treatment significantly affected the establishment of conditioned preferences for alcohol. Whereas pups reared by control dams exhibited reliable appetitive conditioning to alcohol, infants raised by alcohol dams completely failed to develop appetitive conditioning. CONCLUSIONS: The present results suggest that alcohol-related memories generated via infantile interactions with an intoxicated dam counteract subsequent conditioning of alcohol ingestion. In conjunction with prior studies, it is concluded that alcohol-related nursing experiences are capable of promoting alcohol memories with a negative hedonic content.

Alcoholic Intoxication↗
PubMed1980

Hormonal changes during alcohol intoxication and withdrawal.

The endocrine effects of alcohol are briefly reviewed. Alcohol enhances glucose-induced insulin secretion and may thus cause reactive hypoglycemia. However, inappropriate insulin secretion is not the reason for alcohol-induced hypoglycemia in fasted subjects. The direct effects of alcohol in thyroid function in humans are small, although alcoholics often have low concentrations of thyroid hormones in their plasma because of liver damage. Alcohol increases cortisol secretion from adrenal cortex either by increasing ACTH secretion or, more probably, by directly stimulating the adrenals. Alcohol also increases aldosterone secretion. The production of epinephrine and norepinephrine by the adrenal medulla is increased during alcohol intoxication and withdrawal. Plasma testosterone concentration is decreased during hangover and during alcohol withdrawal. The decrease is due to direct effects of alcohol on the testes, because plasma LH concentration is increased simultaneously. Alcohol has no significant effect on the LRH-induced secretion of LH. Plasma growth hormone concentration is decreased during alcohol intoxication and increased during hangover. TRH-induced secretion of prolactin is increased during alcohol intoxication and inhibited during hangover and withdrawal. The last finding suggests that there is dopaminergic overactivity in hypothalamus during alcohol withdrawal.

Alcoholic Intoxication↗
PubMed1992

[Aldosterone and electrolyte content in blood and myocardium of rats after single physical load in acute alcoholic intoxication].

It is shown that acute alcoholic intoxication causes essential changes of aldosterone content and balance of electrolytes in blood plasma of Wistar rat males. The SPL test revealed the inadequate reaction in the mineral-corticoid function of the adrenal glands in the rats with acute alcoholic intoxication. The method of the free choice of the load by the experimental rats is the most optimal way to assess. The rats with acute alcoholic intoxication displayed smaller tolerance to physical load.

Acute Disease↗
PubMed2004

Acute alcohol intoxication during hemorrhagic shock: impact on host defense from infection.

BACKGROUND: Acute alcohol intoxication is a frequent underlying condition associated with traumatic injury. Our studies have demonstrated that acute alcohol intoxication significantly impairs the immediate hemodynamic, metabolic, and inflammatory responses to hemorrhagic shock. This study investigated whether acute alcohol intoxication during hemorrhagic shock would alter the outcome from an infectious challenge during the initial 24 hr recovery period. METHODS: Chronically catheterized male Sprague Dawley rats were randomized to acute alcohol intoxication (EtOH; 1.75 g/kg bolus followed by a constant 15 hr infusion at 250-300 mg/kg/hr) or isocaloric isovolemic dextrose infusion (dex; 3 ml + 0.375 ml/hr). EtOH and dex were assigned to either fixed-volume (50%) hemorrhagic shock followed by fluid resuscitation with Ringer's lactate (EtOH/hem, dex/hem) or sham hemorrhagic shock (EtOH/sham, dex/sham). Indexes of circulating neutrophil function (apoptosis, phagocytosis, oxidative burst) were obtained at baseline, at completion of hemorrhagic shock, and at the end of fluid resuscitation. Bacterial clearance, lung cytokine expression, and myeloperoxidase activity were determined at 6 and 18 hr after an intratracheal challenge with Klebsiella pneumoniae (10 colony-forming units). RESULTS: Mean arterial blood pressure was significantly lower in acute alcohol intoxication-hemorrhagic shock animals throughout the hemorrhagic shock. In sham animals, acute alcohol intoxication alone did not produce significant changes in neutrophil apoptosis or phagocytic activity but significantly suppressed phorbol myristic acid (PMA)-stimulated oxidative burst. Hemorrhagic shock produced a modest increase in neutrophil apoptosis and suppression of neutrophil phagocytic capacity but significantly suppressed PMA-stimulated oxidative burst. Acute alcohol intoxication exacerbated the hemorrhagic shock-induced neutrophil apoptosis and the hemorrhagic shock-induced suppression of phagocytosis without further affecting PMA-stimulated oxidative burst. Fluid resuscitation did not restore neutrophil phagocytosis or oxidative burst. Acute alcohol intoxication decreased (-40%) 3-day survival from K. pneumoniae in hemorrhagic shock animals, impaired bacterial clearance during the first 18 hr postinfection, and prolonged lung proinflammatory cytokine expression. CONCLUSIONS: These results demonstrate that the early alterations in metabolic and inflammatory responses to hemorrhagic shock produced by acute alcohol intoxication are associated with neutrophil dysfunction and impaired host response to a secondary infectious challenge leading to increased morbidity and mortality.

Alcoholic Intoxication↗
PubMed1989

Pharmacology of acute alcoholic intoxication.

Research of the alcohol action mechanism on the SNC in acute alcoholic intoxication (AAI) has been dealt in various ways. On one side the alcohol action--apparently most unspecific--on cellular membranes has been studied. Other authors, instead, have studied more specific alcohol effects on three types of neurotransmitters: opioid peptides, GABA and catecholamines. The effect of alcohol on cellular membranes seems to be beyond any doubt. Alcohol action on specific neurotransmitters is the object of controversy, especially in the case of endogenous opioids. There are data which strongly support the participation of the GABA receptors in the AAI. Modifications produced in the cellular membrane by alcohol action can modify the structure of the function of the membrane receptors. On the other hand, distinct receptors may be localized in the same neuron, while the existence of interactions between different neurotransmitters is well known. Therefore, the various hypotheses previously stated are not mutually exclusive.

Alcoholic Intoxication↗
PubMedDate not supplied

Acute alcohol intoxications in children treated in hospital.

Cases of alcohol intoxication in children are common; they are encountered every day in Finland. Studies other than case studies of alcohol intoxication in children are few. Metabolic acidosis was a frequent finding in juvenile alcohol intoxication. Capillary or arterial blood pH was below normal (less than 7.36) in 61.4% of patients and bicarbonate (less than 22) in 55.3% of patients. pCO2 was varied; the higher the blood alcohol concentration the higher the pCO2. Metabolic acidosis and blood pH correlated with the blood alcohol concentration and consciousness. The lower the blood pH the higher the serum glucose. Hypoglycemia is the most common reported symptom in children under 5 years of age. In the present study three patients were slightly hypoglycemic. Hypokalemia was the most important change (in 12.2%) in serum electrolytes. Alcohol intoxication causes metabolic acidosis and respiratory depression in children. Metabolic acidosis reduces consciousness.

Acid-Base Equilibrium↗
PubMed1986

Effects of acute alcohol intoxication on spinal cord vascular injury.

Previous experimental studies found that acute intoxication may alter the long-term outcome of standardized spinal cord injury resulting in increased spinal cord necrosis and impaired functional recovery. We examined the effects of acute intoxication (blood alcohol concentration of 100 mg/dl) on hemorrhage and axonal conduction three hours after moderate severity spinal cord contusion induced by a constrained stroke pneumatic impactor. The hemorrhagic spinal cord lesion resulting from standardized injury was significantly increased by acute intoxication. Both local hemorrhage at the injury site and rostro-caudal and total extent of hemorrhage were increased. Also, the ability of nerve axons to recover function during the first three hours post-contusion was impaired by intoxication. These findings confirm that increased post-contusion hemorrhage results when spinal cord contusion injury occurs in the presence of acute intoxication, and suggest that increased intramedullary hemorrhage may contribute to previously observed increases in anatomic damage and impaired functional recovery with alcohol intoxication.

Alcoholic Intoxication↗
PubMed1976

[Features of hepatic lesions in patients with chronic alcoholic intoxication].

The authors studied alcoholic hepatosis and hepatic cirrhosis by laboratory, radioisotope and clinical methods. Most of the routine laboratory techniques, excluding hyperurobilinuria were not very informative in alcoholic hepatosis. Much more frequently it was possible to mark disturbances of the bromsulphaleinic and vofaverdine tests. Of special importance in the evaluation of the acuity and depth of the alcohol intoxication was glutamate and sorbitdehydrogenase. The most informative appeared to be radioisotope hepatography in the phase of alcohol hepatosis and scannography in the formation of liver cirrhosis.

Alanine Transaminase↗
PubMed1998

Brain neuronal degeneration caused by episodic alcohol intoxication in rats: effects of nimodipine, 6,7-dinitro-quinoxaline-2,3-dione, and MK-801.

Rats repeatedly intoxicated with alcohol (ethanol, three times daily) over a 4-day period display neuronal degeneration in the dentate gyrus; entorhinal, piriform, insular, orbital, and perirhinal cortices; and in the olfactory nerve fibers and terminals in the olfactory bulb. Postulating a role for excitotoxicity, we have attempted to prevent the degeneration using antagonists that are neuroprotective in this type of brain damage. In an initial study, continuous subcutaneous infusion of a high dose of the glutamate/NMDA receptor antagonist MK-801 (2 mg/kg/day) by itself caused extensive neuronal degeneration in several brain regions and severe behavioral intoxication that precluded survival if combined with high blood alcohol levels (approximately 300 mg/dl). Moreover, the lower, nonneurotoxic blood alcohol levels (approximately 150 mg/dl) that were compatible with survival worsened the MK-801-induced brain damage. In a subsequent experiment, daily intraperitoneal injections of a lower dose of MK-801 (1 mg/kg/day) resulted in no MK-801 toxicity and, when combined with neurotoxic levels of alcohol, no reduction in alcohol-induced neurotoxicity. Nimodipine, a voltage-gated Ca2+ channel blocker, reduced the neuronal damage in the dentate gyrus, but greatly increased it in the piriform cortex when administered intragastrically at 600 mg/kg/day; it provided no protection from alcohol-dependent degeneration when given intragastrically at 100 mg/kg/day. Continuous intracerebroventricular delivery of 0.24 to 0.29 mg/day of 6,7-dinitro-quinoxaline-2,3-dione, a glutamate/alpha-amino-3-hydroxy-5-methyl-4-isoxazole receptor antagonist, failed to diminish alcohol-dependent neuronal damage in any brain region. We conclude that brain damage from episodic "binge" alcohol intoxication is not primarily mediated by excitotoxic mechanisms, implying that other, nonexcitotoxic pathophysiological mechanisms, are involved. Furthermore, MK-801, far from protecting from the alcohol-induced damage, at high doses causes widespread neuropathology that is significantly potentiated by alcohol.

Alcoholic Intoxication↗
PubMed1990

Iron release and erythrocyte damage in allyl alcohol intoxication in mice.

Allyl alcohol administration in a toxic dose (1.5 mmol/kg) to starved mice causes the development of hemolysis in nearly 50% of the animals. Malonic dialdehyde (MDA) appears in plasma of the animals showing hemolysis. The treatment of mice with desferrioxamine after allyl alcohol intoxication completely prevents lipid peroxidation and hemolysis, suggesting the involvement of iron in the allyl alcohol-induced erythrocyte damage. Erythrocytes obtained from intoxicated mice before the development of hemolysis show, upon incubation, release of iron, lipid peroxidation and lysis. Studies carried out with reconstituted systems of erythrocyte lysates, containing ghosts and different fractions of erythrocyte cytosol and incubated in the presence of acrolein (the major metabolite of allyl alcohol), strongly suggest that iron is released from hemoglobin. This iron appears to promote lipid peroxidation which is accompanied by erythrocyte lysis. Thus, the allyl alcohol-induced hemolysis appears to be a model for iron delocalization from iron stores.

1-Propanol↗
PubMed1989

Electroencephalographic study of naloxone effects in the recovery of an acute alcoholic intoxication.

Experimental assays analysing EEG changes during the recovery of an acute alcoholic intoxication were carried out in three groups of cats: 1) Recovery of acute alcoholic intoxication produced by continuous intravenous perfusion of ethanol, 0.06 g/kg/min, during 20 minutes. 2) Recovery of acute alcoholic intoxication by injecting naloxone (400 micrograms/kg), just after finishing alcohol perfusion. 3) Recovery of acute alcoholic intoxication by injecting naloxone (400 micrograms/kg), 15 min after finishing perfusion. Naloxone administered after an acute alcoholic intoxication worsens the recovery of EEG parameters; 1-2 (p less than 0.05), 1-3 (p less than 0.05).

Alcoholic Intoxication↗
PubMed1994

Mechanisms of hypocalcemia and markers of bone turnover in alcohol-intoxicated drinkers.

Studies of hypocalcemia and osteoporosis frequently encountered in heavy users of alcohol have previously been performed on alcoholic people who have already recovered from alcohol intoxication. Bone and mineral metabolism during and after the intoxication may be different. We measured serum parameters of bone and mineral metabolism in 26 alcohol-intoxicated men and in 19 healthy control men. Although serum ionized calcium was 12% (P < 0.0001) lower in the patients than in the controls, serum intact parathyroid hormone was similar in the study groups. As reflected by decreased serum levels of osteocalcin (-43%; P < 0.001), bone formation was depressed in the patients. Serum cross-linked carboxyterminal telopeptide of human type I collagen (ICTP), a novel parameter of bone matrix degradation, was 9% higher in the patients (P = 0.03) than controls. The positive correlation between serum osteocalcin and ICTP in the controls (r = 0.59, P < 0.01) was absent in the patients (r = 0.05, P = 0.8). We conclude that in alcohol-intoxicated alcohol users, the parathyroid glands do not respond normally to a hypocalcemic stimulus, and that depressed bone formation is uncoupled from accelerated bone resorption.

Adult↗
PubMed2002

Early responsiveness to stimuli paired with different stages within the state of alcohol intoxication.

BACKGROUND: Infant rats quickly learn to avoid a sensory cue paired with alcohol as an unconditioned stimulus, particularly when the drug reaches peak blood concentrations. In this study, a tactile cue paired with the onset of alcohol intoxication preceded subsequent presentations of a gustatory conditioned stimulus (CS). The goal was to address the possibility of differential conditioning depending on when stimuli were introduced during the course of the toxic state. METHODS: In experiment 1, rat pups received sequential presentations of a salient texture (sandpaper) and a gustatory cue (saccharin) while intoxicated with a 2.5 g/kg alcohol dose or after receiving saline. Texture location tests and saccharin intake assessments were then performed. A third modality of assessment was defined by a saccharin intake test while pups simultaneously experienced sandpaper. In experiment 2, alcohol-mediated conditioning was followed by tests similar to those of experiment 1, but after pups were re-exposed to either the tactile CS or the alcohol-unconditioned stimulus. RESULTS: Conditioned taste aversions, due to pairing saccharin and the later stage of alcohol intoxication, were reliably established in both experiments. Also in both experiments, this excitatory aversive response was dramatically inhibited when the association between the texture CS and the earlier stage of alcohol intoxication was activated. There were no indications of conditioned motor responses to the tactile CS that might compete with intake behavior of saccharin or distort measurement of an appetitive memory derived from pairing the texture and the earlier stage of intoxication. CONCLUSIONS: Rat pups' expression of an association between a taste signaling aversive consequences of alcohol was eliminated by the presence of a tactile stimulus that originally had signaled the absence of aversive consequences of alcohol intoxication. The results suggest the interaction of inhibitory and excitatory conditioning involving the aversive properties of alcohol.

Alcoholic Intoxication↗