Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Alcoholic Intoxication”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 433 records · Page 24Linked to original sources
PubMed1987

Acute alcohol intoxication disrupts brightness but not olfactory conditioning in preweanling rats.

The present experiments tested the effect of acute alcohol administration on Pavlovian conditioning of 21-day-old rats using conditioned stimuli of two different sensory modalities--olfaction, an early developing sensory capacity functional at birth, and vision, a later developing sensory system not becoming functional until approximately 15 days of age. Conditioning and testing were conducted between 30 and 60 min following gastric infusion with either physiological saline or a mildly intoxicating alcohol dose (1.5 g/kg body weight). Brain alcohol levels were observed to remain at a peak and stable concentration during this period (Experiment 1). Alcohol impaired acquisition or expression of conditioned aversions to a visual cue paired with footshock when presented either as a single-element conditioned stimulus or as part of an odor/visual compound stimulus (Experiment 2), but it had no discernible effect on conditioned aversions to an olfactory stimulus that had similarly been paired with footshock (Experiments 2 and 3). The results suggest that alcohol may impair some aspects of learning but spare others, depending perhaps on the particular sensory modality to be conditioned.

Alcoholic Intoxication↗
PubMed1992

Acute alcoholic intoxication and naloxone. Effects on visual evoked potential.

Experimental assays analyzing visual evoked potential (VEP) changes during an acute alcoholic intoxication were carried out in two groups of cats: One with continuous ethanol (0.06 g/kg.min) i.v. perfusion. Another one with a naloxone (400 micrograms/kg) i.v. injection 10 min before ethylic perfusion. Naloxone potentiates alcohol effects on VEP parameters, and on the appearance of isoelectric postpotential and flat VEP.

Acute Disease↗
PubMed1982

[Dose-dependent cardiodepression in acute alcohol intoxication in the rat].

Isovolumetric pressure-volume relations, parameters of contractility and the resting tension curve were recorded in Wistar rats prior and during acute intoxication with ethylalcohol. Parameters were recorded at blood levels between 6.0% and 2.0% of the intravenously infused alcohol. At the high blood alcohol level, maximal isovolumetric pressure is diminished by 24%, maximal rate of pressure rise by 42%, as compared with controls, whereas enddiastolic pressure increased by 32% and enddiastolic volume by 11%. Significant impairment of hemodynamics is also present at a blood alcohol level of 2.0%. These findings point to a dose-dependent cardiodepression in acute alcohol intoxication.

Alcoholic Intoxication↗
PubMed1992

Effects of alcohol intoxication on the initial assessment of trauma patients.

STUDY OBJECTIVES: To evaluate the influence of alcohol intoxication on the initial assessment and treatment of trauma patients. DESIGN: A prospective study of 2,237 trauma patients 18 years of age or older admitted to a Level I trauma center over a 19-month period. RESULTS: The study population was primarily male (78%) and white (73%) and had sustained blunt trauma (79%). One thousand fifty-three patients (47.1%) had positive blood alcohol concentration (BAC); median BAC in patients with any detectable alcohol was 179 mg/dL. When stratified by injury severity categories and compared with nonintoxicated (BAC less than 100 mg/dL) patients, intoxicated patients with an Injury Severity Score (ISS) of 1 to 15 were more likely to undergo the following: field and/or ED intubation (relative risk [RR], 2.22; 95% confidence interval [CI], 1.7 to 2.7); diagnostic peritoneal lavage (RR, 1.83; CI, 1.43 to 2.3); head computed tomography scanning (RR, 1.18; CI, 1.0 to 1.4); and intracranial pressure monitoring (RR, 1.41; CI, 0.74 to 2.7). The effects were less pronounced for those patients with an ISS of more than 15, except for intracranial pressure monitoring where patients with an ISS of more than 15 were 47% more likely to have intracranial pressure monitoring if intoxicated (RR, 1.47; CI, 1.2 to 1.9). CONCLUSION: Acute intoxication appears to alter the initial assessment of injury severity, resulting in an increased use of invasive diagnostic and therapeutic procedures.

Adolescent↗
PubMed1982

Acute alcohol intoxication, negative affect, and autonomic arousal in women and men.

The present study tested the hypothesis that acute moderate alcohol intoxication is associated with reductions in experimentally-induced negative affect among 64 moderately drinking adult women and men. The effort incorporated a balanced placebo design, multiple measures of affective responses including cardiovascular and electrodermal activity, and control for phase of the sexual cycle among nonoral contraceptive women. Negative effect and psychophysiological responses to intoxication following stress manipulation were a complex function of beverage, expectancy, and gender. Expectation of a moderate alcohol dose among women at the premenstruum was associated with higher levels of self-reported anxiety, whereas alcohol consumption guised as tonic seemed to be related to tension reduction. Alcohol tended to increase autonomic arousal among men, but there were no significant changes in negative affect. Moderate intoxication was associated with increased heart rate regardless of gender, and alcohol expectancy increased levels of skin conductance for men and women.

Adult↗
PubMed1978

N1--P2 component of the auditory evoked potential during alcohol intoxication and interaction of pyrithioxine in healthy adults.

The auditory evoked potential was used to assess the effect of alcohol intoxication (1 g/kg) and pyrithioxine (7 mg/kg) on 9 adult subjects. Its components in the latency range 50--250 msec (N1--P2) were studied for 6 g 30 min, during a constant level of alertness. Four periods were considered: alcohol alone, alcohol plus pyrithioxine, pyrithioxine plus alcohol and placebo. With alcohol alone the N1--P2 amplitude was small in the first part of the test and large in the second part as compared to placebo values. Pyrithioxine antagonism was greatest after alcohol had been resorbed. The placebo period indicated that amplitude changes were not due to long-term habituation, when the subject was kept alert.

Adult↗
PubMed1978

Effect of acute alcohol intoxication on granulocyte mobilization and kinetics.

Granulocyte mobilization into skin abrasions in human volunteers was significantly inhibited by acute alcohol intoxication (45,-800 cells in 8 hr versus 353,000 in normal controls). Alcohol applied locally did not inhibit granulocyte delivery, and protection of the abrasion against heat loss did not reduce the inhibited delivery in intoxicated volunteers. Intoxication inhibited granulocyte adherence and local mobilization in parallel. Alcohol administration to rabbits shifted granulocytes from marginal to circulating pool in a manner similar to epinephrine. Mobilization of bone marrow granulocytes by glucocorticoid or endotoxin administration was not inhibited by intoxication, nor did it prevent the endotoxin-induced shift of granulocytes from circulating to marginal pool.

Alcoholic Intoxication↗
PubMed1995

Cutoff in potency implicates alcohol inhibition of N-methyl-D-aspartate receptors in alcohol intoxication.

As the number of carbon atoms in an aliphatic n-alcohol is increased from one to five, intoxicating potency, lipid solubility, and membrane lipid disordering potency all increase in a similar exponential manner. However, the potency of aliphatic n-alcohols for producing intoxication reaches a maximum at six to eight carbon atoms and then decreases. The molecular basis of this "cutoff" effect is not understood, as it is not correlated with either the lipid solubility or the membrane disordering potency of the alcohols, which continue to increase exponentially. Since it has been suggested that inhibition of N-methyl-D-aspartate (NMDA) receptors by alcohols may play a role in alcohol intoxication, we investigated whether a series of aliphatic n-alcohols would exhibit a cutoff in potency for inhibition of NMDA receptors. We found that although potency for inhibition of NMDA receptors increased exponentially for alcohols with one to five carbon atoms, potency for inhibition of NMDA receptors reached a maximum at six to eight carbon atoms and then abruptly disappeared. This cutoff for alcohol inhibition of NMDA receptors is consistent with an interaction of the alcohols with a hydrophobic pocket on the receptor protein. In addition, the similarity of the cutoffs for alcohol inhibition of NMDA receptors and alcohol intoxication suggests that the cutoff for NMDA receptor inhibition may contribute to the cutoff for alcohol intoxication, which is consistent with an important role of NMDA receptors in alcohol intoxication.

Alcoholic Intoxication↗
PubMed1987

[Acetylcholinesterase and monoamine oxidase in various brain structures in chronic alcoholic intoxication].

The authors studied the rat brain after prolonged (up to 18 months) alcohol intoxication as well as the progeny of female rats after alcohol consumption for 4 months. Some changes in the activity of acetyl cholinesterase and monoamine oxidase in different structures of the brain in parents and progeny were unidirectional while others were not. Other findings included a weight loss during alcoholization and a decline in the fertility and viability of the progeny.

Acetylcholinesterase↗