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PubMedDate not supplied

[Further study of immuno-correcting properties of vitamins A and E in experimental chronic alcoholic intoxication].

The experiments conducted on guinea pigs have shown that chronic alcohol poisoning induced by daily oral intake of 1 ml of 25% ethanol solution during a month has brought to suppression of the T-system immunity. Vitamin A used during 3 days in a dose of 30,000 IU results in partial normalization of the immunological parameters, while vitamin E given during 3 days in a dose of 50 IU provides absolute normalization of the immune status.

Adjuvants, Immunologic↗
PubMed1996

Natural disease and alcohol intoxication amongst drivers of motor vehicles in Singapore from 1989 to 1993: a study of 140 necropsies.

A 5-year retrospective study of 140 necropsies conducted on drivers of vehicles (excluding motorcyclists) involved in fatal motoring events, drawn from 1285 traffic deaths, showed a marked preponderance of males (95%) and of Chinese subjects (87.1%), with over half (53.6%) aged between 20 and 39 years. Approximately a third was free of morphological evidence of natural disease, while the remainder showed evidence of various combinations of ischaemic heart disease (64.3%), hypertensive heart disease (38.6%), chronic obstructive airways disease (25.7%), benign hypertensive nephrosclerosis (15%), cerebral atheroma (15%) and other conditions. While the majority succumbed to the effects or complications of severe trauma, 35 subjects (25%) died from natural (that is, non-traumatic) causes, with 17 or almost half of these having occurred as sudden deaths "at the wheel", not associated with any form of collision. The mean age of the former (traumatic deaths) was 35.3 years while that of the latter (natural deaths) was 55.2 years (P < 0.001). Notably, ischaemic heart disease was the predominant natural cause, accounting for 31 of all such cases, none of which resulted in death or injury to any passenger, pedestrian or another motorist. It was also the cause of death in 12 vocational drivers, corresponding to 0.9% of all traffic deaths during this period. Although 34 drivers (24.3%) had detectable blood ethanol levels at autopsy, of which 28 (20%) exceeded the current legal limit of 80 mg/100 ml, all of the cases where death was attributed to natural causes were free of ethanol. However, 15 subjects (10.7%) who had died from trauma but had significant underlying pathology, comprising 13 cases of ischaemic heart disease, had blood ethanol concentrations well above the legal limit. It is possible that, in at least some of the latter, alcohol consumption might have acutely aggravated the underlying pathology and combined to contribute to the occurrence of these fatal accidents.

Accidents, Traffic↗
PubMed2000

Acute alcohol intoxication and gadolinium chloride attenuate endotoxin-induced release of CC chemokines in the rat.

This work tests the hypotheses that Kupffer cells are a major source of CC-chemokines (MIP-1alpha, MCP-1, RANTES) during acute endotoxemia and that acute ethanol intoxication modulates Escherichia coli lipopolysaccharide (LPS, 1 mg/Kg, i.v.)-induced chemokine release in the rat. LPS stimulated the release of CC-chemokines into the circulation, hepatic sequestration of leukocytes and liver injury. LPS-induced serum chemokines peaked at 1-3 h and could not be detected at 24-h posttreatment. Splenectomy significantly suppressed LPS-induced RANTES release, but not MIP-1alpha and MCP-1. Kupffer cell depletion by gadolinium chloride or acute ethanol intoxication significantly attenuated LPS-induced CC-chemokine release and hepatic injury. Hepatic sequestration of leukocytes during endotoxemia was also suppressed by acute ethanol. LPS downregulated the expression of MIP-1alpha and MCP-1 mRNAs and upregulated RANTES mRNA in Kupffer cells at 3-h post endotoxin. The expression of mRNAs was further suppressed in ethanol plus the LPS-treated group. Ethanol also suppressed the LPS-mediated priming of Kupffer cells for enhanced CC-chemokine release in vitro. Ethanol alone significantly upregulated the expression of CC-chemokine mRNA, and primed the Kupffer cells for enhanced RANTES release. CC-chemokine release and mRNA expression in hepatic sinusoidal endothelial cells were not significantly altered by ethanol, except for MCP-1 release. These data show that acute ethanol may be beneficial in tissue injury during acute endotoxemia.

Acute Disease↗
PubMed1980

The effects of temperature and acute alcohol intoxication on brain stem auditory evoked potentials in the cat.

The effects of core temperature changes (less than 1 degree C) and acute ethanol intoxication (100-400 mg%) on brain stem auditory evoked potentials in cats were studied independently--then together--to distinguish between a putative direct pharmacological action of ethanol on brain stem auditory neurons, as reflected in reported BAEP latency changes, and in indirect action of ethanol mediated through slight changes in central temperatures. The results suggest that the reported BAEP latency effects are attributable, largely if not entirely, to the second mechanism above. No significant temperature-independent BAEP latency alterations occurred at any sublethal blood ethanol concentration or in one dosage that subsequently proved fatal. These findings do not exclude a direct ethanol effect on brain stem auditory neurons but provide no evidence for a temperature-independent effect. Knowledge of secondary BAEP temperature effects associated with drug administration is crucial to proper interpretation of BAEPs in both experimental and clinical applications.

Alcoholic Intoxication↗
PubMed1992

[Alcohol intoxicated bicyclists in Düsseldorf 1986-1990].

Although traffic participation of bicycle riders is steadily increasing only few investigations concerning "riding while intoxicated" are available. This study examines the blood sample records of all blood samples submitted to the Duesseldorfer Institute of Forensic Medicine for blood alcohol analysis from 1986 to 1990 with respect to the participation of bicycle riders. As to the most important epidemiologic data: The proportion of samples from bicyclists increased from 2.6% in 1986 to 4.8% in 1990. Women account for 6.5%. 36.8% are younger than 30 years. Most bicycle riders were apprehended during the months of summer, on the days of the weekend and in the hours around midnight. 67.3% displayed a BAC above the legal limit for bicycle riders of 1.7 g/l. In comparison only 34.5% were judged highly drunken on medical examination. Regarding the group with a BAC above 2.5 g/l expected to be highly intoxicated 37.7% only appeared slightly or moderately impaired rising the suspicion of high alcohol tolerance.

Adult↗
PubMed2000

Moderate sleep deprivation produces impairments in cognitive and motor performance equivalent to legally prescribed levels of alcohol intoxication.

OBJECTIVES: To compare the relative effects on performance of sleep deprivation and alcohol. METHODS: Performance effects were studied in the same subjects over a period of 28 hours of sleep deprivation and after measured doses of alcohol up to about 0.1% blood alcohol concentration (BAC). There were 39 subjects, 30 employees from the transport industry and nine from the army. RESULTS: After 17-19 hours without sleep, corresponding to 2230 and 0100, performance on some tests was equivalent or worse than that at a BAC of 0.05%. Response speeds were up to 50% slower for some tests and accuracy measures were significantly poorer than at this level of alcohol. After longer periods without sleep, performance reached levels equivalent to the maximum alcohol dose given to subjects (BAC of 0. 1%). CONCLUSIONS: These findings reinforce the evidence that the fatigue of sleep deprivation is an important factor likely to compromise performance of speed and accuracy of the kind needed for safety on the road and in other industrial settings.

Adult↗
PubMed2007

Acute alcohol intoxication increases interleukin-18-mediated neutrophil infiltration and lung inflammation following burn injury in rats.

In this study, we examined whether IL-18 plays a role in lung inflammation following alcohol (EtOH) and burn injury. Male rats ( approximately 250 g) were gavaged with EtOH to achieve a blood EtOH level of approximately 100 mg/dl before burn or sham injury ( approximately 12.5% total body surface area). Immediately after injury, rats were treated with vehicle, caspase-1 inhibitor AC-YVAD-CHO to block IL-18 production or with IL-18 neutralizing anti-IL-18 antibodies. In another group, rats were treated with anti-neutrophil antiserum approximately 16 h before injury to deplete neutrophils. On day 1 after injury, lung tissue IL-18, neutrophil chemokines (CINC-1/CINC-3), ICAM-1, neutrophil infiltration, MPO activity, and water content (i.e., edema) were significantly increased in rats receiving a combined insult of EtOH and burn injury compared with rats receiving either EtOH intoxication or burn injury alone. Treatment of rats with caspase-1 inhibitor prevented the increase in lung tissue IL-18, CINC-1, CINC-3, ICAM-1, MPO activity, and edema following EtOH and burn injury. The increase in lung IL-18, MPO, and edema was also prevented in rats treated with anti-IL-18 antibodies. Furthermore, administration of anti-neutrophil antiserum also attenuated the increase in lung MPO activity and edema, but did not prevent the increase in IL-18 levels following EtOH and burn injury. These findings suggest that acute EtOH intoxication before burn injury upregulates IL-18, which in turn contributes to increased neutrophil infiltration. Furthermore, the presence of neutrophils appears to be critical for IL-18-meditaed increased lung tissue edema following a combined insult of EtOH and burn injury.

Alcoholic Intoxication↗