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Results for “Alcoholic Intoxication”

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PubMed1984

Blood acetaldehyde concentration gradient between hepatic and antecubital venous blood in ethanol-intoxicated alcoholics and controls.

After ethanol (0.8 g kg-1 body weight orally) significant concentrations of acetaldehyde (2-20 mumol 1(-1] were found in hepatic venous blood of moderately intoxicated non-alcoholic male Caucasians in spite of the absence of detectable levels (less than 2 mumol 1(-1] in simultaneously taken antecubital blood. In thirteen chronic alcoholics the elevation of blood acetaldehyde was more constant in the hepatic than in the peripheral vein. Fructose infusion caused a marked elevation of acetaldehyde both in the hepatic and peripheral vein of four controls, but not of four alcoholics, who eliminated ethanol about 50% faster than controls. The rate of disappearance of acetaldehyde from sampled and in vitro incubated hepatic venous blood was similar to that observed after addition of acetaldehyde in vitro to ethanol-free control blood (2 nmol ml-1 min-1 at 20 mumol 1(-1) acetaldehyde; Km about 30 mumol 1(-1]. Uptake of acetaldehyde in blood was calculated to explain maximally 30-40% of the concentration gradient between central and peripheral blood.

Acetaldehyde↗
PubMed2006

A novel role for IL-18 in corticosterone-mediated intestinal damage in a two-hit rodent model of alcohol intoxication and injury.

Recent findings from our laboratory have shown that acute alcohol (EtOH) intoxication before burn injury impairs intestinal immunity and barrier functions. To further delineate the mechanism of impaired intestinal barrier function, the present study examined the role of corticosterone (CORT) and interleukin (IL)-18, as CORT and IL-18 are elevated following a combined insult of EtOH intoxication and burn injury. Male rats (approximately 250 g) were gavaged with EtOH to achieve a blood EtOH level of approximately 100 mg/dL prior to burn or sham injury (25% total body surface area). Immediately after injury, a group of rats was treated with CORT synthesis inhibitor metyrapone (25 mg/kg), with or without recombinant (r)IL-18 (50 microg/kg). Another group of rats was treated with caspase-1 inhibitor Ac-YVAD-CHO to block IL-18 production. On Day 1 after injury, there was a significant increase in blood CORT levels, intestinal levels of IL-18, neutrophil chemokines [cytokine-induced neutrophil chemoattractant 1 (CINC-1) and CINC-3], intercellular adhesion molecule-1, myeloperoxidase activity, and intestinal permeability in rats receiving a combined insult of EtOH and burn injury. Treatment of rats with CORT inhibitor or with caspase-1 inhibitor prevented the increase in all of the above parameters following a combined insult of EtOH and burn injury. Moreover, coadministration of rIL-18 in metyrapone-treated rats restored the above parameters, similar to those observed in rats receiving EtOH and burn injury. These findings suggest that a combined insult of EtOH and burn injury results in increased CORT levels, which in turn up-regulates intestinal IL-18 levels and thereby causes altered intestinal barrier function following a combined insult of EtOH intoxication and burn injury.

Alcoholic Intoxication↗
PubMedDate not supplied

Head injury in the presence of alcohol intoxication.

The difficulty of distinguishing between serious head injury and intoxication is presented in the case of an injured patient whose signs and symptoms were attributed to alcohol withdrawal. This report emphasizes the need for a high level of suspicion for all trauma patients, for all health care providers to be familiar with common forms of life-threatening trauma, and how to distinguish between altered levels of consciousness resulting from alcohol intoxication versus intracranial disorders. This case may also demonstrate that a person's wealth and social influence and an institution's orientation to a medical specialty can affect care giver's decisions.

Acute Disease↗
PubMed1988

Effects of acute alcohol intoxication on cerebral blood flow measured with PET.

Regional distribution of cerebral blood flow was assessed in a group of 13 normal social drinkers under baseline conditions and after acute alcohol intoxication. Blood flow measurements were done using 15O-labeled water and positron emission tomography (PET). Each subject underwent two control sessions under baseline conditions and two sessions after alcohol. Seven of the subjects were given 0.5 g/kg of alcohol and six were given 1 g/kg of alcohol p.o. The first and second post-alcohol scans were done 40 and 60 min after alcohol ingestion. The studies revealed that both the high and the low doses of alcohol reduced blood flow to the cerebellum. This effect was significant only for the high doses of alcohol, which also increased blood flow to the right temporal and the prefrontal cortex. The decrease in blood flow of the cerebellum could account for the muscular incoordination induced by alcohol.

Adult↗