Alcohol administration

Stewart, S. and Pihl, R., Effects of alcohol administration on psychophysiological and subjective-emotional responses to aversive stimulation in anxiety sensitive women. Psychology of Addictive Behaviors 8(1), 29-42, 1994. 

Hypersensitivity to benzodiazepines psychoses acute narrow-angle glaucoma children < 6 years lactation concomitant alcohol administration. 

The possible role of the ethanol-inducible isozyme of cytochrome P-450 in the metabolism of carbon disulfide has been examined (Snyderwine et al. 1988). Rats were administered various alcohols (methanol, ethanol, isopropanol, and isobutanol) by gavage. Eighteen hours after alcohol administration, rats were administered carbon disulfide intraperitoneally at doses of 1, 100, or 625 mg/kg. The results showed that pretreatment of rats with these alcohols enhances the metabolism of carbon disulfide by increasing the ethanol-inducible isoform of cytochrome P-450 with isopropanol being most potent. Furthermore, the study authors indicate that alcohol induction of P-450-dependent carbon disulfide metabolism per se is not sufficient to result in carbon disulfide-induced hepatic damage although it does lead to the loss of specific cytochrome P-450 function. 

Hultberg B, Isaksson A, Bugge M. 1988. The effect of porta-caval shunt ammonia infusion and alcohol administration on rat plasma beta hexosaminidase. Liver 8(3) 129-131. 

Ivermectin is rapidly absorbed, is bound to a great extent to plasma protein, and is excreted in the urine or feces either unchanged or as the 3 -0-demethyl-22,23-dihydroavermectin Bia or as the dihydroavermectin Bia monosaccharide. The absorption of IVM is significantly affected by the presence of alcohol. Administration of IVM as an alcoholic solution may result in as much as a 100% increase in absorption. 

A randomised, crossover study in 8 men with psychotic disorders found that quetiapine 250 mg three times daily did not afTect the mean breath-alcohol concentration after they took 0.8 g/kg of alcohol in orange juice. Some statistically significant changes in the performance of psychomotor tests were seen, but these were considered to have little clinical relevance. However, the US manufacturers of quetiapine say that, in clinical studies, the motor and cognitive effects of alcohol were potentiated by quetiapine. Therefore the US manufacturers of quetiapine advise avoiding alcohol, and the UK manufacturers advise caution with the concurrent use of alcohol. Note that drowsiness is the most common adverse effect of quetiapine, occurring in over 10% of patients. Quetiapine may occasionally induce postural hypotension, which could be exacerbated by alcohol administration. 

Any beverage alcohols, wine or beer intended for nonindustrial use, labeled under the Federal Alcohol Administration Act. 

On the other hand, the ethiology of fatty livers caused by alcohol is still debated and manifold effects of alcohol have been reported. In man a fatty liver can result from acute or chronic ethanol ingestion. In the rat a single dose of ethanol or the chronic administration causes an increase in liver lipids (Dilxjzio 1958 Mallov 1955). Mallov (1961) demonstrated an increased mobilization of free fatty acids from the depots, caused by alcohol administration. On the other hand, ScHAPiRO et al. (1964) showed in the perfused liver, that addition of ethanol to the perfusate decreased the secretion of neutral glycerides by the liver. However, with ethanol no decrease in protein synthesis could be shown (Seakins and Robinson 1964), and normal or elevated plasma lipids were found. 

Benzaldehyde is a synthetic flavoring substance, sanctioned by the U.S. Food and Dmg Administration (FDA) to be generally recognized as safe (GRAS) for foods (21 CFR 182.60). Both "pure almond extract" and "imitation almond extract" are offered for sale. Each contains 2.0—2.5 wt % benzaldehyde in an aqueous solution containing approximately one-third ethyl alcohol. 

Completely Denatured Alcohol. Completely denatured alcohol (CD A) escapes the involved financial and administrative controls required of the other classifications of industrial ethanol. No tax is appHed, no bond is required, no permit is needed to enable a customer to purchase CD A. Requirements for records by both producer and user are minimal. These simplified regulations are possible because CDA is denatured with substances that render it totally unfit for beverage purposes. It is also unsuitable where odor is objectionable. CDA and products made from it are, however, governed by special labeling requirements of the BATE. Repackaging of completely denatured alcohol is permitted as long as labeling requirements are met. 

As regards toxicity, pyrazole itself induced hyperplasia of the thyroid, hepatomegaly, atrophy of the testis, anemia and bone marrow depression in rats and mice (72E1198). The 4-methyl derivative is well tolerated and may be more useful than pyrazole for pharmacological and metabolic studies of inhibition of ethanol metabolism. It has been shown (79MI40404) that administration of pyrazole or ethanol to rats had only moderate effects on the liver, but combined treatment resulted in severe hepatotoxic effects with liver necrosis. The fact that pyrazole strongly intensified the toxic effects of ethanol is due to inhibition of the enzymes involved in alcohol oxidation (Section 4.04.4.1.1). 

DOX, as EPI seems to form fewer amounts of ROS and secondary alcohol metabolite, (ii) encapsulation of anthracyclines in uncoated or pegylated liposomes that ensure a good drug delivery to the tumor but not to the heart, (iii) conjugation of anthracyclines with chemical moieties that are selectively recognized by the tumor cells, (iv) coadministration of dexrazoxane, an iron chelator that diminishes the disturbances of iron metabolism and free radical formation in the heart, and (v) administration of anthracyclines by slow infusion rather than 5-10 min bolus (Table 1). Pharmacological interventions with antioxidants have also been considered, but the available clinical studies do not attest to an efficacy of this strategy. 

Chronic administration of opiates and alcohol leads to physical dependence a phenomenon, which is only weakly expressed following chronic administration of psychostimulants or other drugs of abuse. Physical dependence results from neuroadaptive intracellular changes to an altered pharmacological state. Abstinence from chronic opiate or alcohol use leads to a variety of physiological and psychological withdrawal symptoms based on these adaptations of the neuronal system. 

Wernicke s syndrome is a serious consequence of alcoholism and thiamine (vitamin Bx) deficiency. Certain characteristic signs of this disease, notably ophtalmoplegia, nystagmus, and ataxia, respond rapidly to the administration of thiamine but to no other-vitamin. Wernicke s syndrome may be accompanied by an acute global confusional state that may also respond to thiamine. Left untreated, Wernicke s syndrome frequently leads to a chronic disorder in which learning and memory are strongly impaired. This so-called Korsakoff s psychosis is characterized by confabulation, and is less likely to be reversible once established. 

When administering acetaminophen, the nurse assesses the overall health and alcohol usage of the patient before administration. fatients who are malnourished or abuse alcohol are at risk of developing hepatotoxicity (damage to the liver) with the use of acetaminophen. 

Alcohol sulfates are easily metabolized by mammals and fishes either by oral or intraperitoneal and intravenous administration. Several labeled 35S and 14C alcohol sulfates have been used to determine their metabolism in experiments with rats [336-340], dogs [339], swines [341], goldfish [342], and humans [339]. From all of these studies it can be concluded that alcohol sulfates are absorbed in the intestine of mammals and readily metabolized by to and p oxidation of the alkyl chain and excreted in the urine and feces, but are also partially exhaled as carbon dioxide. Fishes absorb alcohol sulfates through their gills and metabolize them in a similar way to that of mammals. 

From the detailed studies performed either using individual alcohol sulfates and alcohol ether sulfates or formulated products by oral administration and skin contact, no evidence of carcinogen risk was found. Similar conclusions were obtained when these sulfates or formulated products were tested for mutagenic and teratogenic properties. 

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