Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the course of celiac plexus alcohol block, facial flushing, palpitations, and hypotension are occasionally incurred in some patients. We hypothesized that the phenomenon represents acetaldehyde syndrome, not response to increased blood levels of ethanol as might be supposed. In order to prove our hypothesis, we selected five patients scheduled to undergo celiac plexus alcohol block, and, with their consent, we measured blood concentration of ethanol and acetaldehyde before and for 6 hr after the block. We also determined the phenotypes of aldehyde dehydrogenase (ALDH) in their hair roots. We found that "flushers" are found exclusively among subjects without ALDH I, and that their blood levels of acetaldehyde were significantly higher than those of "non-flushers" within 10 min after the block. The flushers also gave histories of facial flushing after ingestion of small amounts of ethanol. On the basis of such histories one can anticipate whether acetaldehyde syndrome is likely or unlikely to accompany the block.
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PMID:Acetaldehyde syndrome after celiac plexus alcohol block. 377 61

Evidence is reviewed linking clinical effects of ethanol with actions on the sympathetic and parasympathetic nervous systems. The studies reported include a series of investigations by the authors. Acutely, ethanol causes peripheral vasodilation and may also result in changes in heart rate and blood pressure. Ethanol may contribute to acute problems which may present clinically, including micturition syncope, accidental hypothermia and facial flushing. However, increased sympathetic nervous activity plays a role in causing hypertension and other symptoms during ethanol withdrawal in chronic alcoholics. Some chronic alcoholics may have neuropathy involving sympathetic nerves, and this can result in distal sweating loss and occasionally in orthostatic hypotension. Also, hypothalamic lesions associated with Wernicke's encephalopathy may result in hypothermia. Neuropathy involving parasympathetic nerves in not uncommon in alcoholics with other evidence of nervous system damage, but it is generally asymptomatic. Occasionally, vagal neuropathy may cause disorder of gastrointestinal motility, and neuropathy affecting the sacral innervation may be a factor in alcoholic impotence.
Drug Alcohol Depend 1986 Dec
PMID:The effects of acute and chronic ingestion of ethanol on the autonomic nervous system. 381 27

The hypolipidemic activity of the tetraester of pantethine with 3-(3-pyridinemethoxycarbonyl)propionic acid (MG 28362) was assessed in various experimental conditions versus the corresponding activities of nicotinyl alcohol (NA), nicotinyl alcohol hemisuccinate (NAH), nicotinic acid (NAC), and pantethine tetranicotinate (PTN). In the normolipidemic rat, MG 28362 causes a more durable reduction of non-esterified fatty acids (NEFA) and serum triglycerides than the reference products. NEFA values return slowly to pretreatment levels without causing the rebound effect typical of most nicotinic acid derivatives. Likewise in the test of ethanol-induced hypertriglyceridemia, MG 28362 shows more pronounced and sustained activity compared to the reference products. It is also more effective on Triton hyperlipidemia and on diet-induced hypercholesterolemia; in the latter test, MG 28362 caused no triglyceride accumulation in the liver. Even at high dosage levels, MG 28362 did not cause the characteristic flushing of nicotinic acid congeners. Last, the new substance displays a fairly marked antiaggregating activity on blood platelets, some anti-hypoxic activity, and a generally low order of toxicity.
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PMID:Pharmacological study of a new hypolipidemic drug of prolonged activity, the tetraester of pantethine with 3-(3-pyridinemethoxycarbonyl)propionic acid. 384 36

A rise in blood acetaldehyde concentrations following alcohol ingestion was significantly inhibited when healthy nonflushing subjects were administered a clinical dose of pantethine orally. However, similar findings were not observed in flushing (alcohol-sensitive) subjects lacking hepatic low Km aldehyde dehydrogenase (ALDH). The blood ethanol concentrations were not altered by this treatment in either flushing or nonflushing subjects. Acetaldehyde (45 microM) added in vitro to whole blood and plasma obtained 1 hr after pantethine administration disappeared as the incubation continued similarly as with blood and plasma obtained prior to pantethine treatment. Pantethine-related metabolites, such as taurine, pantetheine, coenzyme A, and pantothenate, activated ALDH in vitro. Hepatic acetaldehyde levels following ethanol loading of rats treated with pantethine were much lower than in untreated rats. The pantethine action observed only in nonflushing subjects might be due to an accelerated oxidation of acetaldehyde by the activation of low Km ALDH by pantethine-related metabolites formed in the liver.
Alcohol Clin Exp Res
PMID:Lowering of blood acetaldehyde but not ethanol concentrations by pantethine following alcohol ingestion: different effects in flushing and nonflushing subjects. 389 99

A sensitive high performance liquid chromatography method has been used to measure aldehyde dehydrogenase (ALDH) activity in hair roots from Caucasian and Japanese subjects. Kinetic studies confirmed previous isoelectric focusing results that hair roots from Caucasians have two forms of ALDH, one low Km form and another high Km form, while hair roots from Japanese individuals who show a flushing reaction after ethanol intake lack, or have low activity of, the low Km form. By taking the ratio of the activities measured at a low (3 microM) and a high (75 microM) concentration of the substrate (3,4-dihydroxyphenylacetaldehyde), a suitable index for ALDH deficiency was obtained. The ratio varied between 1.6 and 3.5 for Caucasians and between 7 and 23 for Japanese flushers, and it was 2.5 for a Japanese nonflusher. The current method allows a more quantitative and qualitative assessment of the ALDH isozyme pattern in hair roots than that obtained with the isoelectric focusing technique.
Alcohol Clin Exp Res
PMID:Application of a high performance liquid chromatography method for screening of aldehyde dehydrogenase isozyme deficiency in hair roots from different ethnic groups. 390 4

Abuse of alcohol (ethanol) and abuse of an increasing number of drugs (e.g. analgesics and sedatives) are among the outstanding social and medical problems of many industrialized countries including Switzerland. Since alcohol consumption has profound effects on both the pharmacokinetic and pharmacodynamic actions of a variety of drugs, the rational use of drugs in alcoholics is an increasingly difficult task and requires a thorough understanding of the physiologic, biochemical, pharmacologic and toxic actions of alcohol. Clinically the most important targets of alcohol action are the liver and the central nervous system (CNS), both of which are frequently involved in the mediation of potentially fatal interactions between drugs and alcohol. In practice the most important of these interactions include (a) inhibition of hepatic (cytochrome P450 dependent) drug oxidation by acute alcohol ingestion resulting in increased bioavailability of drugs that are predominantly excreted by hepatic metabolism, (b) inhibition of acetaldehydedehydrogenase by some drugs with production of an acute flushing reaction to alcohol, (c) increased sensitivity of the CNS to a variety of sedative drugs following acute alcohol ingestion leading to enhanced CNS toxicity of most psychoactive drugs, (d) stimulation of hepatic drug oxidation and decreased CNS sensitivity to sedatives after chronic alcohol abuse, thus explaining the "metabolic" and pharmacodynamic tolerance of these patients towards psychoactive agents, and (e) depressed drug metabolism and increased CNS sensitivity to sedative and hypnotic drugs in patients with cirrhosis of the liver. The mechanisms and practical consequences of the clinically most important influences of acute and chronic alcohol ingestion on the pharmacokinetics and the pharmacodynamic actions of drugs are outlined.
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PMID:[Alcohol, alcoholism and drugs]. 391 83

Research that deals with the causes of alcoholism has been hampered by the absence of factor analyses that deal specifically with ethanol's aftereffects. We factor analyzed 100 alcoholics' reports of the effects that they experience after alcohol consumption. Five factors emerged--Hangover, Euphoria, Flushing, Seizures, and Sleepiness. They are described and discussed. Future investigators may find them helpful in assessing theories on the etiology of alcoholism and in studies of ethanol's effects on subsets of alcohol abusers.
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PMID:Factor analysis of the aftereffects of drinking in alcoholics. 397 32

The drinking behavior and alcohol-induced facial flushing of 1646 Japanese men (50.9% flushers and 48.0% nonflushers) were analyzed from questionnaires completed by their wives. The results indicate a relationship between flushing and various indices of sensitivity to alcohol and low rates of alcohol-related problems. It is proposed that alcohol-induced flushing acts as an inhibitory factor against excessive alcohol use and consequent problems due to drinking.
J Stud Alcohol 1985 May
PMID:Alcohol-induced facial flushing and drinking behavior in Japanese men. 401 Feb 94

Alcohol-sensitive Japanese subjects with facial flushing and an increase in heart rate during ethanol intoxication exhibited marked individual variation in accumulation of acetaldehyde. This variation correlated well with the intensity of the above mentioned physiological responses. Oral pretreatment with 10 mg/kg 4-methylpyrazole, which inhibited the ethanol elimination rate by 15-25%, strongly suppressed both acetaldehyde accumulation and the associated responses. Under this condition, the sensitivity to acetaldehyde appeared to be reduced, and the correlation between the acetaldehyde level and the physiological responses disappeared. The effectiveness of even a low dose of 4-methylpyrazole suggests its clinical usefulness for alleviation of acute acetaldehyde toxicity in alcohol-hypersensitive Japanese individuals as well as in disulfiram-treated alcoholics.
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PMID:Suppression of acetaldehyde accumulation by 4-methylpyrazole in alcohol-hypersensitive Japanese. 402 Dec 29

We evaluated the roles of endogenous opioid peptides and histamine in the pathophysiology of alcohol-induced facial flushing in rosacea. Non-diabetic patients with rosacea ingested 360 ml of 6% ethanol after receiving either subcutaneous naloxone hydrochloride or oral chloropheniramine maleate. Only pretreatment with naloxone blocked the alcohol-induced rosacea flushing (AIRF), suggesting an active role of endogenous enkephalin and/or endorphin in this vascular reactivity. In this respect, AIRF is similar to chlorpropamide alcohol flushing and menopausal flushing.
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PMID:Alcohol-induced rosacea flushing blocked by naloxone. 621 51


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