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Ethanol intake

Rats of the Charles Foster strain were allowed to swim in a 20 cm deep plastic tub. They swam actively, paused for sometime and continued swimming. The period of immobilization with the head seldom protruded over the surface of water was recorded for each rat. The duration of immobilization is directly proportional to the depressive like state. The highly active rats are characterized by a period shorter than 130 sec and the lowly active ones by the period longer than 300 sec. It is the lowly active rats that are potential alcoholics (Paul et al., 1992). These rats were selected for tests involving ethanol consumption. In a random population of rats the [Pg.18]


The production rate of acetic acid was 2kg-h 1, where the maximum acetic acid concentration was 12%. Air was pumped into the fermenter with a molar flow rate of 200 moMi-. The chemical reaction is presented in (E. 1.1) and flow diagram in Figure 9.5. Determine the minimum amount of ethanol intake and identify the required mass balance for the given flow sheet. The ethanol biochemical oxidation reaction using A. aceti is ... [Pg.239]

Anxiolytics with little abuse potential, such as buspirone, and antidepressants that have a benign side-effect profile and may reduce ethanol intake warrant careful evaluation in the treatment of anxious and depressed alcoholic patients. [Pg.40]

Naranjo CA, Sellers EM, Chater K, et al Non-pharmacological interventions in acute alcohol withdrawal. Clin Pharmacol Ther 34 214—219, 1983 Naranjo CA, Sellers EM, Roach CA, et al Zimelidine-induced variations in alcohol intake hy nondeptessed heavy drinkers. Clin Pharmacol Ther 35 374-381, 1984 Naranjo CA, Sellers EM, Sullivan ]T, et al The serotonin uptake inhibitor citalopram attenuates ethanol intake. Clin Pharmacol Ther 41 266-274, 1987 Naranjo CA, Sullivan ]T, Kadlec KE, et al Differential effects of viqualine on alcohol intake and other consummatory behaviors. Clin Pharmacol Ther 46 301 -309,1989 Naranjo CA, Kadlec KE, Sanhueza P, et al Fluoxetine differentially alters alcohol intake and other consummatory behaviors in problem drinkers. Clin Pharmacol Ther 47 490 98, 1990... [Pg.50]

MACLURE M (1993) Demonstration of deductive meta analysis ethanol intake and risk of myocardial infarction. Epidemiol Rev. 15 1-24. [Pg.237]

Arnone M, Maruani J, Chaperon F. Selective inhibition of sucrose nd ethanol intake by SR141716a, an antagonist of central cannabinoid (CB1) receptors. Psychopharmacology 1998 132 104-106. [Pg.126]

Social habits (e.g., cigarette smoking, excessive ethanol intake) and medications (Table 83-1) can also cause ED. [Pg.949]

According to Valimaki et al. (V2) moderate ethanol intake induces a slight increase of Lp(a) (F6, M14). Huang (H40) observed an increase of Lp(a) after abstinence from alcohol use by alcohol-dependent patients. [Pg.103]

Concurrent use with ethanol may alter the patterns of drug use. While low to moderate doses of ethanol do not influence the amount of cannabis self-administered by humans, there is evidence that chronic THC administration can increase ethanol intake (McMillan and Saodgrass 1991 Chaitand Perry 1994). [Pg.433]

McMillan DE, Snodgrass SH. (1991). Effects of acute and chronic administration of delta 9-tetrahydrocannabinol or cocaine on ethanol intake in a rat model. Drug Alcohol Dependence. 27(3) 263-74. [Pg.562]

Blanchard BA, Click SD. 1995. Sex differences in mesolimbic dopamine responses to ethanol and relationship to ethanol intake in rats. Recent Dev Alcohol 12 231-241. [Pg.243]

Olive ME, Koenig HN, Nannini MA, Hodge GW. 2002. Elevated extraceUular erf levels in the bed nucleus of the stria terminalis during ethanol withdrawal and reduction by subsequent ethanol intake. Pharmacol Biochem Behav 72 (1-2) 213-220. [Pg.251]

Ethanol can increase the levels of many enzymes involved in metabolism of xenobiotics. Prolonged ethanol intake causes irreversible damage in the central nervous system and in the liver, resulting in marked decreased capacity for detoxification of xenobiotics and thereby increased sensitivity to a number of chemicals (KEMI 2003). [Pg.249]

Kniepert E, Siegemund A, Rosenkranz M, et al. 1991. Toxic effects of carbon tetrachloride during short and long term ethanol intake in rats. Arch Toxicol Supp114 263-265. [Pg.169]

Glyburide has high potency and its duration of action extends at least over 24 hours. It is metabolized in the liver. It can cause serious hypoglycemia. As is the case with chlorpropamide, a minority of patients can react with flushes after ethanol intake when on glyburide medication. [Pg.397]

Insulin resistance/hyperinsulinemia Ethanol intake of more than 30 ml per day Anxiety-induced hyperventilation or panic attacks Chronic pain... [Pg.580]

Fernandez-Teruel A, DriscoU P, Gil L, Tobena A, Escorihuela RM (2002) Enduring effects of environmental enrichment on novelty seeking, saccharin and ethanol intake in two rat lines (RHA/Verh and RLA/Verh) differing in incentive-seeking behavior. Pharmacol Biochem Behav 73 225-231... [Pg.63]

Holter SM, Danysz W, Spanagel R (2000) Novel uncompetitive N-methyl-D-aspartate (NMDA)-receptor antagonist MRZ 2/579 suppresses ethanol intake in long-term ethanol-experienced rats and generalizes to ethanol cue in drug discrimination procedure. J Pharmacol Exp Ther 292 545-552... [Pg.292]

Shanmugasundaram, E. R., and K. R. Shanmugasundaram. An Indian herbal formula (SKV) for controlling volun- SO076 tary ethanol intake in rats with chronic alcoholism. J Ethnophar-macoll986 17(2) 171-182. [Pg.457]

Naranjo CA, Sellers EM, Jullivan JT, et al. The serotonin uptake inhibitor citalopram attenuates ethanol intake. Clin Pharmacol Ther 1987 41 266-274. [Pg.309]

Savolainen, H., Vainio, H., Helojoki, M. Elovaara, E. (1978) Biochemical and toxicological effects of short-term intermittent xylene inhalation exposure and combined ethanol intake. Arch. Toxicol., 41, 195-205... [Pg.1207]

Sukul NC, Ghosh S, Sinhababu SP, Sukul A. 2001. Strychnos nux-vomica extract and its ultra high dilution reduce voluntary ethanol intake in rats../ Alt Comp Medl 187-193. [Pg.118]

D.G. McCarver, R. Byun, R.N. Hines, M. Hicheme, W. Wegenek, A Genetic Polymorphism in the Regulatory Sequences on Human CYP2E1 Association with Increased Chloroxazone Hydroxylation in the Presence of Obesity and Ethanol Intake , Toxicol. Appl. Pharmacol., 152, 276-281 (1998). [Pg.23]

An extract of Radix puerariae, a herb long used in traditional Chinese medicine for alcohol addiction and intoxication, suppresses the free-choice ethanol intake of ethanol. The isoflavonoids... [Pg.335]

Landolt HP, Roth C, Dijk DJ, Borbely AA. Late-aftemoon ethanol intake affects nocturnal sleep and the sleep EEG in middle-aged men. J Clin Psychopharmacol 1996 16 428 136. [Pg.287]

McCarver DG, Byun R, Hines RN, Hichme M, Wegenek W. A genetic polymorphism in the regulatory sequences of human CYP2E1 association with increased chlorzoxazone hydroxylation in the presence of obesity and ethanol intake. Toxicol Appl Pharmacol 1998 152 276-281. [Pg.199]

The clinical importance of ALDH2 deficiency for alcohol ingestion rests on the chemical reactivity and therefore toxicity of the ethanol-derived substrate acetaldehyde. It may produce facial flushing and a drop in blood pressure with tachycardia (94), i.e., effects which are perceived as an unpleasant sensation. These tend to occur after ethanol intake if the enzymatic removal of acetaldehyde is not fast enough. The unpleasantness, or even an embarassed reaction to the visual flushing, have been deterrents of excessive ethanol consumption and thereby of alcoholism. In Japan however, the deterrent effect of these sensations has been claimed to be gradually diminishing (95). [Pg.235]

From these studies it appears that in rats with a high ethanol intake obtained by selective breeding or by the sweet-fading techniques and on a limited access paradigm of operant ethanol self-administration, neuroleptics consistently reduce responding for ethanol. This effect seems specific for ethanol, since responding for water was unimpaired. [Pg.341]

KiianmaaK, Andersson K, Fuxe K (1979) On the role of ascen ding dopamine systems in the contral of voluntary ethanol intake and ethanol intoxication. Pharmacol Biochem Behav 70 603-608. [Pg.383]

Mitochondrial oxidative stress and mitochondrial GSH defense affects transcription factor activation. Oxidant stress in mitochondria not only can promote the loss of mitochondrial GSH and mitochondrial functions, but also can promote extramito-chondrial activation of NF-kB and therefore may affect nuclear gene expression. Mitochondria are targets of cytokines leading to the overproduction of reactive oxygen species induced by ceramide, a lipid intermediate of cytokine action and closely associated with apoptosis. Chronic ethanol intake depletes liver mitochondrial glutathione due to an ethanol-induced defect in the transport of GSH from cytosol into the mitochondrial matirix. This sensitizes liver cells to the prooxidant effects of cytokines and prooxidants generated by the oxidative metabolism of ethanol. [Pg.350]

The paracetamol-alcohol interaction is complex acute and chronic ethanol intake has opposite effects. [Pg.133]


See other pages where Ethanol intake is mentioned: [Pg.527]    [Pg.203]    [Pg.238]    [Pg.662]    [Pg.453]    [Pg.496]    [Pg.324]    [Pg.288]    [Pg.18]    [Pg.336]    [Pg.565]    [Pg.160]    [Pg.164]    [Pg.169]    [Pg.270]    [Pg.1906]   
See also in sourсe #XX -- [ Pg.18 ]




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