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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study evaluates the efficacy of prostaglandin E2 (PGE2) as an oxytocic agent for the augmentation of delay in labor in 40 consecutive patients matched with another group of 40 patients (treated with intravenous oxytocin) as to age, parity, maturity, cervical dilation at time of augmentation, and analgesia. Delay in labor was diagnosed clinically when there was arrest in the descent of the presenting part and/or arrest of dilatation of the cervix. All patients were continuously monitored by means of a presenting part electrode and an intrauterine pressure catheter. Both oxytocin and PGE2 were administered via a constant infusion Palmer pump. Standard dosage increments were used until adequate contractions were achieved and no deleterious effect on the fetus was observed. 0.75 ml of 1 mg/ml ampoule of PGE2 in ethanol was diluted in 500 ml normal saline. Initial rate of infusion was 0.285 mcg/minute for a minimum of 30 minutes; the dose was subsequently doubled at intervals of 1 hour until adequate contractions were achieved. Initial rate for infusion for oxytocin was 2mu/minute; the dose was doubled every hour until adequate contractions were noted. Further cervical dilatation and descent of the presenting part occurred in all cases. Mean Apgar scores at 1 and 5 minutes respectively were 7.53 and 9.50 for the PG group, and 6.93 and 9.18 for the oxytocin group. No perinatal deaths occurred. Mean birthweight was 3.34 kg for the PG group and 3.39 kg for the oxytocin group. The oxytocin group exhibited significantly higher augmentation/delivery interval (7.32 hours vs. 5.2 for the PG group, p 0.001), mean basal uterine tone (13.23 vs. 7.38, p 0.001), mean frequency of contraction (4.39 vs. 3.61, p 0.01), and incidence of side effects (nausea, vomiting, and pyrexia). A fetal heart rate of less than 100 beats/minute was seen in 3 patients in the PG group and 7 in the oxytocin group.
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PMID:A comparison of intravenous prostaglandin E2 and intravenous oxytocin for the augmentation of labour complicated by delay. 445 29

College students in Oklahoma completed a self-administered questionnaire to compare the drinking behaviors of culturally active American Indians (N = 34 men and 24 women) an Whites (N = 181 men and 250 women). Significantly more Indians were classified as drinkers, but they had begun drinking at a somewhat later age. Both groups indicated a preference for beer, and they were quite similar in quantity and frequency of beer consumption. White students reported drinking significantly more wine and distilled spirits, and drinking more often in public places, such as bars, pubs, restaurants and parked cars; Indians drank more in their own homes and in the homes of friends. White students tended to cite hedonistic reasons for drinking whereas Indians reported escapist or social reasons and drinking to "get high." Drinking-related problems were reported somewhat more often by Indian students, notably so by Indian women. Indians were more inclined to report the more serious drinking problems of being arrested, blacking out, interference with school or work, an difficulties in human relationships. White students more often cited problems of nausea or vomiting, drinking and driving, doing something that was later regretted and damaging property. It was suggested that the higher Indian arrest rate could be indicative of police bias and that the reports of problem drinking among Indian women be investigated further.
J Stud Alcohol 1984 Sep
PMID:Alcohol consumption patterns among American Indian and white college students. 633 98

Oral amantadine 100 mg and bromocriptine 2.5 + 2.5 mg, alone and in combination with ethanol (1 g/kg), were investigated in two placebo-controlled, double-blind and cross-over trials. In the first trial the psychomotor effects of amantadine and bromocriptine were compared to those of placebo, and in the second trial ethanol was added to the treatment. Bromocriptine lowered serum prolactin levels, thus confirming its absorption. Amantadine and bromocriptine alone had no psychomotor effects but unpleasant sensations, nausea and dizziness were reported after bromocriptine. Ethanol impaired performance in terms of impaired coordinative and reactive skills, lowered tapping speed, prolonged critical flicker interval and reduced gaze nystagmus angle (P less than 0.05 to 0.001; two-way ANOVA). Subjectively, ethanol induced mental slowness, clumsiness and impairment of performance (P less than 0.05 to 0.001). Amantadine and bromocriptine failed to counteract any of these ethanol-induced changes. It is concluded that in man, an acute dopaminergic activation by amantadine or bromocriptine does not significantly modify the psychomotor effects of ethanol.
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PMID:Failure of amantadine and bromocriptine to counteract alcoholic inebriation in man. 650 9

A total of 70 patients presenting with suspected acute trazodone poisoning were notified to the Poisons Unit (National Poisons Information Service for England) from August 1980 until March 1983. Detailed follow-up information was obtained on 41 patients, 22 of whom were thought to have ingested trazodone alone. In these latter patients drowsiness (11), ataxia (5), nausea/vomiting (4) and dry mouth (2) were the manifestations of toxicity reported most frequently, only 2 patients became unconscious (grade 2 or 3 coma), and all recovered uneventfully with no more than minimal supportive therapy. The presence of trazodone was confirmed in 8 out of 9 patients from whom specimens (blood and urine) were received. The highest plasma trazodone concentrations (15 and 19 mg/l, respectively) were both associated with only drowsiness and ataxia. However, in 2 further patients moderate plasma trazodone concentrations (4.2 and 8.2 mg/l, respectively) were associated with deep (grade 3-4) coma, although 1 of these latter patients had also ingested ethanol (plasma concentration 3.0 g/l). Although acute trazodone poisoning does not appear to be associated with cardiac arrhythmias or convulsions, these results emphasise that drowsiness and ataxia are commonly encountered, while coma may occur in severe cases. The possible contribution of metabolites of trazodone to toxicity and the potentiating effect of co-ingested drugs or alcohol must be remembered.
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PMID:Acute trazodone poisoning: clinical signs and plasma concentrations. 671 57

We propose that alcohol is a food and that drinking alcohol is fundamentally a feeding habit. Many feeding habits are acquired by Pavlovian conditioning in which the flavor of food [conditioned stimulus (CS)] is adjusted by the aftereffects of the ingested meal [unconditioned stimulus (US)]. Thus, repletion of nutritive deficits or recuperation from illness enhances flavor palatability, whereas toxicosis or nausea reduces it. After reviewing the major functional and neurophysiological features of this homeostatic conditioning process, we relate them to the flavor (CS) and effect (US) of alcohol. We present evidence suggesting that the caloric effects of low-dose alcoholic drinks may help to establish and maintain alcohol habits through conditioned palatability changes. Included is a general treatment of the antagonistic interactions between such homeostatic conditioning and the behavioral mechanisms used to defend again peripheral insults such as electric shock. In closing, we discuss the implications for modifying alcoholic habits.
Recent Dev Alcohol 1984
PMID:Alcohol-ingestive habits. The role of flavor and effect. 672 72

Ten healthy male volunteers were exposed for 4 h to two concentrations [6 and 11.5 mumol/l (636 and 1,218 mg/m3)] of m-xylene or/and given single doses (0.4 and 0.8 g/kg) of ethyl alcohol. Exposure to two xylene concentrations combined with the higher dose (0.8 g/kg) of alcohol was also conducted. Vestibular functions (positional nystagmus with electronystagmography, body balance) and visual function (flicker fusion) were measured. Both alcohol doses increased body sway and the intensity of nystagmus more than either concentration of xylene did, but they had little effect on visual functions. The effects of alcohol on vestibular functions were dose-dependent. The effects of xylene alone on the vestibular system were rather small, and those on the visual functions negligible. The combined effect of alcohol and the lower concentration of xylene (6 mumol/l) on body sway was additive, but the higher xylene concentration (11.5 mumol/l) antagonized the effect of alcohol on body sway and positional nystagmus. Two subjects experienced nausea and vomited exposure to alcohol and the higher xylene concentration. Mild impairment in visual functions was noted in the combined exposure. Alcohol significantly increased the blood m-xylene concentrations, a finding that suggests that their antagonism was pharmacodynamic rather than pharmacokinetic.
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PMID:Effects of xylene and alcohol on vestibular and visual functions in man. 696 75

Ingestion of a moderate dose of ethanol (0.8 g/kg) by volunteers prior to 4-h inhalation exposure to m-xylene (6.0 or 11.5 mmol/m3) caused marked alterations in xylene kinetics. After ethanol intake the blood xylene level rose about 1.5-2.0-fold and urinary methylhippuric acid excretion declined by about 50% suggesting that ethanol decreased the metabolic clearance of xylene by about one half during xylene inhalation. This effect was noticeable up until a few hours after completed xylene exposure. Urinary excretion of 2,4-xylenol, the minor m-xylene metabolite, was generally not decreased by ethanol and sometimes the reverse seemed to be the case. The disturbance of xylene kinetics can be hypothesized to be caused mainly by ethanol-mediated inhibition of microsomal metabolism. When four volunteers who ingested ethanol prior to m-xylene inhalation at the higher concentration were monitored for blood acetaldehyde, transiently raised levels were found without notable effects on ethanol elimination. This observation may explain why some individuals experienced dizziness and nausea during the combined ethanol-xylene exposure.
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PMID:Metabolic interaction between m-xylene and ethanol. 709 64

Acute ethanol ingestion inhibits the metabolism of the common industrial solvents trichloroethylene and dimethylformamide. The solvents in turn may interact with ethanol metabolism as shown by an accumulation of acetaldehyde and occasional symptoms of alcohol intolerance. It was recently found that mutual metabolic interaction occurs even in the context of ethanol ingestion (0.8 g/kg in single dose) combined with subsequent inhalation exposure to m-xylene (6.0 & 11.5 mmol/m3 (140 & 280 ppm), over 4 h). Ethanol impaired the metabolic clearance of m-xylene, raised the blood xylene concentration, and decreased the urinary excretion of methylhippuric acid. Thus, ingestion of ethanol is a noticeable source of error in the biological monitoring of xylene uptake. Some people appear to be susceptible to combined ethanol-xylene exposure and may develop nausea and dermal flush.
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PMID:Acute solvent-ethanol interactions with special reference to xylene. 713 27

A serious, relatively unrecognized, occupational health problem involves the interaction of ethyl alcohol and chemical agents used in industry. Workers who drink alcohol and are exposed to certain chemical agents may experience adverse health effects such as nausea, dizziness, headache, and liver damage. This report reviews the synergistic interactions of ethanol with compounds such as the thiurams, amides, oximes, halogenated hydrocarbons, and metals. Also discussed is the effect of ethanol as a cofactor with vinyl chloride in the etiology of cancer.
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PMID:The interaction of ethyl alcohol and industrial chemicals. 717 Oct 89

Amit and Sutherland's conclusions concerning the use of conditioned taste aversions for alcoholism treatment are critically evaluated. Their conclusion that painful electric shock is contraindicated as a basis for alcohol taste aversions is consistent with the animal and human literature which depicts nausea as a more biologically appropriate US for taste aversion formation. However, Amit and Sutherland also conclude that alcoholics will not develop illness-induced alcohol aversions because animal studies show that aversion acquisition is disrupted by preconditioning familiarity with the conditioned stimulus (CS) - flavor - or unconditioned stimulus (US) - illness. This conclusion is untenable because Amit and Sutherland only considered animal conditioning methods that differed markedly from aversion therapy practices. Other animal studies modeled after aversion therapy procedures clearly show CS and US preexposure effects to be transitory phenomena. Moreover, experimental and clinical data show humans to be quite susceptible to taste aversion formation, and that many alcoholics do form strong alcohol aversions under appropriate conditioning parameters. Additional implications of the animal literature for effective aversion therapy are explored, and the paper concludes with a discussion of covert sensitization, a promising verbal aversion therapy which has resulted in the development of strong alcohol aversions in many volunteer subjects at the Augusta Veterans Administration Medical Center.
Drug Alcohol Depend 1980 Feb
PMID:A reconsideration of the relevance of recent animal studies for development of treatment procedures for alcoholics. 718 41


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