Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bromocriptine (0.5-6.0 mg/day) was administered to seven unmedicated chronic schizophrenic and two schizoaffective patients. Transient slight improvement was noted in four patients and marked improvement in one other. Clinical improvement was associated with nausea and drowsiness. These doses of bromocriptine stimulated serum growth hormone and inhibited serum prolactin levels in some subjects. These results suggest that bromocriptine may stimulate dopamine autoreceptors and, through this mechanism, attenuate symptoms in a small proportion of psychiatric patients.
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PMID:Effect of low-dose bromocriptine in treatment of psychosis: the dopamine autoreceptor-stimulation strategy. 641 30

The space adaptation syndrome is one of the more vexing problems confronted by our nation's astronauts during their journeys. This syndrome may be a variant of motion sickness, although this possibility has been questioned. Physostigmine, a centrally active cholinesterase inhibitor which increases brain acetylcholine, was found to cause a motion sickness-like syndrome--in psychiatric patients and normals--including nausea, emesis, malaise, dysphoria, increases in serum ACTH, beta-endorphin, cortisol, and prolactin, Neostigmine, a non-centrally acting cholinesterase inhibitor, and saline placebo caused no such effects. The above effects closely parallel those of motion sickness. Thus, the effects of physostigmine may be a convenient model for screening for treatments for motion sickness or space adaptation syndrome, or for predicting who will develop these syndromes.
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PMID:A cholinomimetic model of motion sickness and space adaptation syndrome. 648 3

The tolerance and prolactin (PRL) release-inhibiting action of the 8 alpha-aminoergoline, mesurlergine, were investigated. In a blind crossover study in six subjects with hyperprolactinemia, 0.5 mg mesulergine induced fewer side effects than did 2.5 mg bromocriptine, while the PRL release-inhibiting effect of the two was of the same order. Six different subjects with suspected PRL-secreting pituitary adenomas who (repeatedly) had to discontinue bromocriptine because of nausea, vomiting, or symptoms of orthostatic hypotension were treated for 20 mo with mesulergine (1 to 2 mg/day). Mesulergine did not induce side effects and its actions resembled those of bromocriptine. Mesulergine induced cessation of galactorrhea and resumption of normal menstrual cycles in five subjects, while in one subject an insufficient luteal phase persisted. No abnormalities in routine blood parameter estimations were observed. In two of three subjects there was shrinkage of a pituitary tumor after 12 to 15 mo on mesulergine. Mesulergine did not directly inhibit PRL release by cultured normal rat pituitary cells and human prolactinoma cells and it antagonized the action of dopamine in a dose-dependent manner. This suggests that the dopaminergic action is carried out by a metabolite of mesulergine, while the parent drug probably prevents the well-known side effects of dopamine-agonistic drugs by its dopamine receptor blocking activity. Because of its acceptability, mesulergine might be important in the treatment of hyperprolactinemia and perhaps also of acromegaly and Parkinson's disease.
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PMID:Mechanism of action and tolerance of mesulergine. 648 83

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

Plasma levels and urinary excretion of the dopamine agonist, transdihydrolisuride (TDHL), were measured by radioimmunoassay in healthy male volunteers given TDHL 50 micrograms i.v. and oral doses of 200, 400 and 800 micrograms. Plasma prolactin was also measured by radioimmunoassay. Following i.v. injection, the concentration of TDHL declined with a half-life of 37 +/- 19 min. The total clearance was 38 +/- 27 ml/min/kg and the apparent volume of distribution was 1.3 +/- 0.41/kg. The bioavailability of oral TDHL was proportional to the dose; after 200, 400 and 800 micrograms the bioavailability was 20 +/- 25%, 31 +/- 24% and 48 +/- 26%. TDHL was almost totally metabolized and less than 0.5% of the dose was excreted unchanged in urine in 24 h. Plasma prolactin levels were depressed by 66 +/- 15%, 75 +/- 11% and 80 +/- 7% after TDHL 200 micrograms, 400 micrograms and 800 micrograms. The effect lasted for more than 12 h after the lowest dose and for more than 24 h after 400 and 800 micrograms. Side effects, mainly nausea and headache, only occurred at the two highest dose levels.
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PMID:Pharmacokinetics and pharmacodynamics of the ergot derivative, transdihydrolisuride, in man. 651 Apr 62

Metrizamide (Amipaque), a water soluble nonionic contrast medium has less toxic effect in comparison with other contrast media, and it is now widely used for myelography, cisternography, ventriculography and cerebrospinal fluid dynamic imaging. However, as the number of cases in which this medium has been utilized has gradually increased, incidents of toxic manifestations have been reported. Among these, there are a considerable number of case reports referring to metrizamide encephalopathy, but only a few authors reported the appearance of triphasic waves on EEG when they occurred. The authors experienced one case of metrizamide encephalopathy accompanied by frequent appearance of triphasic waves on EEG. A 31-year old male was admitted to our hospital with the complaint of right homonymous hemianopsia. At that time he was fully conscious and mentally alert. On CT, 39 mm X 45 mm partially enhanced isodense mass was revealed on the enlarged sella turcica. Laboratory findings showed high titer of prolactin (10200 ng/ml). Premedication of 100 mg phenobarbital i.m. was followed by the tomography of the sella turcica, using 8 ml of 250 mgI/ml metrizamide injected into L 3-L 4 subarachnoid space. Several hours after the examination, he complained of slight nausea and was kept in bed with his head placed in an elevated position. The next morning, he was found to be in a drowsy state. He was disoriented and could not respond adequately to questions asked. His naming of daily necessities was also poor, although he knew how to use them.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of metrizamide encephalopathy with triphasic waves on EEG]. 654 77

Dopaminergic (DA) transmission is a major regulator of pituitary prolactin (PRL) secretion. Strategies to assess abnormalities of DA regulation in mental illness have thus included comparisons of patients' and normals' serum PRL levels before and after the administration of DA agonists and antagonists. These clinical research strategies suffer from a number of shortcomings. There is a wide interindividual variability of normal basal PRL levels, and intraindividual variability has been little studied. Large interindividual variability of PRL responses to DA antagonist challenges has also been observed in normals and reported to be strongly correlated to variation in serum levels of the challenge drug. Assessment of DA agonist challenges is hampered by the fact that low basal levels of serum PRL make suppression difficult to measure; a further problem is the confounding effect of nausea when these drugs are given in high doses. In this study of normals, individual basal serum PRL levels were found to be stable over a mean period of 10 months, with interindividual variance vastly greater than intraindividual variance. Thus, state alterations in mental illness may best be studied using a longitudinal design for measurements of PRL levels in patients, thereby avoiding confounding interindividual variability. Moreover, it appears that alterations of PRL levels between groups or within patients, even though within the normal range, may have individual physiological significance. A study of the PRL responses to haloperidol (hal) and hal + apomorphine (apo) challenges in normals revealed a strong correlation despite a highly significant 51% reduction in PRL response with the addition of apo. Because this correlation is dependent upon a normal or limited range of DA regulation, the study of these two responses in abnormal populations may be more revealing of DA abnormalities than the study of PRL responses to single DA agonist or antagonist challenges.
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PMID:Prolactin studies in normals: implications for clinical research. 657 96

The present study examined the relationship between plasma prolactin (PRL) and central blood volume (CBV) in man. 6 adult males lay in a lower body pressure box at a thermoneutral ambient temperature (27 degrees C) on three occasions. On each occasion a 70-min control period was followed by a 20-min exposure to a lower body pressure of either 0 mm Hg, -20 (lower body negative pressure; LBNP), or +10 mm Hg (lower body positive pressure; LBPP), followed by a 60-min recovery period. Blood was drawn and urine collected at 30-min intervals. Blood pressure and heart rate were monitored at 30-min intervals during control and recovery periods and at 10-min intervals during lower body pressure exposure. Neither 0 mm Hg, LBNP, nor LBPP altered plasma osmolality, sodium, or potassium levels. Increasing CBV by LBPP increased systemic blood pressure (p less than 0.01) but had no effect on heart rate, plasma PRL, or urine osmolality. LBNP, in contrast, increased heart rate (p less than 0.05). Half of the subjects undergoing LBNP developed presyncopal symptoms, characteristic of a vasovagal reaction which includes precipitous hypotension. Subjects developing these symptoms tended to exhibit an increase in plasma PRL and an increase in urine osmolality. Asymptomatic subjects demonstrated no change in plasma PRL or urine osmolality. In addition, subjects exhibiting a PRL response to LBNP had a higher control period plasma PRL baseline (231%) than did asymptomatic subjects. These data suggest that while plasma PRL levels are not sensitive to nonhypotensive changes in CBV, they do respond to hypotensive decreases in CBV and/or its associated nausea.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma prolactin responses to acute changes in central blood volume in man. 664 22

Sodium bromide was administered orally in capsules to healthy volunteers in doses of 0, 4 or 9 mg Br-/kg/day using a double-blind design. Each treatment was given to seven males for 12 weeks and to seven non-pregnant females (not using oral contraceptives) over three full cycles. Special attention was paid to possible effects on the endocrine and central nervous systems. At the start and end of the study, a full medical history, the results of a physical examination, haematological studies and standard clinical chemistry and urine analyses were recorded for each subject. These showed no changes for individuals following treatment, except for some incidence of nausea associated with bromide-capsule ingestion. Mean plasma-bromide concentrations at the end of treatment were 0.08, 2.14 and 4.30 mmol/litre for males and 0.07, 3.05 and 4.93 mmol/litre for females of the 0-, 4- and 9-mg Br-/kg/day groups, respectively. Plasma half-life was about 10 days. In the females taking 9 mg Br-/kg/day (but in no other group) there was a significant (P less than 0.01) increase in serum thyroxine and triiodothyronine between the start and end of the study but all concentrations remained within normal limits. No changes were observed in serum concentrations of free thyroxine, thyroxine-binding globulin, cortisol, oestradiol, progesterone or testosterone, or of thyrotropin, prolactin, luteinizing hormone (LH) and follicle-stimulating hormone before or after the administration of thyrotropin-releasing hormone and LH-releasing hormone. Analysis of neurophysiological data (EEG and visual evoked response) showed a decrease in delta 1- and delta 2-activities and increases in beta-activities and in mean frequency (Mobility parameter) in the groups on 9 mg Br-/kg/day, but all the findings were within normal limits.
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PMID:The influence of sodium bromide in man: a study in human volunteers with special emphasis on the endocrine and the central nervous system. 668 22

A 10-day random double-blind study on the effect of bromocriptine versus placebo in severe alcohol-withdrawal symptoms was conducted in 60 alcoholics. The effect of bromocriptine--a dopamine agonist--was significantly better than placebo in ameliorating the following symptoms: anxiety, restlessness, depression, tremor, sweating and nausea as well as the total score of these symptoms. Also in the evaluation of specific symptoms according to a symptom check list of psychiatric, behavioural and social aspects, and in a global evaluation, bromocriptine was clearly superior to placebo. Serum prolactin studied on the first and tenth day of the survey showed a significant increase occurring in the placebo-treated patients. Side effects related to the use of bromocriptine were negligible. Our findings support recent experimental evidence that alcohol-withdrawal symptoms, at least in part, are related to a transient dopaminergic dysfunction in the brain.
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PMID:Bromocriptine in the treatment of the alcohol-withdrawal syndrome. 676 59


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