Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

2-Chloro-11-(2-dimethyl-aminoethoxy)dibenzo [b,f]thiepine (zotepine) is a new neuroleptic drug with a chemical structure different from known neuroleptics. The psychopharmacological effects of zotepine in mice, rats and dogs were studied and compared with those of commercially available neuroleptics. Haloperidol and perphenazine were the most active and thioridazine was the least active in hibiting apomorphine-induced gnawing and circling movement, methamphetamine-induced gnawing and circling movement, conditioned avoidance response, motor activity, dopamine-induced pancreatic secretion and apomorphine-induced vomiting. These drugs also had the same order of potency in inducing catalepsy and increasing dopamine turnover and prolactin release. Chlorpromazine, propericiazine and thiothixene were intermediate in potency. Zotepine equalled chlorpromazine in most activities, however, it was clearly less active than chlorpromazine in potentiation of barbiturate sleep and cardiovascular effect.
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PMID:Pharmacological study of [2-chloro-11-(2-dimethylaminoethoxy) dibenzo[b,f]thiepine] (zotepine), a new neuroleptic drug. 4 13

Bromocriptine, a lysergic acid derivative with a bromine atom at position 2, has been found to have unique effects on the dopamine receptors in the pituitary and central nervous system and peripherally. It is rapidly and completely absorbed from the gut and is mainly excreted in the bile and faeces. It seems to have a particular specificity for the pituitary prolactinotrophe although it does have other effects in different diseases states. In spite of the fact that it is an ergot derivative, it is remarkably free of ergot vascular side effects in the doses needed for therapeutic benefit. The most common adverse effect are nausea, vomiting and postural symptoms. These can be overcome by starting at low doses and increasing the therapeutic levels. Its major use is in the suppression of prolactin in states where this hormone is elevated irrespective of cause. It has also been used in the treatment of acromegaly and is under investigation for use in other disease states probably linked with prolactin system or dopaminergic receptors.
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PMID:Pharmacology of bromocriptine in health and disease. 22 67

A new peripheral dopamine agonist which causes dopaminergic renal vasodilation, was tested for central dopaminergic activity. SK & F 38393 stimulated the dopamine-sensitive adenylate cyclase in homogenates of rat caudate, as a partial agonist, and caused contralateral rotation in rats with unilateral 6-OHDA lesions of substantia nigra. Rotation was shown to be due to a direct effect on supersensitive dopamine receptors. Stimulation of cAMP formation and rotation were blocked by dopamine antagonists. In contrast to other dopamine agonists, SK & F 38393 did not cause stereotypy, emesis or inhibition of prolactin release, nor did SK & F 38393 affect dopamine turnover. The results suggest that SK & F 38393 may selectively stimulate supersensitive central dopamine receptors in vivo or may activate only a certain subclass of dopamine receptors including the receptor in the renal vasculature and the adenylate cyclase coupled postsynaptic receptor in the caudate.
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PMID:The central effects of a novel dopamine agonist. 56 69

A series of rigid analogs of apomorphine lacking aromatic hydroxyl substitutents were evaluated for dopaminergic properties. Three compounds, N-methyl-N-propyl-2-aminotetralin (Me-Pr-2-AT), N-N-dipropyl-2-aminotetralin (Di-pr-2-AT) and N,N-dipropyl-2-aminoindane (Di-Pr-2-AI) induced emesis in dogs, contralateral circling in unilaterally lesioned rats, and inhibited prolactin secretion. The induced circling responses, however, were attenuated by prior treatment with alpha-methyl-p-tyrosine methyl ester (AMPTME) and the compounds were weak inhibitors of 3-H-dopamine binding in calf caudate homogenates. The possibility that these agents may be metabolically activated in vivo is discussed.
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PMID:Dopaminergic effects of non-hydroxylated rigid analogs of apomorphine. 57 41

28 women with amenorrhea-galactorrhea were investigated endocrinologically and treated with bromocryptine 2.5 mg twice daily, ranging from 18 to 150 days. These women were classified into 6 with hypothyroidism, having prolactin (PRL) over 30 ng/ml, thyroid stimulating hormone (TSH) over 8 mcU/ml, luteinizing hormone (LH)6-20 mlU/ml and greater than follicle stimulating hormone (FSH); 8 with radiologically diagnosed pituitary tumors, LH, FSH, and increased PRL; 9 with similar endocrine profiles and suspected pituitary tumors; and 3 with high PRL considered idiopathic. 5 of the hypothyroid group were followed, and achieved ovulation, reduced TSH, PRL, and lactation, and 3 became pregnant. Of the 8 with tumors, 5 menstruated, 4 ovulated, 3 conceived, 3 had reduced lactation, 2 had reduced PRL, and 1 failed to respond clinically; 9 with suspected tumors took bromocryptine for at least 20 days, resulting in 4 pregnancies and 3 with regular menses. The 3 idiopathic cases showed lower PRL and regular ovarian function, 1 pregnancy, yet 1 developed pseudocyesis and recurrent galactorrhea. 2 women had to stop bromocryptine because of vomiting. This drug is longer-acting than L-dopa and safer than estrogen-progestagen combinations in cases of pituitary tumors. Bromocryptine reduces galactorrhea and associated hypothyroidism temporarily.
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PMID:Bromocryptine therapy in cases of amenorrhea-galactorrhea. 57 72

This study reports a case of allergy to ergot-derived drugs in a patient with a prolactin (PRL)-secreting microadenoma. The anamnesis revealed allergic reactions to the administration of analgesics and antibiotics. The administration of dopamine agonist drugs, such as bromocriptine (BRC; 2.5 mg) or lisuride (0.2 mg), induced after a few minutes the appearance of nausea, vomiting, postural hypotension, headache, edema of the glottis with dispnea and acroedema. The edemas disappeared a few hours after the administration of antihistaminic drugs while nausea, vomiting, postural hypotension and headache persisted for a few days. Therefore, the patient was tested with another dopamine agonist non-ergot-derived drug, quinagolide (CV 205-502), which did not cause side effects or allergic reactions. Furthermore, not only was the responsiveness to the drug optimal but it also normalized the PRL levels, and menses reappeared after more than a 5-year amenorrhea. This report suggests that ergot-derived drugs, such as lisuride and BRC, seldom induce allergic reactions apart from common side effects. Consequently, the feasibility of using a new drug with a different molecular structure (non-ergot derived) effective in the therapy of hyperprolactinemic syndromes represents a good alternative to conventional therapy.
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PMID:Usefulness of CV 205-502 in a case of allergy to ergot-derived drugs. 130 52

The neuroendocrine response to L-5-hydroxytryptophan was compared in 37 prepubertal children who met the Research Diagnostic Criteria for major depressive disorder with that in 23 normal children with no lifetime history of any psychiatric disorder and very low rates of depression in both first- and second-degree relatives. Intravenous L-5-hydroxytryptophan (0.8 mg/kg) was given over a 1-hour interval after preloading with oral carbidopa, an inhibitor of peripheral but not central L-5-hydroxytryptophan metabolism. L-5-Hydroxytryptophan, a precursor of serotonin, increases serotonin turnover in the central nervous system when given after carbidopa. Seven (19%) of the 37 children with major depressive disorder and two (9%) of the 23 normal children had nausea or vomiting and therefore did not complete the full infusion. They were subsequently excluded from data analysis. After this stimulation, prolactin, cortisol, and growth hormone secretion were compared between diagnostic groups. The depressed children secreted significantly less cortisol (effect size, 0.70) and significantly more prolactin (effect size, 0.83). There was a sex-by-diagnosis interaction in prolactin response to L-5-hydroxytryptophan and, on examination, the prolactin hypersecretion was seen in depressed girls but not in depressed boys compared with same-sex controls. There was no significant stimulation of growth hormone in either group. These findings are consistent with dysregulation of central serotonergic systems in childhood major depression.
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PMID:Neuroendocrine response to L-5-hydroxytryptophan challenge in prepubertal major depression. Depressed vs normal children. 144 21

Women who are of normal weight and have bulimia nervosa exhibit multiple neuroendocrine disturbances. We hypothesized that bingeing and vomiting behavior could be contributory because food consumption in healthy volunteers increases plasma cortisol and prolactin secretion and suppresses growth hormone secretion. Thus, we investigated the effects of bingeing and vomiting on the circadian pattern (measurements every 20 min for 24 hr) of these hormones in comparison to healthy control women eating normally. Bingeing and vomiting were associated with modest increases in cortisol and prolactin and reductions in growth hormone secretion. However, this bingeing or purging did not alter mean 24-hr pattern of cortisol and growth hormone secretion as values for bulimics were similar to controls. While mean daytime patterns of prolactin secretion were similar in bulimics and controls, bulimic patients had a significant reduction of nocturnal prolactin levels. In summary, bingeing and vomiting does not appear to have a substantial influence on hormonal secretion. However, bulimic women have blunted nocturnal prolactin patterns.
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PMID:Circadian patterns of cortisol, prolactin, and growth hormonal secretion during bingeing and vomiting in normal weight bulimic patients. 189 60

A simple open study was undertaken in order to assess the value of the dopamine-agonist lisuride in the treatment of patients with two types of hyperprolactinemia: Six patients with pituitary adenoma and two with "idiopathic hyperprolactinemia". All patients were started on a dose of 0.2 mg per os per day until values of serum prolactin became normal (two to eleven months in the first group), except for two that required increment to 0.4 mg/day after the first four months without effect; both responded satisfactorily to the increased dose. Side effects were mild nausea end occasional vomiting, except in one case of the first group, which abandoned the treatment due to intense vomiting. One of the patients of "idiopathic hyperprolactinemia" required the dose to be increased to 0.4 mg/day after the first four months and finally responded after two more months with the higher dose. The second patient of this group did not respond even to a dose of 1 mg/day, which was otherwise well tolerated.
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PMID:[Treatment of the hyperprolactinemic states with lisuride in a simple open study]. 193 25

Patients previously treated with H2-receptor blocking agents (cimetidine or ranitidine) exhibited a complex neurobehavioral and gastroenteric syndrome, including anxiety, insomnia, anorexia, growing thin, irritability, tachycardia, diarrhoea, nausea, vomiting, abdominal pain, headache, vertigo. These symptoms were dramatically reduced by administration of cimetidine or ranitidine, and reappeared with a new suspension of the therapy. The withdrawal syndrome from H2-receptor antagonists was reversed by treatment with domperidone (10 mg three times per day), a potent hyperprolactinaemic drug which does not cross the blood brain barrier. These results suggest that the drop in prolactin levels that occurs when cimetidine or ranitidine are suspended may contribute to the development of the withdrawal syndrome.
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PMID:[The H2-antagonist therapy withdrawal syndrome: the possible role of hyperprolactinemia]. 198 22


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