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)

Eighteen patients received repeated administrations of cisplatin in relatively large amounts (55-75-100 mg/m2) given systemically by drop infusion. As antiemetic treatments, the following were scheduled: on the day before; prednisolone 30mg (3 X p.o.), immediately before; methylprednisolone 500mg (i.v.), and 3 hours after administration of cisplatin ; methylprednisolone 500mg (i.v.) and domperidone 60 mg (suppo.). Domperidone was given twice a day for one week. Nausea, vomiting and anorexia were studied objectively for two weeks. At a dose of 75 mg/m2 of cisplatin, the occurrence and the duration of nausea and vomiting were effectively reduced by the regimen; nausea was observed in 67% of all cases (average duration: 3.3 days) and vomiting was experienced in 40% (1.2 days). Anorexia was observed in 67% of cases and lasted longer (5.2 days). The severity and duration of these side effects of nausea, vomiting and anorexia seemed to appear in a manner related to the dose of cisplatin given, but even at a dose of 100 mg/m2, the regimen described above reduced the patients' discomfort to acceptable levels. No remarkable side effect of this anti-emetic regimen was evident.
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PMID:[Effect of combined use of adrenocortical hormones and domperidone as anti-emetics during cisplatin therapy]. 403 53

Evaluation of the activity of anti-emetic drugs in randomized controlled trials has, in most cases, demonstrated the superiority of treatment over placebo administration for the control of chemotherapy-induced emesis (see Table 15). The degree of control of emesis relates both to the intensity of the emetogenic stimulus and to the effectiveness of the anti-emetic agent employed. Prochlorperazine is a relatively weak anti-emetic. The drug exhibits modest activity in the treatment of emesis produced by mild emetogenic stimuli, but is relatively ineffective in the treatment of patients on moderate to severely emetogenic drugs. Domperidone has demonstrated activity against moderately emetogenic stimuli but has not been evaluated in cisplatin-treated patients. The cannabinoids have proved efficacious in the treatment of emesis induced by more severe emetogenic stimuli. THC therapy, however, has been limited in some studies by toxicity. High-dose metoclopramide has demonstrated efficacy in small series of patients in the treatment of cisplatin-induced vomiting. Dexamethasone activity as a single agent is in doubt but the drug may improve the efficacy of metoclopramide when used in combination. For the future, the use of combinations of anti-emetics with differing sites of action and non-overlapping toxicities, may lead to further improvement in efficacy. Combinations of centrally-acting drugs such as the cannabinoids plus dopamine antagonists such as metoclopramide or domperidone, are worth evaluating. The control of anticipatory nausea and vomiting is another major area of interest which has, as yet, not been studied in any depth. A single comparative trial has been reported in the literature (50) and in this study, behavioural therapy rather than drug therapy was evaluated. There may be a place for the evaluation of behavioural therapy in combination with drugs exhibiting anxiolytic properties such as the benzodiazepines and the cannabinoids. Finally, new anti-emetic drugs with an improved therapeutic index will be welcomed by the patient.
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PMID:Advances in anti-emetic therapy. 609 68

Twelve antagonists of apomorphine-induced emesis in dogs were studied in different tests to evaluate their antiemetic specificity. Ten of these antagonists were neuroleptics: benzquinamide, clebopride, bromopride, prochlorperazine, haloperidol, chlorpromazine, thiethylperazine, metoclopramide, droperidol, and pimozide blocked conditioned responding in dogs and apomorphine-induced stereotyped behavior in rats. The use of these compounds as anti-emetics entails a risk of neurological side effects. Metopimazine and domperidone were devoid of neuroleptic activity. Metopimazine, however, showed potent alpha-adrenergic blocking activity, showed histamine H1 antagonism, and induced palpebral ptosis. Therapeutic doses of metopimazine are, therefore, likely to produce sedation and side-effects related to autonomic blockade, Domperidone showed potent antiemetic activity and, up to high doses, no other central or peripheral effects. Therefore, domperidone is the only specific antiemetic known.
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PMID:Antiemetic specificity of dopamine antagonists. 613 May 55

The main treatment of the acute migraine attack remains sleep, sedation, an anti-nauseant and analgesics, and in some patients 1 or 2 mg of ergotamine tartrate. Drugs containing large amounts of caffeine should not be used. Absorption of drugs may be impaired in a migraine attack. Metoclopramide is probably the anti-emetic of choice because it is an effective anti-nauseant and promotes normal gastrointestinal activity. Domperidone has a similar action but is said not to go through the blood-brain barrier, so is less likely to cause extrapyramidal reactions. All drugs, including analgesics such as aspirin and paracetamol, are best given in a soluble or effervescent form. Where vomiting occurs early in the attack, suppositories may be indicated. Ergotamine tartrate is necessary in about one third of attacks and is best given by suppository or by inhalation. Doses higher than 2 mg per attack or 6 mg in one week may cause toxic symptoms, the early signs of which are headache, nausea, vomiting and a feeling of not being very well. The non-drug treatments of an acute attack include pressing on the temporal artery, hot and cold compresses and relaxation.
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PMID:Treatment of the acute migraine attack--current status. 640 72

Systemic administration of apomorphine, angiotensin II, neurotensin and leucine-enkephalin induces emesis in dogs in a dose-dependent fashion. Receptors for Leu-enkephalin and angiotensin II but not apomorphine show receptor desensitization, such that a second systemic administration 5 min after the first is ineffective. Domperidone blocked the emetic response to apomorphine but not to Leu-enkephalin or angiotensin II. Naloxone selectively blocked the Leu-enkephalin response, while saralasin blocked responses to both angiotensin II and Leu-enkephalin, but not apomorphine. Chlorpromazine prevented the emetic response to all agents, suggesting a dopamine receptor in the emetic pathway on the brain side of the blood-brain barrier. In dogs with ablation of the area postrema the emetic response to apomorphine and all peptides was prevented.
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PMID:Peptide-induced emesis in dogs. 672 20

Domperidone is a dopamine antagonist that does not readily enter the central nervous system. Given parenterally or orally it increases gastric emptying of liquids and increases lower oesophageal sphincter pressure in healthy subjects. The antiemetic and pharmacodynamic profile of domperidone is similar to that of metoclopramide, although domperidone has a lower propensity to cause extrapyramidal side effects. Domperidone effectively alleviates symptoms of chronic postprandial dyspepsia and nausea and vomiting due to a wide variety of underlying causes and in some studies has been superior to metoclopramide. Vomiting associated with the administration of moderately emetic cytotoxic drugs is controlled in the majority of patients. Alleviation of the dose-limiting peripheral side effects (nausea and vomiting) of the anti-Parkinsonian drugs bromocriptine and levodopa, enables a higher optimum dose, with consequent improvement in Parkinsonian symptoms. Domperidone does not aggravate the extrapyramidal side effects of neuroleptic drugs. Control of cytotoxic-induced, and postprandial nausea and vomiting in children has been achieved with domperidone without evidence of extrapyramidal side effects. Indeed, side effects have seldom occurred with therapeutic doses of domperidone.
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PMID:Domperidone. A review of its pharmacological activity, pharmacokinetics and therapeutic efficacy in the symptomatic treatment of chronic dyspepsia and as an antiemetic. 675 78

In two dogs the effect of domperidone (0.5 mg/kg BW i.v.) on retroperistaltism produced by apomorphine (3-10 mg s.c.) was studied. Reverse peristalsis was characterized by strong and long lasting contractions of the duodenum. Domperidone inhibited, in 10 out of 11 experiments, reverse peristalsis and reflux of intestinal contents. It is well known that domperidone inhibits emesis in dogs and humans but it has not been studied whether preceding retroperistaltism is also inhibited. Therefore the effect of domperidone on retroperistaltism was investigated in two dogs.
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PMID:Inhibition of reverse peristalsis of the intestine by domperidone. 694 9

In catastrophe situations ether is an important alternative to the usual anaesthetics being easy to manage and economical. We wanted to study the effects of the new antiemetic Domperidone on vomiting after either anesthesia. Two groups of patients were anaesthetized for general surgical procedures by means of the EMO (Epstein-Macintosh-Oxford) Vaporizer. Half an hour before the end of the operation one group received 0.2 mg/kg domperidone while the randomized control group received no prophylactic antiemetic medication. The domperidone group showed better, statistically significant, results (p less than 0.05). Domperidone proved to have a good prophylactic antiemetic effect which does not cause side effects or circulatory alterations. In preparation for catastrophe situations ether anesthesia under improved conditions was again included in the regular training programme.
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PMID:[Domperidone after ether anaesthesia. Prevention of postoperative hyperemesis (author's transl)]. 709 38

Domperidone, a new gastrokinetic with potent antiemetic properties is devoid of central effects, up to high dose levels. To assess the CNS activity of domperidone and metoclopramide, the inhibition of intracranial self-stimulation (ICS) in two different situations, and the influence on EEG in dogs were studied. The dissociation between the antiemetic and central effects of both compounds were evaluated in dogs given a stereotypogenic dose of apomorphine. A significant and dose-related inhibition of ICS (conditioned situation) was obtained with 0.8 and 1.6 mg/kg i.v. domperidone and with 0.125, 0.25 and 0.50 mg/kg i.v. metoclopramide. The ED50 values were 0.79 mg/kg and 0.25 mg/kg respectively. The effect was most pronounced 4 hr after administration with domperidone and 15 min after administration with metoclopramide. In the EEG studies, no specific structure-related effects were found but the total potency was increased with domperidone 0.8 and 1.6 mg/kg i.v. and with metoclopramide 0.063, 0.125, 0.25 and 0.50 mg/kg i.v. This increase was due to a decrease in fast frequencies, an increase of slower frequencies and a slight increase of the amplitude. Sleep-like patterns were not observed with either compound. In the apomorphine-test in dogs, the ratio between the i.v. ED50 values for antagonism of stereotypy and of emesis was 180 (1.8/0.01) for domperidone and 2.67 (0.64/0.24) for metoclopramide. Thus, central effects and antiemetic effects are concomitant with metoclopramide, whereas with domperidone, extremely large doses are required to obtain central effects.
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PMID:Neuropharmacological comparison between domperidone and metoclopramide. 719 63

Apomorphine (0.03 mg . kg-1 s.c.) and morphine (0.5 mg . kg-1 s.c.) produced gastric relaxation and vomiting in the conscious dog. Domperidone (0.1-1 mg . kg-1 i.v.), haloperidol (0.1 mg . kg-1 i.v.) and pimozide (0.025 mg . kg-1 i.v.) selectively blocked the gastric relaxation as well as the vomiting caused by apomorphine. Naloxone (0.07 mg . kg-1 i.v.) selectively blocked the gastric relaxation and the vomiting caused by morphine; after naloxone, morphine produced a delayed gastric relaxation in 2 experiments out of 7. These results suggest that for gastric relaxation as well as for vomiting, apomorphine and morphine act on different receptors. Fentanyl elicited marked gastric relaxation, blocked by naloxone, but did not elicit vomiting. After fentanyl, morphine and apomorphine no longer produced gastric relaxation and vomiting. This observation shows that the known blocking effect of fentanyl at the vomiting center does not affect its gastric relaxing effect.
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PMID:Gastric relaxation and vomiting by apomorphine, morphine and fentanyl in the conscious dog. 720 14


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