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The combinations were relatively stable, with all drugs maintaining over 90% of their initial chemical potency for at least 1 week. There were no evident changes in either the physical appearance or pH values of the solutions over the course of the study.
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In this prospective, randomized, double-blind trial, patients who had undergone breast surgery and were experiencing PONV during the first 3 hours after anesthesia received either granisetron 40 microg/kg IV, droperidol 20 microg/kg IV, or metoclopramide 0.2 mg/kg IV. Patients were observed for 24 hours after administration of study drug. Emetic episodes were recorded by nursing staff who were blinded to treatment assignment.
To investigate the effects of acute hyperprolactinemia on the 24 h LH pulsatile pattern, 11 women in the early follicular phase (EF, days 3 and 4) and 8 postmenopausal women (PMW) were studied before and during administration of metoclopramide, a dopamine receptor antagonist. Sequential 24 h infusions of either metoclopramide (MCP, 30 micrograms/kg/h) or normal saline were conducted and pulsatile LH activity assessed for 48 hrs. In both EF women and PMW, a prompt (within 90 min, p less than 0.001) and sustained (greater than 45 micrograms/L, p less than 0.001) release of PRL was induced by MCP infusions. MCP-induced hyperprolactinemia failed to modify the LH pulsatile activity in both EF women and PMW. These observations suggest that acute hyperprolactinemia due to dopaminergic blockade has no discernible effect on LH pulsatility and that the reduced LH pulse frequency observed in association with endogenous hyperprolactinemia may result from different neuroendocrine mechanism(s) and/or is time dependent.
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The substituted benzamide drugs YM 09151-2 and clebopride potently inhibited apomorphine-induced stereotyped behaviour in the rat and caused displacement of the specific binding of [3H]spiperone to D-2 binding sites on striatal membranes in low nanomolar concentrations. Other substituted benzamide drugs including metoclopramide, sultopride and flubepride also inhibited stereotyped behaviour to a greater or lesser degree, but were less potent in displacing [3H]spiperone from D-2 sites. YM 09151-2 and clebopride only weakly displaced specific binding of [3H]piflutixol to D-1 sites on rat striatal membranes, and only weakly inhibited striatal dopamine stimulated adenylate cyclase activity, when compared with cis-flupenthixol. The other substituted benzamide drugs did not displace [3H]piflutixol or inhibit dopamine stimulation of adenylate cyclase activity in the concentration range used. Clebopride and YM 09151-2 were highly lipophilic with apparent partition coefficient (log P') values equivalent to those of classical neuroleptic compounds, such as cis-flupenthixol. In contrast, the other substituted benzamide drugs were markedly less lipophilic. A log P' value of approximately 2 was required before inhibition of adenylate cyclase activity or displacement of [3H]piflutixol binding occurred. However, in excess of this value there was no correlation between either inhibition of adenylate cyclase activity or displacement of [3H]piflutixol binding and the lipophilicity of the various compounds. We conclude that potent lipophilic substituted benzamide drugs, like other members of the substituted benzamide series, are selective D-2 receptor antagonists. Inherent steric factors within the drug series would appear to dictate activity at D-1 and D-2 sites, although lipophilicity may contribute to actions in these environments.
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The effects of serotonin (5-hydroxytryptamine) on ventilation were investigated by continuous measurements of intrabuccal pressure in unrestrained eel. Intravenous administration of 5-hydroxytryptamine (30 micrograms.kg-1) caused a large increase in ventilatory frequency (+ 100%) and amplitude (+ 140%). The 5-hydroxytryptamine-induced hyperventilation was blocked by the 5-HT3-receptor antagonists metoclopramide (1.0 mg.kg-1) or MDL72222 (1.0 mg.kg-1), and was insensitive to the 5-HT1/2-receptor antagonist methysergide (3.0 mg.kg-1) and to the 5-HT4-receptor antagonist DAU 6285 CL (3.0 mg.kg-1). The hyperventilatory response to 5-hydroxytryptamine could be mimicked by the 5-HT3 receptor agonist 1-phenylbiguanide (300 micrograms.kg-1). These results strongly implicate the 5-HT3-receptor as the mediator of the 5-hydroxytryptamine-induced hyperventilation in eel.
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The early and delayed groups were similar in age (median 62 years vs. 64 years; P=0.17), sex (males 65% vs. 63%; P=0.91), and postoperative cases (31% vs. 33%; P=0.82) and had similar proportions who received mechanical ventilation (95% vs. 95%; P=1.00), an inotrope or vasopressor (63% vs. 70%; P=0.17), renal replacement therapy (8% vs. 10%; P=0.71), opiates (77% vs. 80%; P=0.60), antibiotics (89% vs. 91%; P=0.72) and metoclopramide (46% vs. 55%; P=0.11). A significantly larger proportion of the early group received an aperient (54% vs. 29%, P<0.001) and experienced diarrhoea (38% vs. 27%, P=0.04), but the groups had similar proportions affected by constipation (42% vs. 43%, P=0.91).
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Chest pain is an alarming symptom; it justifies many visits to the emergency department (ED). The etiology is often unknown. Chest wall pain in the presence of migraine headache, although not a common occurrence, is intriguing when it resolves with antimigraine treatment.
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From the study cohort (n = 681,104), 3239 sudden cardiac death cases were matched to 12,572 controls. The adjusted odds ratio (95 % confidence interval) for sudden cardiac death with current use of domperidone alone was 1.71 (0.92-3.18) versus non-use of study medications, 1.26 (0.68-2.34) versus current PPI use, and 0.40 (0.17-0.94) current metoclopramide use. The adjusted odds ratio (95 % confidence interval) relative to exposure to no study drug for domperidone >30 mg/day (eight cases, five controls) was 3.20 (0.59-17.3) and 1.65 (0.89-3.07) for age ≥61 years (27 cases, 49 controls). The odds ratio (95 % confidence interval) was 3.17 (1.72-5.83) for within-person periods of domperidone use versus non-use in the case-crossover analysis.
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The clinical development of ondansetron for the prevention and treatment of postoperative nausea and vomiting has been progressing for 5 years, and continues as new directions of research are being addressed. Large multicentre studies have demonstrated the efficacy of ondansetron in the prevention and treatment of postoperative nausea and vomiting, but no large comparator studies have been reported. Several studies are now being undertaken to compare ondansetron with other currently used antiemetics such as droperidol and metoclopramide, assessing efficacy, safety, pharmacoeconomic, and quality of life parameters. The majority of studies to date have been performed in gynaecological surgery patients receiving general anaesthesia--a population that experiences a high incidence of postoperative nausea and vomiting. Clinical development of ondansetron is therefore progressing to establish its efficacy in a wider surgical population, including paediatrics, the elderly, non-gynaecological surgery, and as retreatment in patients with failed prophylactic antiemetic therapy.
Domperidone and cisapride, both reduced the number of abdominal constrictions when given orally or intraperitoneally. Domperidone (5 mg/kg) inhibited it to the extent of 57.0 % after po and 54.6 % after ip. The inhibition after cisapride (5 mg/kg) was 65.1 % (po) and 71.6 % (ip). Naloxone pretreatment reduced this inhibition (57.0 % vs 10.3 % for domperidone and induced hyperalgesia by antagonizing the inhibition and enhanced analgesia to the extent of 28.4 % for cisapride). The reaction time was increased by domperidone (10 mg/kg, ip) from 1.6 s +/- 1.0 s to 14.8 s +/- 0.5 s and cisapride (10 mg/kg, ip) from 3.3 s +/- 1.0 s to 14.8 s +/- 0.5 s.
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In S2CM09, 92 patients treated 118 headaches during mild pain. Rates of pain-free response were higher 2 hours after dosing with sumatriptan 50 mg (51%) or 100 mg (67%; P < 0.05) compared with placebo (28%), and were higher with early treatment of mild pain compared with treatment of moderate/severe pain at 2 hours (sumatriptan 50 mg: mild pain, 51%; moderate/severe pain, 31%; P < 0.05; sumatriptan 100 mg: mild pain, 67%; moderate/severe pain, 36%) and 4 hours (50 mg: 75% vs 56%; 100 mg: 90% vs 61%; P < 0.05). Early intervention also resulted in less redosing than when moderate/severe pain was treated (50 mg: 21% vs 32%; 100 mg: 20% vs 29%). More attacks treated early with sumatriptan 50 or 100 mg were associated with normal function 4 hours after dosing compared with placebo (70% and 93% vs 46%, respectively). Sustained pain-free response rates 2 to 24 hours after early dosing with sumatriptan 50 or 100 mg were also higher (34% and 53%, respectively) compared with treatment of moderate/severe pain (19% and 24%, respectively). Early treatment with sumatriptan 100 mg produced significantly higher pain-free rates at 2 hours after dosing (P < 0.001) than did ergotamine plus caffeine (S2BT25: 69% vs 34%, respectively) or aspirin plus metoclopramide (S2BT26: 73% vs 25%, respectively).
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The release of cerebral acetylcholine from terminals in the cerebral cortex has been shown to be regulated by 5-hydroxytryptamine (5-HT) but it is not known which subtype of the 5-HT receptor is involved. 5-HT receptor agonists increase acetylcholine levels in vivo, indicating a reduced turnover, and reduce release of acetylcholine from striatal slices in vitro. Depleting 5-HT by inhibiting synthesis or by destroying the neurons containing 5-HT potentiates acetylcholine release, and increases acetylcholine turnover in the cerebral cortex and hippocampus. Selective antagonists for the 5-HT3 receptor subtypes which seem to have effects on mood and activity may exert their effect through the regulation of acetylcholine release in the cortex and limbic system. Radioligand binding studies show a high density of 5-HT3 receptors in the cholinergic-rich entorhinal cortex and we provide evidence that a reduction in cortical cholinergic function can be effected in vitro by 5-HT3 receptors.
We have studied the effect of i.v. metoclopramide on renal vascular resistance in nine healthy volunteers. Peak systolic and end-diastolic frequencies were measured using duplex Doppler ultrasound of a renal interlobar artery, before and after the administration of i.v. metoclopramide 10 mg, and the resistance index derived. There was no significant change in mean arterial pressure or resistance index following metoclopramide.
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A predictive decision analytic model using previously published clinical and economic evaluations, and costs of medical care in Canada.
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Metoclopramide administered intravenously (i.v.) immediately before injection of propofol, after mixing with propofol, or after a rubber tourniquet for 1 min before propofol injection will reduce pain induced by propofol injection. In this study, these three different techniques in reducing propofol injection pain with metoclopramide were compared with lidocaine or saline to evaluate the most effective method in reducing propofol injection pain.
Alizapride, a new antiemetic of the benzotriazole-line, enterally given, has been used in a randomized double blind trial including 40 patients suffering from radiogenic gastro-intestinal syndrome. Compared to metoclopramide, alizapride caused a faster regression of inappetence and of the frequency of daily vomiting. Drug-induced side-effects could not be seen.
The effect of metoclopramide on presynaptic dopamine receptors was investigated in the cat cardioaccelerator nerve preparation. Metoclopramide, a substituted benzamide derivative, antagonized inhibitory action of apomorphine on positive chronotropic responses induced by sympathetic nerve stimulation in cat hearts, in vivo. Neither phentolamine, an alpha-adrenergic blocking agent, nor indomethacin a prostaglandin synthesis inhibitor, antagonized the effect of apomorphine. Apomorphine did not alter the positive chronotropic effects of intravenously administered noradrenaline. Metoclopramide potentiated stimulation-induced positive chronotropic responses. These results suggest that metoclopramide blocks the presynaptic dopamine receptors at the cat heart.
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The authors describe an evaluation of the Du Pont Prep. off-line automatic centrifugal sample processing system, used in the authors' Drug Investigation Unit over the past two years. In comparison to liquid-liquid extraction, the authors found that assay precision has generally been improved, absolute recovery was quantitative, reliability has been good and the use of the system has resulted in notable labour saving. However, the cost per test based on a seven-year amortization of capital cost shows that the system is more expensive. Assays for urinary opiates, serum tricyclic antidepressants, serum isoxicam, serum valproate, serum metoclopramide and serum pindolol are presented and the merits of the method are compared with those for manual liquid-liquid extraction procedures.
From november 1981 to january 1982, 80 consecutive patients received high dose metoclopramide, adjoined to different cancer chemotherapy regimens containing cisplatine, dacarbazine, actinomycin D or mithramycin. Nineteen of them (23,75%) had no chemotherapy induced nausea or vomiting, 30 (37,5%) had nausea alone or vomited only once, and 17 (21,3%) had 3 to 5 episodes of vomiting. The overall efficacy of high-dose metoclopramide was 83,7 per cent. It has been seen whatever the chemotherapeutic agents used, and was inchanged for the following courses in 33 of 37 patients who received 2 to 4 courses. In 25 out of 33 patients who had already received the same chemotherapy without high dose metoclopramide, the digestive tolerance have been improved by the antiemetic treatment. Toxicity of high dose metoclopramide had been encountered in 17 (21,5%) of the patients and necessited this treatment to be stopped in 10. There were mainly extrapyramidal syndroms, diarrhea and drownsiness. The toxicity of high dose metoclopramide was of concern mainly in patients younger than 30, and/or when dosage escalation have been attempted.
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In connection with all highly or very highly emetogenic chemotherapies, an antiemetic prophylaxis should be initiated on the day of therapy, especially when using platinum or most of the cyclophosphamide-based regimes for cancer treatment. The recommended prophylaxis consists of a combination of 5-HT(3) antagonists with a corticosteroid. To combat the so-called delayed emesis on the days following therapy, all patients should undergo an oral corticoid therapy, possibly in combination with MCP (especially platinum-therapy patients), less frequently with 5-HT(3) antagonists. With these means of prophylaxis emesis can be prevented/avoided completely in most patients, and nausea can at least be reduced. It is sufficient to administer a single dose of 5-HT(3) antagonists prior to chemotherapy. For ondansetron and granisetron, the best documented substances within this class of drugs, 8 mg (ondansteron) and 3 mg (granisetron) are considered standard dosages. Among the corticoids, most data have been accumulated for dexamethasone. A standard dose of 10 to 20 mg can be administered prior to chemotherapy. Right after and especially on the days following chemotherapy higher dosages seem to be indicated.
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We investigated the relationships among gastrointestinal sounds, gastrointestinal manometric findings, and small intestinal transit time in healthy fasted humans.
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Patients at our Stoma Outpatient Clinic underwent baseline evaluation, and those with symptoms of constipation (prolonged periods between bowel movements, passage of pasty or hardened fecal effluent, and associated symptoms such as abdominal discomfort or bloating, flatulence, and pain with passage of effluent into the stoma) received individualized dietary recommendations that typically included an increase in dietary fiber and fluid intake, along with increased fluid intake. The outcomes of dietary changes were evaluated during a follow-up visit 3 months later. If dietary changes alone did not improve constipation symptoms, we prescribed a psyllium-based bulk-forming agent, an osmotic stool softener, and a probiotic, with or without a prokinetic agent such as metoclopramide taken 3 times daily.