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Seven male volunteers were given apomorphine (14-20 micrograms/kg) subcutaneously on a total of ten occasions. Nausea was experienced on six occasions and on four occasions there was no effect. Venous samples were taken before injection, at peak nausea and 20 min later for assay of factor VIII
OBJECTIVE
The mechanism of the antiemetic actions of corticosteroids is not known. The purpose of this study was to evaluate if betamethasone can prevent nausea, vomiting or increase of vasopressin induced by apomorphine. Metoclopramide, a dopamine antagonist, was used as a control
This study investigated whether the indices of dopaminergic function, yawning and growth hormone release induced by apomorphine, as well as the drug-induced nausea and hyperthermia, show sensitization or tolerance to repeated injections. Five normal volunteers received 12 injections of apomorphine
Based on studies in animals and humans, it has been suggested that nausea activates the hypothalamo-neurohypophyseal system with resultant increases in circulating concentrations of oxytocin or vasopressin. The purpose of these studies was to determine in humans whether nausea is associated with
Apomorphine, a centrally-acting emetic, was administered subcutaneously (50 micrograms/kg) to nine normal subjects (four male, five female; aged 22-36 years) and four patients with idiopathic diabetes insipidus (DI) (one male, three female; aged 24-49 years). In the normal subjects this stimulus
BACKGROUND
Nausea and vomiting can occur in Parkinson's disease (PD) patients initiated on apomorphine subcutaneous injections and antiemetic prophylaxis is recommended per product labeling. Data suggest long-term antiemetic prophylaxis may not be needed, although this has not been systematically
The side effect profile of apomorphine SL (2-6 mg) has been determined in clinical studies of over 5000 patients using over 120 000 doses. Apomorphine, 2 and 3 mg, has been shown to have an excellent safety profile. The most commonly occurring side effects (<7%), nausea, headache and dizziness, tend
BACKGROUND
As Parkinson's disease (PD) progresses,despite optimized pharmacotherapy, patients experience more frequent fluctuations between symptomatic improvement ("on" times) and the return of motor features ("off" times). Apomorphine, the first injectable dopamine agonist available in the United
Dopaminergic stimulation by apomorphine causes severe adverse effects such as vomiting and sedation. We compared the effectiveness of the serotonin 5-HT(3) antagonistic antiemetic drug ondansetron in a single oral dose with the standard regimen using domperidone TID 2 days prior to stimulation. In a
Pretreatment with pimozide (0.2-1.2 mg/kg) reduced a conditioned taste aversion produced by apomorphine (0.4 mg/kg) in a dose-related manner. This pretreatment effect was pharmacologically specific as shown by the inability of pimozide to prevent a conditioned taste aversion produced by nicotine
Apomorphine, a non-ergot derivative, is a potent, directly acting dopamine receptor agonist with high affinity to D4, lower to D2, D3, D5, the lowest to D1-like dopamine receptors as well as to serotonin and adrenoreceptors. Subcutaneous apomorphine is currently used in Parkinson's disease as an
Apomorphine (Apokyn) is now available for rescue treatment of "off" episodes in patients with advanced Parkinson's disease. It must be injected subcutaneously. Apomorphine in a variety of formulations has been used in Europe for many years. Like other dopamine agonists it can cause nausea and
Apomorphine, a potent dopamine agonist with mixed D1 and D2 properties, has long been recognized to have antiparkinsonian effect. Its oral administration is limited by both its hepatic first pass metabolism and adverse side effects (nausea, vomiting, azotemia). It is now widely used by subcutaneous
Apomorphine, a dopamine-agonist was applied as s. c. infusions to 7 patients with idiopathic Parkinson's disease. The indications were longlasting akinetic episodes (4 patients) and therapeutically resistant invalidating motoric fluctuations ("on-off") as well as hyperkinesia (3 patients) on
As Parkinson's disease progresses, fluctuations between akinesia, or hypomobility ("off" times), and mobility ("on" times) increase in frequency despite optimized pharmacotherapy. Motor fluctuations include predictable shortening of therapeutic effects, nocturnal or early morning akinesia, random