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)

Sleep induction has been studied in humans after the administration of apomorphine, a direct stimulant of the central dopaminergic system. The drug induced sleep and vomiting in healthy volunteers while it had no significant effect on 10 Parkinsonism patients treated for a long period with L-dopa. Apomorphine given to a group of Parkinsonism patients not receiving any specific treatment, and with a lower degree of disease severity, induced vomiting and sleep with a pattern similar to that in healthy subjects. A relationship between the dopaminergic system and sleep induction is suggested.
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PMID:Dopamine receptors and sleep induction in man. 44 84

The mechanisms underlying the frequent association of nausea and vomiting with elevations of plasma vasopressin(PAVP) were studied in man and rat. After oral water loads (N = 16), plasma osmolality fell in all human subjects and was associated with a decline in PAVP in 14 asymptomatic human subjects. In 2 human subjects, nausea occurred and was associated with increases in PAVP, without changes in blood pressure. During ethanol infusion (N = 28), PAVP was suppressed unless nausea supervened. In 4 nauseated human subjects, PAVP escaped from ethanol inhibition and rose to levels 10 times basal, despite the absence of hemodynamic changes. Apomorphine, a potent dopamine agonist and emetic agent, was administered to human volunteers in doses of 7 to 24 microgram/kg. There was no increase in PAVP in 3 human subjects who remained asymptomatic (7 to 16 microgram/kg). Ten human subjects experienced nausea after 16 microgram/kg, which was followed shortly by marked increases in PAVP. Emesis occurred in 5 human subjects given 16 to 24 microgram/kg, and was followed by PAVP levels similar to those seen with nausea alone. In 7 human subjects from the nausea group, the repeat study (16 microgram/kg) after pretreatment with dopamine antagonist (haloperidol, N = 4; fluphenazine, N = 3) resulted in complete blockage of apomorphine-induced AVP release. In rats, which lack an emetic reflex, apomorphine doses of 200 microgram/kg induced only slight increases in PAVP when compared to the response to 16 microgram/kg in man. These studies indicate that stimulation of the emetic reflex results in AVP-release in man. Nausea-mediated AVP release supervenes over concomitant osmolar or pharmacologic (ethanol) inhibition.
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PMID:Influence of the emetic reflex on vasopressin release in man. 54 11

Apomorphine, a dopaminergic receptor stimulant, was tested and compared in subemetic doses (0.76 mg subcutaneously) to levodopa (500 mg orally) as a stimulant of growth hormone release in 10 normal volunteer subjects (five male, five female). The administration of levodopa failed to cause a normal increment in serum growth hormone levels (greater than 5 ng/ml from base line) in four patients, produced a borderline normal response in two patients with a normal response in four patients. Apomorphine stimulation produced a borderline normal response in one patient and a normal response in the remaining nine patients. The peak response to apomorphine administration was 26.94 +/- 6.60 ng/ml and to levodopa 9.76 +/- 2.67 ng/ml (p less than 0.025). There was no statistical difference between men and women in whom apomorphine testing was utilized. Side effects (nausea, vomiting) were seen in three patients tested with levodopa and in four patients tested with apomorphine. Such symptoms began within 20 minutes of apomorphine administration, persisted from 30 to 40 minutes and disappeared abruptly. All patients treated with apomorphine noted transient drowsiness.
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PMID:Apomorphine-stimulated growth hormone release. 60 13

Apomorphine-induced vomiting is often used for preclinical efficacy testing of putative antiemetics in normal volunteers. The usual technique of individual intravenous titration for finding the threshold emitic dose of apomorphine in each subject is slow and tedious. We used a uniform dose of 0.05 mg/kg apomorphine given subcutaneously to test the antiemetic action of metoclopramide and votracon in ten healthy, young male volunteers. All ten subjects vomited in response to this dose of apomorphine when pretreated with placebo. Pretreatment with metoclopramide prevented vomiting in all subjects, and votracon prevented vomiting in two. Apomorphine, 0.05 mg/kg, subcutaneously appears to be an appropriate challenge dose for testing compounds for antiemetic activity in normal human volunteers.
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PMID:An apomorphine-induced vomiting model for antiemetic studies in man. 62 80

Apomorphine in sub-emetic doses inhibits gastric emptying without producing nausea or vomiting. This discovery was applied to 21 persons to find out correlation between gastric emptying rate and alcohol absorption. In the 60 minutes after a single oral ingestion the shape of the alcohol-tolerance curve is considerably flatter after administration of apromorphine as compared to controls. The peak blood alcohol concentration occurs later and is significantly lower. These findings suggest that absorption of ethyl alcohol after a single oral alcohol ingestion can be controlled to a considerable extent by the gastric emptying rate.
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PMID:[Changes of alcohol resorption through apomorphine in subemetic dosage]. 65 83

Apomorphine proved to be more effective as an emetic in dogs after s.c. administration than after i.m. injection with doses of 0.04 and 0.1 mg/kg. This effect is explained by an anti-emetic effect mediated by mu-receptors in the vomiting centre in the brain, which, in contrast to the chemoreceptor trigger zone, is within the blood-brain barrier. A certain delay between the stimulation of D2-receptors in the chemoreceptor trigger zone (causing emesis) and mu-receptors in the vomiting centre (producing anti-emesis) therefore results, leading to a self-limiting emesis. Blockade of the mu-receptors by naloxone increased and prolonged the effect of apomorphine. A relatively narrow range of apomorphine concentrations on s.c. administration is then effective to stimulate the chemoreceptor trigger zone, but can hardly inhibit the vomiting centre, and must therefore be considered the most suitable route for administration of apomorphine.
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PMID:Apomorphine-induced emesis in the dog--routes of administration, efficacy and synergism by naloxone. 238 6

Apomorphine (0.05 mg/kg intravenously) was given to conscious dogs, and gastrin levels were measured in peripheral venous blood with a radioimmunoassay. Apomorphine induced an increase of gastrin levels which peaked at 5 min. The peripheral dopamine D-2/DA2 receptor antagonist domperidone (0.2 mg/kg), but not halopemide (0.1-1 mg/kg) nor the D-1/DA1 receptor antagonist SCH 23,390 (0.1 mg/kg), blocked the gastrin response to apomorphine. Both domperidone and halopemide, but not SCH 23,390, blocked the apomorphine-induced vomiting. These results suggest that apomorphine increases gastrin levels by an action at D-2/DA2 receptors, which are situated outside the blood brain barrier and differ from the receptor inducing the vomiting.
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PMID:Effects of dopamine receptor antagonists on gastrin and vomiting responses to apomorphine. 288 24

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 caused nausea (and vomiting in seven of nine) with a latency of 9.5 +/- 0.9 min which was followed by a large increase in plasma arginine vasopressin (AVP) concentration (from 0.9 +/- 0.2 pmol/l to 249 +/- 104 pmol/l at 15 min after the onset of symptoms; mean +/- SEM, P less than 0.01). There was a small but significant increase in plasma oxytocin (OXT) concentration (from 1.6 +/- 0.4 pmol/l to 6.2 +/- 3.4 pmol/l; P less than 0.05). Mean arterial pressure (MAP) fell slightly (from 87 +/- 1.9 mm Hg to 71 +/- 4.4 mm Hg; P less than 0.05) 15 min after the onset of nausea; there was no change in blood haematocrit or plasma osmolality and sodium concentration. In the DI patients apomorphine produced nausea (with vomiting in three of four) with a latency of 10.0 +/- 1.4 min but failed to cause an increase in either plasma AVP or OXT. In the DI patients the fall in MAP did not reach statistical significance (83 +/- 4 mm Hg to 71 +/- 11 mm Hg); there was also no change in haematocrit, osmolality or sodium concentration. Ipecacuanha, an emetic with both peripheral and central actions, was administered orally to seven normal subjects (three male, four female; aged 22-36 years) six of whom also underwent apomorphine tests.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Responses of plasma oxytocin and arginine vasopressin to nausea induced by apomorphine and ipecacuanha. 290 23

1. The LD50 for a 7-day period following intraperitoneal injection of apomorphine-HCl was calculated to be 158 mg/kg in rainbow trout. 2. Intraperitoneal injection of apomorphine at doses of 60 mg/kg or greater caused vomiting of plastic balls which had been placed in the stomachs of rainbow trout. 3. Apomorphine-induced effects included vomiting, vomiting behavior, toxicity, increased respiration, impaired motor control and equilibrium, and increased aggression. 4. The vomiting control mechanism of trout may be similar to that described in mammals.
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PMID:Apomorphine-induced vomiting in rainbow trout (Salmo gairdneri). 290 37

Experiments were performed on 52 dogs exposed to irradiation at a dose of 5-80 Gy or injected with 0.02-0.5 mg/kg apomorphine. The apomorphine effect was also studied in 18 healthy male volunteers. Apomorphine injected to dogs reproduced to a certain extent the pattern and sequence of gastrointestinal, sensorimotor and circulatory lesions constituting the primary radiation reaction. The apomorphilne dosage ED50-ED90, in terms of vomiting, roughly corresponded to irradiation at a dose of 5-10 Gy. The basic difference was that the time of onset and duration of specific symptoms after irradiation were several times longer than after apomorphine injection. It is suggested that the common pathogenetic component in the primary reaction to irradiation and its apomorphine model is the phasic change in the activities of brain dopaminergic systems.
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PMID:[Various physiological characteristics of primary radiation reaction and its apomorphine model]. 322


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