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)

Ondansetron, a 5-HT3 antagonist proposed for use in the treatment of chemotherapy-induced emesis, was first given to man in 1984 and in the 4 years subsequent to this, the drug was given to more than 220 different healthy volunteers. In pharmacodynamic studies, there was evidence to suggest that ondansetron was gastroprokinetic but reduced transit time through the small bowel. Ondansetron was of no benefit in a model of motion sickness. The pharmacokinetics of ondansetron have been defined in volunteers using intravenous and oral dosage regimens proposed for the clinic. Ondansetron had a terminal plasma half-life of 3.0-3.5 h and plasma clearance (principally metabolic) of the order of 600 ml/min, and there was no evidence of accumulation at steady state. The absolute oral bioavailability of ondansetron was 59%. Metabolic studies showed the drug to be excreted predominantly in urine and faeces, with a metabolite profile in urine similar to that seen in the animal species used for toxicological testing. Ondansetron is both safe and well tolerated at daily doses of up to 64 mg given to volunteers.
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PMID:The clinical pharmacology of ondansetron. 253 95

Three kinds of neurotransmitters (histamine, acetylcholine, and catecholamine) are thought to be important in the neural processes of motion sickness because antihistaminics, scopolamine, and amphetamine are effective in preventing motion sickness. In this study, we examined the neurochemical and neuropharmacologic features of motion sickness in rats. Based on our results, we propose the following hypotheses for the neurochemical mechanisms of motion sickness: (1) the histaminergic neuron system is involved in the signs and symptoms of motion sickness, including vomiting; (2) the acetylcholinergic neuron system is involved in the processes of habituation to motion sickness, including neural store mechanisms; and (3) the catecholaminergic neuron system in the brain stem is not related to the development of motion sickness.
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PMID:Neurochemical mechanisms of motion sickness. 257 85

5-Hydroxytryptamine3 antagonists have been reported to prevent emesis elicited by cisplatin and radiation. This study investigated the possibility that drugs with this mechanism of action may be useful in preventing emesis elicited by other stimuli. The drugs ICS 205-930 (0.1 and 1.0 mg/kg) and MDL 72222 (0.1 and 1.0 mg/kg) were administered SC to cats before challenging them with either provocative motion or an emetic dose of xylazine. In no instance was a significant reduction in emesis evident. Zacopride was also administered before motion testing (0.01 to 10.0 mg/kg) and found to not have efficacy. To test the possibility that species or route of administration were factors in the negative results, 1.0 mg/kg of ICS 205-930 was administered SC before IV infusion of 7.5 mg/kg of cisplatin. There was a total suppression of emesis for the duration of the six-hour observation periods. This result verifies other work which found 5-hydroxytryptamine3 antagonists to be effective in preventing emesis elicited by cancer chemotherapeutic treatments. However, there is no evidence that they are effective in other syndromes, such as motion sickness and xylazine-induced emesis.
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PMID:Blockade of 5-hydroxytryptamine3 receptors prevents cisplatin-induced but not motion- or xylazine-induced emesis in the cat. 273 31

Characteristics of motion sickness and effects of possible prophylactic drugs were studied using Suncus murinus (house musk shrew) for its potential use as an experimental model in motion sickness. Mild reciprocal shaking (amplitude: 10-40 mm; frequency: 0.5-3.0 Hz) induced vomiting in most of Suncus murinus within 2 min. Adaptation was observed when the motion stimulus was repeated with an interval of 2 to 3 days. During the repetitive motion training, both the ratio of sensitive animals and the number of vomiting episodes decreased, and the time from the start of shaking to the first vomiting was extended. Subcutaneous injection of scopolamine (100 mg/kg), chlorpromazine (8 mg/kg), promethazine (50 mg/kg), diphenhydramine (20 mg/kg), chlorphenylamine (20 mg/kg) and methamphetamine (2 mg/kg) decreased the emetic effect of motion sickness, but pyrilamine (20 mg/kg), meclizine (20 mg/kg) and dimenhydrinate (32 mg/kg) were not effective or very weak. These results indicate that the Suncus murinus is sensitive to the motion stimulus and antiemetic drugs are effective as prophylaxis. The Suncus murinus is useful as a new experimental animal model for motion sickness.
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PMID:Suncus murinus as a new experimental model for motion sickness. 289 27

The possible role of the alpha-2 adrenoceptors in xylazine-induced vomiting and in motion sickness was investigated. Cats were divided into two groups according to motion sickness susceptibility and were observed after s.c. injections of xylazine. The incidence of vomiting increased with the dose, and at each dose, the high susceptibility group had a greater emetic incidence than the low susceptibility group. In another experiment with cats divided into two groups according to motion sickness susceptibility, s.c. administration of yohimbine effectively antagonized the xylazine-induced emesis in both susceptibility groups. The cats in the latter experiment were then challenged with a motion sickness stimulus, after s.c. pretreatment with yohimbine. Yohimbine failed to prevent motion sickness but did occasion an unexplained variability in the incidence of vomiting. These findings suggest that the emetic effect of xylazine results from stimulation of alpha-2 adrenoceptors but that these receptors are not fundamental to feline motion sickness. The fact that susceptibilities to xylazine-induced emesis and to motion sickness are correlated suggests a point of interaction other than the area postrema, which is known to be essential for xylazine-induced vomiting but not for motion sickness in the cat.
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PMID:Xylazine emesis, yohimbine and motion sickness susceptibility in the cat. 300 84

The aim of this research was to quantify the development of habituation or intensification of experimental motion sickness induced in Bolivian squirrel monkeys by repeated exposures to horizontal rotation. Incidence, frequency, and latency of vomiting responses were recorded from monkeys rotated daily in a transparent testing chamber at 30 rpm for periods of 1 or 2 hours. Data showed that more than half of the subjects revealed habituation in terms of increased latencies for vomiting. Some showed a tendency to vomit increasingly earlier with multiple daily exposures to rotation. The development of habituation and intensification was evident as early as the second day of rotation. The number of emetic episodes per day decreased as a consequence of repeated rotation, but intensification of vomiting frequency did not occur beyond the fifth day.
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PMID:Intensification and habituation of experimental motion sickness in squirrel monkeys by repeated horizontal rotation. 308 28

It has been suggested by numerous researchers that the development of conditioned food aversion (CFA) in experimental animals represents the presence of a subjective state of illness. Squirrel monkeys with proven susceptibility to rotation-induced vomiting were given surgical bilateral labyrinthectomies, a procedure known to abolish signs and symptoms of motion sickness in human beings. Postoperatively, labyrinthectomized monkeys neither vomited nor revealed any reduction in food consumption when exposed to provocative rotation. Other samples of monkeys known to be refractory to horizontal rotation and to sinusoidal vertical motion also exhibited little tendency to acquire a conditioned aversion to banana. But monkeys who had sham operations and those who revealed weak-to-strong signs of motion sickness exhibited a marked CFA (significant reduction in food intake). The strength of CFA was much greater when elicited in the test vehicle when compared with response in the home cage. The findings are interpreted as support for a limited application of CFA procedures for inferring the presence of motion-induced nausea and malaise.
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PMID:Subjective concomitants of motion sickness: quantifying rotation-induced illness in squirrel monkeys. 312 Jan 18

Rats eat kaolin after treatment with poisons or rotation. Thus, eating of nonnutritive substances such as kaolin, so-called pica, is an illness-response behavior of rats analogous to vomiting in humans. For use of rotation-induced pica as a behavioral index of motion sickness in rats we examined what kind of rotation was effective for inducing pica in rats and whether the vestibular apparatus was necessary for its induction. Rats ate much kaolin after double rotation with continuously changing centrifugal and angular accelerations, but little after single rotation with no accelerative changes. However, even double rotation failed to induce pica in bilaterally labyrinthectomized rats. Thus, rotation-induced pica in rats was induced in the same way as motion sickness in humans, suggesting that it resulted from motion sickness in rats. We conclude that pica can be used as a behavioral index of motion sickness in rats.
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PMID:Pica as an index of motion sickness in rats. 326 13

After a brief description of the newest and special form of motion sickness known as "space sickness" arising in space flight, and the various hypotheses on its aetiopathogenesis, motion sickness in general and the air or plane sickness deriving from atmospheric flying are discussed. The aetiopathogenesis of air sickness derives from abnormal stimulations that are primarily vestibular but also visual and somesthesic, and generated by irregular movements or variations in attitude of the plane. Reflex action than produces effects that are primarily neurovegetative (nausea, vomiting, pallor, scialorrhea, sweating, bradycardia) and neuropsychological (depression, drowsiness, headache, discomfort and general debility with altered cenesthesia). After a description of the symptoms, the prevention and treatment of air sickness are discussed.
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PMID:[Motion sickness in the aerospace environment]. 331 14

Diminished gastric motility and lack of bowel sounds have been observed in astronauts aboard the Space Shuttle (4). In this study subjects were given scopolamine 0.6 mg with d-amphetamine 5 mg with and without neostigmine 15 mg. Neostigmine 15 mg alone was also compared with placebo for effect on gastric emptying time. In an additional test, subjects performed head movements in a rotating chair to an end-point of motion sickness short of vomiting. Ten ounces of isotonic saline containing 1 mCl of Tc 99mDPTA was ingested 2 h after the medications and immediately after rotation. The counts from stomach contents were monitored with a Picker small field of view gamma camera every 30 s for 1 h. Gastric motility was inhibited by scopolamine and amphetamine with 14% residual count at the end of 1 h. When neostigmine was added to this combination the results were in the placebo range. Motion sickness produced a profound inhibition of gastric emptying with a 47% residual count. The results indicate that the gastric stasis encountered in space is due mainly to motion sickness with a minimal contribution from the antimotion sickness drugs.
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PMID:Nuclear medicine evaluation of motion sickness and medications on gastric emptying time. 331 99


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