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)

In 87 children aged 2-9 yr, oral droperidol and oral droperidol plus diazepam were compared as premedicants in a controlled double-blind clinical trial. Atropine was given orally to all the patients. Droperidol was well absorbed and produced good sedation, associated with a low incidence of vomiting after operation. Droperidol plus diazepam did not appear to offer any advantage over droperidol alone. Anxiety and extrapyramidal effects were not observed and may have been obviated by the addition of atropine. Droperidol syrup was noted to be more palatable than other oral premedicants in use.
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PMID:A controlled clinical trial of oral droperidol and droperidol plus diazepam for premedication in children. 33 85

Three cases are reported where 1/2-2 bulbs of Zigadenus were ingested. This resulted in vomiting, cramping and nausea, starting within 1-2 hours and lasting 4-5 hours. Both the heart rate and blood pressure were affected, generally, but not consistently, decreased. Atropine, when used for the cardiovascular effects, increased the heart rate, but had minimal action on the blood pressure. There was little toxic effect on respiration, central nervous system, or temperature. The one case of increased temperature was though to be due to an unrelated illness. Treatment of such cases should include emesis (or lavage, if emesis is contraindicated), activated charcoal, and saline cathartic. Symptomatic cases need an iv and possible administration of atropine, a sympathometic and/or a ganglionic blocking agent. Since there is considerable variation in what symptoms will be seen with the different species of Zigadenus, each case must be treated symptomatically; first with good supportive care, then possibly with administration of the above agents.
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PMID:Three cases of Zigadenus (death camus) poisoning. 51 64

The antiemetic effects of droperidol, diphenidol, and placebo were compared in 210 patients subjected to minor gynecologic or urologic procedures. Atropine (0.6 mg), meperidine (1 mg/kg) body mass, and either droperidol (5 mg), diphenidol (40 mg), or 2 ml of 0.9% saline were administered IM, 1 hour before general anesthesia. Trial drugs were presented in coded ampules so that the study was conducted double-blind. Droperidol appeared superior to both diphenidol (p less than 0.01) and placebo (p less than 0.001) in the prevention of vomiting, and reduced the incidence of nausea when compared to saline (p less than 0.05). Forty-four patients experienced side effects, which occurred with similar frequency in the 3 groups studied.
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PMID:Nausea and vomiting after anesthesia and minor surgery. 56 92

These agents act as anticholinesterases. Signs of toxicity are: overactivity of the parasympathetic nervous system, nausea, vomiting, diarrhea, sweating, abdominal cramps and copious secretions. Large doses may cause sustained depolarization of the motor end plate, leading to muscular paralysis. Death may ensue from respiratory failure. The extensive and often careless use of insecticides, fungicides and pesticides makes organophosphates a particular pediatric hazard. Atropine and pralidoxime chloride are effective for therapy.
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PMID:Organophosphates--a pediatric hazard. 113 Feb 47

The safety of outpatient surgery depends mainly on patient selection, the type of operation, and the anesthetic technique. Subjects of this study were 500 women who as outpatients underwent tubal electrocoagulation through a laparoscope. After an interval of 1 week to 4 months postoperatively, each was sent a questionnaire regarding postanesthetic complications. The questionnaire was returned by 418 patients (83.6%). Several anesthetic agents had been used. Premedication was given only to very nervous patients (18%). Atropine .4 mg was given to all just before the operation. The trachae of all patients were untubated after a dose of succinylcholine and in 60% of cases 3-6 mg of D-tubocurare. There were no immediate anesthetic complications. Most patients were discharged within 3 hours. Postanesthetic complications were common. Muscle pains occurred in 45%, many lasting 2-5 days. Sore throat followed in 28.2% but was usually mild. Headache, nausea, vomiting, cough, and sputum were noted in 8-17%. A mild dizziness was sometimes a complaint. Inability to concentrate was experienced by 30% of patients for over 2 days. In 32.9 %, return to usual work took up to 48 hours; in 57.9%, it was 2-5 days w hile the others required over 5 days. 81% of the patients reported that they would accept the procedure again, while 16.7% would refuse. Return to preoperative mental status usually took several days and in a few over 5 days. Too early use of alcoholic beverages or driving an automob ile were warned against. Most patients considered that the advantage of having the operation as outpatients made up for the discomforts.
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PMID:Anaesthetic complications in surgical out-patients. 115 42

We performed strabismus surgery on 170 children on an outpatient basis. Endotracheal intubation was utilized in all cases as the means of delivery of the anesthetic agent. Atropine used alone as a preoperative medication reduced the incidence of postoperative vomiting. Parental acceptance of this method of surgery was best when the child was discharged from the hospital awake and alert in the shortest possible time.
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PMID:Brief hospital admissions for pediatric strabismus surgery. 116

Under control (intact and laparotomized) conditions, arterial pressure of urethan-anesthetized ferrets rose significantly in response to intragastric copper sulfate (CuSO4; 10 ml of 5 mg/ml). CuSO4 was emetic 75-90% of the time, and a cardiovascular response always immediately preceded and accompanied emetic responses. The cardiovascular response was significantly reduced or abolished by hexamethonium (0.35 mg/kg) pretreatment combined with atropine methyl bromide (1 mg/kg). Addition of the alpha 2-receptor antagonist 2,3-dichloro-alpha-methylbenzylamine HCl (DCMB, 10 mg/kg) and the beta-receptor antagonist propranolol (3 mg/kg) to the hexamethonium and atropine combination prevented its reduction of the cardiovascular response. Given individually, these agents did not alter cardiovascular response, nor did yohimbine (0.30 mg/kg), RS(+/-)-zacopride (0.30 mg/kg), or granisetron (0.50 mg/kg). Only RS(+/-)-zacopride significantly reduced incidence of emesis. Atropine methyl bromide alone, with hexamethonium, or with hexamethonium, propranolol, and DCMB significantly delayed the first emetic episode. Conversely, bilateral abdominal vagotomy significantly reduced the number of vomiting animals without affecting cardiovascular response. These results suggest that the neural pathways mediating the two events are not identical. In another series of experiments, a significantly greater proportion of animals vomited in response to intragastric CuSO4 than to intraduodenal CuSO4, suggesting that the primary site of CuSO4 action in the ferret is the stomach.
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PMID:Surgical and pharmacological dissociation of cardiovascular and emetic responses to intragastric CuSO4. 135 43

Pyridostigmine is known as a pre-treatment drug against intoxication with organophosphorus nerve agents. During the Persian Gulf war, we encountered a cluster of nine cases of pyridostigmine self-poisoning, of which three presented with mixed drug poisoning. The clinical and laboratory features of pyridostigmine toxicity are presented. Doses ranged between 390 and 900 mg. Pyridostigmine ingestion resulted in mild to moderate cholinergic symptoms such as abdominal cramps, diarrhea, emesis, nausea, hypersalivation, urinary incontinence, fasciculations, muscle weakness and blurred vision. No central nervous system manifestations were evident. The symptoms developed within several minutes and lasted up to 24 h. All patients underwent gastric emptying followed by administration of activated charcoal. Atropine (1-8 mg) was required in only three patients. Measurement of serum cholinesterase inhibition was found to be a reliable and sensitive diagnostic tool in pyridostigmine poisoning. No clear correlation was found between the extent of cholinesterase inhibition and the incidence or severity of the cholinergic signs. The clinical recovery was faster than the spontaneous recovery of the enzyme. Pyridostigmine intoxication is self-limited and well tolerated by young healthy adults.
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PMID:Acute pyridostigmine overdose: a report of nine cases. 175 42

The gastrointestinal motor correlates of vomiting consist of two contractile events, 1) a giant retrogradely propagated contraction of the upper small intestine, the retrograde giant contraction (RGC) and 2) a series of post-RGC phasic contractions that occur primarily in the lower small intestine. The effects of cholinergic, dopaminergic, serotonergic, and opioid receptor antagonists and an opioid receptor agonist on vomiting and its gastrointestinal motor correlates initiated by apomorphine (APO), CuSO4, or cholecystokinin octapeptide (CCK-8) were determined in awake dogs. Atropine blocked the retrograde giant contraction only, and hexamethonium blocked all jejunoileal motor responses activated by APO, CuSO4, or CCK-8. Domperidone blocked all effects of APO only, whereas haloperidol, methysergide, 1-(1-naphthyl) piperazine, and fentanyl blocked or inhibited responses to both APO and CuSO4. None of the dopaminergic, serotonergic, or opioid receptor antagonists or the opioid receptor agonist affected the gastrointestinal motor responses to CCK-8. Cinanserin or Sch 23390 had no effect on any of the responses activated by APO, CuSO4, or CCK-8. These results suggested that D2 dopaminergic and 5-HT2 serotonergic receptors of the emetic central pattern generator mediate vomiting and its gastrointestinal motor correlates, whereas opioid receptors may mediate tonic inhibition of these responses. In addition, peripheral muscarinic or nicotinic cholinergic receptors but not peripheral 5-HT2, dopaminergic, or opioid receptors mediate the gastrointestinal motor correlates of vomiting.
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PMID:Functional localization of specific receptors mediating gastrointestinal motor correlates of vomiting. 256 2

Grayanotoxin-III (GTX-III) is a constituent in leaves of Pieris japonica D. Don which exhibits, in vitro, the ability to open voltage-sensitive sodium channels in various excitable tissues. Effects of systemic administration of GTX-III were studied in vivo using Std-ddy mice. Salivation, vomiting and paralysis of the hind paws invariably occurred in mice injected intraperitoneally with 0.1 or 0.25 mg/kg of GTX-III. The writhing response to an intraperitoneal injection of acetic acid was considerably diminished by pretreatment of animals with the toxin. The grayanoid also caused a profound attenuation of the response to caudal compression, while inducing no significant alteration of that to thermal injury. Pretreatment with GTX-III resulted in a significant decrement of the time required for loss of the righting reflex induced by pentobarbital, with a concomitant delay in recovery. Mice injected with the toxin exhibited a significant and restorable suppression of coordination, and a long-lasting suppression of spontaneous locomotor activity in both horizontal and vertical directions. Neither tetrodotoxin (1-5 micrograms/kg, i.p.) nor Ro15-1788 (1-5 mg/kg, i.p.) prevented the GTX-III-induced suppression of locomotion. Atropine (5-10 mg/kg, i.p.) failed to antagonize the GTX-III-induced suppression but protected against salivation induced by the toxin without affecting other symptoms. Intracerebroventricular injection of quisqualic acid (0.5 microgram), one of the agonists for central glutamate receptors, but not that of tetrodotoxin (5 ng) prevented the GTX-III-induced suppression of horizontal movement. These results suggest that GTX-III may elicit its depressant action on horizontal locomotion possibly through interacting with central glutamatergic neurons rather than activating voltage-sensitive sodium channels in the brain. Possible involvement of muscarinic cholinergic neurons in the GTX-III-induced salivation is also suggested.
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PMID:Preventive action of quisqualic acid against grayanotoxin-induced suppression of locomotor activity in mice. 307 Apr 32


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