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)

Six premature infants (birth weights 920-1320 g) developed marked abdominal distension after birth, and contrast enema examination showed a microcolon. Four of the six were born to mothers with toxemia who received magnesium sulfate. Bilious emesis was absent in all six, despite marked distension and failure to pass meconium. None of the patients had aganglionosis or cystic fibrosis; five of six were followed without surgery and recovered spontaneously. The sixth had perforation 8 hr after contrast enema and required bowel diversion; this infant also survived. This appears to be an equivalent form in small premature infants of the "small-left-colon syndrome" seen in term infants. Surgery should be reserved for complications; it is not necessarily indicated by the finding of a microcolon in such patients.
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PMID:Microcolon of prematurity: a form of functional obstruction. 348 69

The records of 147 cancer patients who received at least three courses of cisplatin-containing chemotherapy in the Arizona Cancer Center clinic between 1982 and 1985 were reviewed to determine the safety and tolerance of cisplatin administered in the outpatient setting. Cisplatin was administered at doses of 50-120 mg/m2 every 3-4 weeks. The drug was added to 400 ml of 10% mannitol, was brought up to 1-L volume with normal saline containing 3 g of magnesium sulfate, and was administered iv over 1 hour. An additional liter of normal saline was administered over approximately 1 hour in patients who received cisplatin doses of 70-120 mg/m2. Courses were interrupted if the serum creatinine was greater than 1.5 mg/dl just prior to the next scheduled dose. The median total doses of cisplatin per patient were 487, 595, and 683 mg/m2 and complete plus partial response rates were 64%, 71%, and 78% for those patients who received 50-60, 70-90, and 100-120 mg/m2/course, respectively. Cisplatin-containing therapy was tolerated without evidence of renal failure and with only moderate to severe emesis in 25% of the patients. Calculated creatinine clearances dropped only 4.9%, 13.9%, and 14.9% between Courses 1 and 6 in patients receiving cisplatin doses of 50-60, 70-90, and 100-120 mg/m2, respectively. We conclude that cisplatin doses of 50-120 mg/m2 can be administered safely and with acceptable tolerance in the outpatient setting.
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PMID:Safe, rapid administration of cisplatin in the outpatient clinic. 353 27

Effects of various emetic and antiemetic drugs were studied using Suncus murinus for its potential use as an experimental model in emetic research. Subcutaneous injection of nicotine bitartrate (10-15 mg/kg), veratrine sulfate (0.5-1.0 mg/kg), emetine dihydrochloride (40-80 mg/kg) and oral administration of copper sulfate (20-100 mg/kg) caused dose-dependent emesis in suncus. The ED50 of nicotine, veratrine, emetine and copper sulfate were 7.9, 0.4, 47.6 and 21.4 mg/kg, respectively. However, subcutaneously injected apomorphine hydrochloride (0.1-100 mg/kg), digitoxin (0.5-1.0 mg/kg) and orally administered emetine dihydrochloride (10-80 mg/kg) did not induce the vomiting. Chlorpromazine and promethazine decreased the emetic effect of nicotine, veratrine and copper sulfate, but scopolamine hydrobromide was not effective. These results indicate that the Suncus murinus is sensitive to various emetic and antiemetic drugs and can be used as a new experimental animal model for the emesis. Emetic behavior of suncus was discussed in comparison with other animals.
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PMID:Suncus murinus: a new experimental model in emesis research. 360 Jan 92

In unanesthetized cats the emetic action of an injection of nicotine into the cerebral ventricle through chronically implanted cannulae was investigated. Nicotine injected in doses of 0.02-1.0 mg produced dose-dependent vomiting, which was abolished after ablation of the area postrema. However, copper sulfate given intragastrically evoked vomiting in cats with an ablated area postrema. The emetic response to intracerebroventricular (ICV) nicotine as well as the vomiting produced by intragastric copper sulfate was depressed or abolished in cats pretreated with ICV reserpine. On the other hand, the emetic response to ICV nicotine and to intragastric copper sulfate was virtually unchanged in cats pretreated with ICV 6-hydroxydopamine and 5,6-dihydroxytryptamine. The duration of vomiting produced by intragastric copper sulfate, but not that of ICV nicotine, was potentiated in cats pretreated with hemicholinium-3. Ganglionic blocking agents, mecamylamine and hexamethonium, injected ICV prevented the vomiting elicited by ICV nicotine. On the other hand, selected anti-muscarinic drugs, alpha and beta adrenergic receptor antagonists, dopamine antagonists, antihistamines and a 5-hydroxytryptamine antagonist all injected into the cerebral ventricle had virtually no effect on the vomiting induced by ICV nicotine. It is postulated that nicotine evokes vomiting by its action on nicotinic receptors within the area postrema but not on catecholaminergic or serotonergic neurones. Finally, acetylcholine could also be involved in the inhibition of the complex mechanisms underlying the central regulation of vomiting.
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PMID:Further studies on nicotine-induced emesis: nicotinic mediation in area postrema. 360 20

Ketamine was administered to 47 women aged 14-41 years who were about to undergo induced abortions. The patients received 2.5 mg of lorazepam 2 hours before the operation and 7.5 mg/kg of ketamine diluted in orange juice or water 45 minutes before. In all cases, sleep and transfer to the operating table were accomplished in calm and semidarkness. Intravenous tubes were inserted and .02 mg/kg of atropine sulfate was administered. Patients considered still conscious were given intravenous injections of ketamine 1 mg/kg. Perioperative evaluation of the quality of anesthesia was done using a 4-level scale based on reactions to stimuli. Ketamine .5 mg/kg was administered intravenously each time significant reactions were obtained. 45 minutes after oral ketamine administration, 8 patients were still conscious and received additional anesthesia. 9 of the 39 patients asleep at the preoperative evaluation required additional anesthesia during the procedure. The immediate postoperative period was calm in all cases, even though some patients later reported having had disagreeable hallucinations. 46.8% had vomiting. The frequency of vomiting declined from 54.4% to 28.8% when pure water was substituted for orange juice as the vector for the preoperative oral ketamine. Correct responses to simple questions were obtained an average of 12.4 minutes postoperatively, but all patients had periods of somnolence lasting 4.8 hours on average. 15 had partial recollections of the surgery. 78.8% of the patients stated that the anesthesia used was excellent or good. 8.5% felt it was average, and 10.6% felt it was poor. Very few publications mention oral use of ketamine. The failure rates of 17% during the preoperative evaluation and 23% during the operation were not negligible and were probably due to the very low bioavailability of ketamine administered orally and the variability of digestive absorption of ketamine from 1 subject to another. The method appears to be appropriate for use in induced abortions, but better management is required to reduce failure rates and control side effects of vomiting and disagreeable postoperative hallucinations.
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PMID:[Anesthesia with oral ketamine]. 362 Oct 17

Programmed ventricular stimulation was used to test oral bethanidine sulfate in 10 patients with life-threatening ventricular arrhythmias. These patients had previously documented, recurrent, sustained ventricular tachycardia (VT) and/or ventricular fibrillation (VF) complicating stable heart disease. During control electrophysiologic studies, VT could be induced in all 10 patients: 6 with nonsustained VT, 3 with sustained VT, and 1 with VT/VF. After control, bethanidine 20-30 mg/kg was administered orally and beginning 60 minutes later, programmed ventricular stimulation was repeated. After bethanidine administration, VT could be induced in nine patients; in four, the VT was essentially unchanged from that induced during control studies. In four others, worse VT was induced after bethanidine. The remaining two patients had a potentially beneficial response to the drug. Bethanidine was poorly tolerated: seven patients had symptomatic orthostatic hypotension that persisted for several days despite concurrent protriptyline therapy. Furthermore, in four patients, spontaneous VT or VT/VF occurred 3-8 hours after the last dose. Nausea, vomiting, flushing, and blood pressure elevation were also noted. Bethanidine sulfate in the dosages used usually does not prevent the induction of VT by programmed ventricular stimulation and frequently causes serious toxicity. These findings suggest that the drug would be ineffective and poorly tolerated for long-term therapy in patients with serious ventricular arrhythmias.
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PMID:Bethanidine sulfate in paroxysmal ventricular tachycardia: toxicity and antifibrillatory actions. 377 63

Seventeen patients in whom uterine activity responded favorably to parenteral magnesium sulfate were given oral magnesium gluconate for continued tocolysis. The mean serum magnesium level before therapy was 1.44 +/- 0.22 mg/100 ml, whereas 2 hours after initiation of oral magnesium it was 2.16 +/- 0.32 mg/100 ml (p less than 0.05). One patient had nausea without vomiting or diarrhea. These data suggest that magnesium ingested orally can raise the serum magnesium level significantly.
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PMID:Tocolysis with oral magnesium. 382 80

Five cardiology centers conducted open-label prospective trials of meobentine sulfate, an intravenously and orally available analog of bethanidine, to assess its potential for treatment of recurrent, drug refractory ventricular tachycardia (VT) or fibrillation (VF), and complex ventricular arrhythmias. The study population comprised 26 patients (mean age, 61 years); 18 were men. Coronary artery disease was present in 15, cardiomyopathy in six, and valvular heart disease in three. Patients presented with both VT and VF (seven), sustained VT alone (12), or frequent ventricular ectopy (PVCs) and nonsustained VT (seven). Of the 26 patients, 5 were enrolled in antiarrhythmic studies (chronic PVC suppression) and 21 were enrolled in programmed electrical stimulation (PES) studies. Two of five in the chronic PVC study showed greater than 75% arrhythmia suppression. Among 21 patients in PES studies, there were eight intravenous (16 mg/kg) and 19 oral trials (400 to 1000 mg every 6 hours, 3 days/dose interval). Five of 22 patients showed efficacy at repeat PES study (neither VT nor VF), one showed partial efficacy, and four were not restudied because of clinical arrhythmia (three) and/or adverse effects (two). Overall, three patients (12%) were continued on the drug for an extended period of time. Adverse experience included hypotension in 50% and gastrointestinal effects (nausea, vomiting, or diarrhea) in 56% (oral trials only). Adverse reactions led to drug discontinuation in six and dosage reduction in eight patients. Thus, meobentine may prevent induction of VT or VF or reduce frequency of complex PVCs in selected patients refractory to other antiarrhythmic agents, but the response rate is relatively low. Symptomatic hypotension or gastrointestinal adverse effects are common and may limit utility of meobentine as a chronic oral antiarrhythmic agent.
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PMID:Meobentine sulfate: antiarrhythmic and electrophysiologic effects assessed by programmed electrical stimulation and ambulatory monitoring in patients with complex ventricular tachyarrhythmia. Report of a multicenter evaluation. 390 15

A pair of siblings with clinical symptoms of cyclic vomiting and ketoacidosis were found to have a biochemical triad of normoglycemia, ketoacidosis and elevated levels of alpha-hydroxy- and alpha-aminobutyrate in plasma and urine. Methionine loading studies in both sibs produced prompt rises in plasma methionine and alpha-aminobutyrate levels, with a subsequent increase in urinary alpha-hydroxybutyrate, as well. Leukocytes from both siblings showed normal oxidation of [3-14C]propionate. Increased inorganic sulfate excretion after methionine loading implied an intact transsulfuration pathway in both siblings. On the basis of the studies detailed in this report, we conclude that these siblings suffer from a defect in alpha-ketobutyrate oxidation, a newly described defect of organic acid metabolism.
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PMID:Defect in alpha-ketobutyrate metabolism: a new inborn error. 391 15

In five conscious dogs prepared with a gastric cannula and platinum monopolar electrodes in the antrum, duodenum, and jejunum, the effect of dopamine or copper sulfate on the myoelectric activity was studied. During phase I of interdigestive myoelectric activity, retching, and/or vomiting occurred in 1.6 +/- 0.2 (mean +/- SE) min after intravenous bolus injection of dopamine (50 micrograms/kg) or in 8.7 +/- 1.8 min after intragastric administration of copper sulfate (2%, 50 mg). Immediately prior to the retching and/or vomiting act, a group of disordered myoelectric activities occurred, including retrograde-moving trains of spike activity starting from the jejunum and the subsequent tachyarrhythmia in the antrum. These motility changes also occurred in the two anesthetized dogs so studied. Both the retching and/or vomiting act and the abnormal myoelectric activity which were induced by dopamine and by copper sulfate were prevented by intravenous administration of a peripheral dopamine blocker, domperidone, 5 mg, in 100% and 70%, respectively. Although domperidone could not prevent the retching and/or vomiting induced by copper sulfate in three of 10 experiments, it delayed the onset of vomiting from 8.7 +/- 1.8 to 14.5 +/- 5.3 min. A possible role of peripheral dopamine receptor on the motility disorders associated with retching and/or vomiting has been suggested.
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PMID:Studies on mechanism of retching and vomiting in dogs. Effect of peripheral dopamine blocker on myoelectric changes in antrum and upper small intestine. 396 72


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