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)

Double-blind clinical trials involving the use of phenothiazines as analgesics or potentiators of analgesics (aspirin, meperidine, morphine sulfate) and adverse effects of phenothiazines are reviewed and evaluated. Promethazine, promazine and propiomazine were not found to possess analgesic or potentiating properties. One chlorpromazine study contained important design and reporting deficiencies which precluded a recommendation for use of chlorpromazine in the treatment of pain. Methotrimeprazine was determined by numerous authors to have analgesic properties; however, most of the studies also were deficient in design or data presented, or both. Adverse reactions to phenothiazines, including hypotension, sedation, drowsiness, extrapyramidal symptoms, tardive dyskinesia, cardiac toxicity and agranulocytosis, are often more common and severe than those attributed to narcotic analgesics. Because of the lack of data supportive of analgesic activity and the adverse reactions associated with phenothiazines, use of these agents in the management of pain should be discouraged. The prophylactic use of phenothiazine for narcotic analgesic-induced emesis also is, in most cases, a questionable practice.
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PMID:Phenothiazine analgesia--fact or fantasy? 3 54

The effects of orally administered zinc sulfate in 52 patients with mild to moderate acne vulgaris were compared to those of a placebo capsule. The numbers of comedones, papules, pustules, infiltrates, and cysts were counted at each visit over a 12-week period. Forty patients completed the study. Zinc appeared to have a somewhat beneficial effect on pustules but not on comedones, papules, infiltrates, or cysts. Fourteen patients (50%) in the zinc group had side effects of nausea, vomiting, or diarrhea. Six patients (21%) in the zinc group could not tolerate the nausea and withdrew from the study.
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PMID:Zinc sulfate in acne vulgaris. 15 30

Acute digoxin poisoning, its recognition and management, are reviewed. The uses of syrup of ipecac, gastric lavage, activated charcoal, cholestyramine, colestipol, edetate sodium and cathartics as measures to terminate the drug exposure are discussed. Measures to hasten digoxin elimination, such as the use of furosemide, hemodialysis and digoxin-specific antibodies are reviewed. Supportive management may include treatment with atropine, phenytoin, lidocaine, propranolol, glucose, insulin and sodium polystyrene sulfonate. Proper management of digoxin poisoning involves the use of standard decontamination procedures (emesis or gastric lavage). Activated charcoal is strongly recommended, followed by rapidly acting cathartics. Antiarrhythmic therapy usually involves atropine sulfate and phenytoin sodium.
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PMID:Acute digoxin poisonings: review of therapy. 34 83

In 37 children with Campylobacter enteritis seen over a 6-month period, ages ranged from 2 weeks to 15 years. The sex ratio (male:female) was three:two. Fever, diarrhea, and bloody stools occurred in about 90% of patients. Blood appeared in the stools characteristically 2 to 4 days after onset of symptoms. Over 90% of older children developed abdominal pain. Vomiting was mild and occurred in 30% of patients. Dehydration was not a feature. Infection occurred in all social classes and was not associated with parental occupation, travel, or animal contact. The illness often presented characteristically and a rapid laboratory diagnosis could be made in patients presenting acutely by direct phase-contrast microscopy of stools. The organism persisted in the stools for up to seven weeks in untreated patients, but could no longer be cultured after 48 hours of therapy with erythromycin, to which all strains were highly sensitive. Significant serologic responses were elicited using a serum bactericidal assay. The Skirrow-type selective medium used by us could be improved by increasing the concentration of polymyxin B sulfate to 5 microgram/ml.
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PMID:Campylobacter enteritis in children. 43 Feb 87

Sensitivities of the stomach and duodenum to oral copper sulfate emesis were compared in dogs. 1) Dogs equipped with a stainless stell cannula in the middle of the duodenum were challenged to the oral threshold emetic dose of copper sulfate administered by a gastric tube. When the cannulas were opened, the oral thresholds were not effective to elicit vomiting in the most cases (1/13). Fairly rapid and high rate recoveries of copper through the open cannula were noted. With the closed cannulas, the thresholds were highly effective (16/16). 2)In the dogs with a cannula at the upper part of the jejunum, the oral threshold doses were always effective whether the canula was opened (9/9) or closed (11/11). Recovery rates of copper from the cannula were usually poor. 3) The oral thresholds administered into the proximal end or the middle of the duodenum through a PVC tubing were equally effective. 4) Although copper sulfate might irritate the stomach and upper duodenum to evoke vomiting, these results suggested a higher sensitivity of the lower duodenum.
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PMID:Site of emetic action of oral copper sulfate in dogs. (II) Importance of lower duodenum. 74 5

Magnesium deficiency can occur in congestive heart failure, after diuresis with furoxemide, ethacrynic acid and mercurials, and with digitalis intoxication, diabetic acidosis, acute and chronic alcoholism, delerium tremens, cirrhosis, malabsorption syndromes, protracted postoperative cases, open heart surgery, the diuretic phase of acute tubular necrosis, and with hypoparathyroidism, primary aldosteronism, juxta-glomerular hyperplasia and pancreatitis. Two cases of serious ventricular arrhythmias associated with magnesium depletion are described. Clinical manifestations are vague but center around neurologic symptoms such as weakness, tremors, stupor, coma, nausea, vomiting and anorexia. Serious cardiac arrhythmias also occur with magnesium depletion. Magnesium appears to be very useful in hypomagnesemic or digitalis-toxic tachyarrhythmias. Magnesium may also be valuable in normomagnesemic tachyarrhythmias. Ten to fifteen milliliters of a 20 percent magnesium sulfate solution, given intravenously over 1 minute, followed by a slow 4 to 6 hour infusion of 500 ml of 2 per cent magnesium sulfate in 5 per cent dextrose in water is recommended. Recurrence of arrhythmias is common and a second infusion of magnesium sulfate may be necessary. Hypermagnesemia occurs frequently in renal insufficiency, and magnesium therapy may then be contraindicated. Serum levels above 5.5 meq/liter should be avoided. Loss of deep tendon reflexes and a decrease in respiratory rate can be used as guides to magnesium therapy. A plea is made for frequent analysis of serum magnesium so that more knowledge can be gained regarding this important biologic element in cardiovascular disorders.
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PMID:Magnesium deficiency and cardiac disorders. 80 29

A study was designed to examine the effects of intraventricularly (i.vt.) administered morphine, apomorphine and epinephrine on the small intestine. Adult cats of either sex were implanted chronically with extracellular, monopolar electrodes at equal intervals along the entire small intestine. A collison cannula was placed in the left lateral cerebral ventricle in each animal. In animals that did not respond with emesis, morphine sulfate (200 micron g) administered i.vt. increased the incidence of spike potentials over the proximal three-quarters of the small intestine almost immediately. The response to i.vt. morphine was abolished by pretreatment with i.vt. naloxone HC1 (200 micron g) and was not obtained after peripheral (i.p.) injection of morphine at the same dose effective centrall. Now change in the number of spike potentials occure after i.vt. administration of two other potent emetic agents, apomorphine HC1 (200 micron g) and epinephrine HC1 (15O micron g), in animals that did not respond with emesis. The results suggest that the increased incidence of spike potentials after i.vt. morphine is a naloxone-sensitive, centrally mediated event not associated with activation of the central emetic mechanism.
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PMID:Centrally mediated intestinal stimulation by morphine. 87 14

Adult cats were administered oral threshold doses of copper sulfate every week. As the cats vomited in 70 out out 80 cases, the reproducibility was 88%. Peripheral vomiting threshold dose was 40 mg/head or less, while the threshold dose for oral copper sulfate emesis after T4 transection and vagotomy was more than 160 mg/head. The following method is thus proposed for application in evaluating an antimetic for oral copper sulfate. Adult cats are to be given the emetic once a week. The threshold dose should be determined in three dose levels; 10, 20, 40 mg/head. The cats with a threshold of more than 40 mg or latency of less than 5 min or of more than 45 min are to be excluded. Inhibition of emesis or a considerable prolongation of latency is the sign of an antimetic action. A positive action of an antiemetic must be followed by another test with the threshold dose of copper sulfate alone. If the cat does not respond to the threshold dose after 2 administrations, the case must be excluded. It is considered positive when 3 cases are inhibited among 4 or more than 50% among more than 5.
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PMID:[Reproducibility of emesis by orally administrated copper sulfate in cats]. 98 87

Long marketed antiemetics, which are still used in medicine or veterinary medicine and whose sites of actions were either assumed to be peripheral or unknown, were subjected to evaluation as antiemetics, against oral copper sulfate emesis. In cats, ethyl aminobenzoate 0.5 g/head, cerium oxalate 0.1 g/head, pinelliae tuber 0.5 g/head and gelatin 2.0 g/head were not effective. In dogs, ethyl aminobenzoate 0.5 g/head, pinelliae tuber 2.0 g/head and hange-syasintoo 2.0 g/head were not effective. Cerium oxalate 0.1 g/head was found to have a slight antiemetic action.
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PMID:[Effectiveness of several antiemetics in vomiting induced by orally administrated copper sulfate in cats and dogs]. 98 88

A new compound, dl-cis-1-benzoyloxy-2-dimethylamino-1,2,3,4-tetrahydronaphthalane (YAU-17) was found to produce sciatic nerve block, corneal and intradermal anesthesia in guinea-pigs, which markedly exceeded the effect of procaine and lidocaine. YAU-17, when given orally to mice, was much less toxic than any other drugs tested, though YAU-17 showed a considerably high acute toxicity by i.v. route. Oral administration of YAU-17 was effective in antagonizing the emetic response of dogs to intragastric phenylalanine isopropyl ester, but produced no distinct inhibition against vomiting elicited by oral copper sulfate. Furthermore, it possessed a spasmolytic activity which was comparable to that of papaverine, and showed an effect of suppressing the mucosal intrinsic reflex in the dog intestine. These pharmacological properties of YAU-17 were qualitatively similar to those of oxetacaine which was used as one of the reference compounds.
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PMID:Pharmacological studies on a new 1-benzoyloxy-alkylaminocycloalkane derivative (YAU-17) with special reference to its mucosa anesthetic activity. 98 56


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