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)

Although consequences of zinc deficiency have been recognized for many years, it is only recently that attention has been directed to the potential consequences of excessive zinc intake. This is a review of the literature on manifestations of toxicity at several levels of zinc intake. Zinc is considered to be relatively nontoxic, particularly if taken orally. However, manifestations of overt toxicity symptoms (nausea, vomiting, epigastric pain, lethargy, and fatigue) will occur with extremely high zinc intakes. At low intakes, but at amounts well in excess of the Recommended Dietary Allowance (RDA) (100-300 mg Zn/d vs an RDA of 15 mg Zn/d), evidence of induced copper deficiency with attendant symptoms of anemia and neutropenia, as well as impaired immune function and adverse effects on the ratio of low-density-lipoprotein to high-density-lipoprotein (LDL/HDL) cholesterol have been reported. Even lower levels of zinc supplementation, closer in amount to the RDA, have been suggested to interfere with the utilization of copper and iron and to adversely affect HDL cholesterol concentrations. Individuals using zinc supplements should be aware of the possible complications attendant to their use.
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PMID:Zinc toxicity. 240 97

The antiemetic activity of zacopride against a variety of emetogenic agents has been determined in dogs. Zacopride was highly effective in inhibiting emesis due to a wide range of cancer chemotherapeutic agents, particularly cisplatin. It was well absorbed orally since the dose of zacopride required to inhibit cisplatin-induced emesis in dogs by 90% was 28 micrograms kg-1 both by i.v. and p.o. routes. Further, zacopride (1 mg kg-1 p.o.), administered after the onset of cisplatin-induced emesis, reduced the number of subsequent emetic episodes by 91%. Zacopride at 0.1, 1, or 3.16 mg kg-1 p.o. or i.v., reduced the number of emetic episodes due to dacarbazine, mechlorethamine, adriamycin, actinomycin D, or peptide YY by 100, 100, 86, 96 and 79%, respectively. However, zacopride was not effective in inhibiting emesis due to either apomorphine, copper sulphate, protoveratrine A, histamine, or pilocarpine. No adverse effects attributed to zacopride were observed. Zacopride is thus a unique and potent antiemetic agent as it selectively inhibits the emetic response to cancer chemotherapy agents and peptide YY.
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PMID:The antiemetic profile of zacopride. 256 16

A 4-month-old Pomeranian pup was examined because of anorexia, salivation, and persistent vomiting. Initial laboratory testing revealed marked hemolytic anemia with spherocytosis. Survey abdominal radiography revealed 4 metal objects which, when removed by gastrotomy, were identified as pennies. Of 4 pennies, 3 were minted since 1983 and were heavily pitted over the surface and rim. Partially digested pennies were composed of a copper-plated high zinc concentration alloy. Further laboratory testing indicated a marked increase in serum zinc concentration in the pup (28.8 mg/L), confirming metal toxicosis. Serum zinc concentrations decreased during recovery.
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PMID:Zinc-induced hemolytic anemia caused by ingestion of pennies by a pup. 275 99

In unanesthetized cats the emetic action of dimethylphenylpiperazinium (DMPP) was investigated, after it was injected into the cerebral ventricles through chronically implanted cannulae. DMPP injected in 0.2-2.0 mg doses into the cerebral ventricle produced dose-dependent vomiting, which was abolished after ablation of area postrema. However, copper sulfate given intragastrically evoked vomiting in cats with an ablated area postrema. Further, the emetic response to ICV DMPP and to intragastric copper sulfate was depressed or abolished in cats pretreated with ICV reserpine. The emetic response to ICV DMPP, but not that caused by intragastric copper sulfate, was potentiated in cats pretreated with ICV 5,6-dihydroxytryptamine. Ganglionic blocking agents, mecamylamine and hexamethonium, injected ICV prevented the vomiting elicited by ICV DMPP. On the other hand, selected anti-muscarinic drugs, alpha and beta adrenergic antagonists, dopamine antagonists, antihistamines and a 5-hydroxytryptamine (5-HT) antagonist all injected into the cerebral ventricles had virtually no effect on the vomiting induced by DMPP. It is postulated that DMPP evokes vomiting by its action on nicotinic receptors of nerve cells within the area postrema but not on catecholaminergic, serotonergic, or cholinergic receptors. Finally, 5-HT and acetylcholine could also be involved in the inhibition of the complex mechanisms underlying the central regulation of vomiting.
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PMID:Dimethylphenylpiperazinium-induced vomiting: nicotinic mediation in area postrema. 286 24

The emetic action of noradrenaline was investigated in unanesthetized cats, after it was injected into the cerebral ventricles through chronically implanted cannulae. Intracerebroventricular injection of noradrenaline produced dose-dependent and shortlasting emesis, which was abolished after ablation of the area postrema. However, copper sulphate, given orally, evoked emesis in cats with an ablated area postrema. The selective alpha-2 adrenoceptor antagonist, yohimbine, as well as the mixed alpha-1 and alpha-2 adrenoceptor blocking drugs, phentolamine, tolazoline, phenoxybenzamine and dihydroergotamine, but not the selective alpha-1 adrenoceptor antagonist, prazosin, all injected into the cerebral ventricles, attenuated or blocked the emesis evoked by intracerebroventricular injection of noradrenaline. Of the alpha-adrenoceptor antagonist, only yohimbine produced dose-dependent inhibition of the emesis induced by noradrenaline. On the contrary, selected beta-adrenoceptor blocking agents, an antimuscarinic drug, a ganglionic blocking agent, an antihistamine, dopamine antagonists and a 5-hydroxytryptamine antagonist, all injected into the cerebral ventricles, had no significant effect on the emesis induced by noradrenaline, similarly injected. The emetic response to intracerebroventricular injection of noradrenaline, as well as to intragastric administration of copper sulphate was not altered in cats pretreated with intracerebroventricular injections of alpha-methyl-p-tyrosine and bretylium. On the other hand, the emetic response to intracerebroventricular injection of noradrenaline and to intragastric administration of copper sulphate was attentuated or blocked in cats pretreated with reserpine intracerebroventricularly. Moreover, in cats pretreated with intracerebroventricular injection of 6-hydroxydopamine and hemicholinium, the emesis induced by intracerebroventricular administration of noradrenaline but not that produced by intragastric injection of copper sulphate, was depressed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Noradrenaline-induced emesis. Alpha-2 adrenoceptor mediation in the area postrema. 288 65

The emetic and antiemetic effects of opioid agonists were studied in awake dogs. The mu-agonists morphine, fentanyl and methadone, in sedative doses, prevented the emetic response to apomorphine and copper sulphate; only morphine induced emesis, at doses lower than those required to prevent emesis. The delta-agonist [D-Ala2,Met5]enkephalinamide (DALA) and [Leu5]enkephalin induced emesis in some of the dogs studied but had no antiemetic activity. The kappa-agonists bremazocine and ethylketocyclazocine (EKC) did not induce emesis but, at sedative doses, prevented the emetic response to apomorphine. The emetic effect of DALA was antagonized by naloxone in some dogs; the antiemetic effect of morphine, bremazocine and EKC was blocked by both naloxone and MR 2266. The non-opioid sedatives diazepam, phenobarbital and xylazine, administered in sedative doses, did not prevent apomorphine-induced emesis. Our results suggest that a delta-receptor is involved in the emetic effect and a mu- and/or or kappa-receptor in the antiemetic effect of opioids.
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PMID:Emetic and antiemetic effects of opioids in the dog. 302 91

Administration of lithium chloride and copper sulfate to adult monkeys caused marked elevations in plasma vasopressin (AVP) levels without significant increases in plasma oxytocin (OT) levels. Emesis was produced in five of the seven animals given these agents, in support of nausea as the main stimulus to AVP release. A similar pattern of AVP release without OT release was found after administration of cholecystokinin (CCK). Although most monkeys vomited in response to 10 micrograms/kg of CCK, a significant increase in plasma AVP levels also was produced with a dose of 1 microgram/kg, which did not produce emesis in any animal. These findings are in marked contrast with previous results in rats, which indicated that lithium chloride, copper sulfate, and CCK each stimulated OT rather than AVP release. Despite this interspecies difference, the significant neurohypophysial hormone secretion in response to both nausea-producing agents and CCK suggests that AVP secretion in monkeys, similar to OT secretion in rats, might reflect activation of central pathways mediating nausea and/or inhibition of food intake, even when overt illness is not produced.
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PMID:Vasopressin release in response to nausea-producing agents and cholecystokinin in monkeys. 303 8

Effects of the clathrate compound of mobenzoxamine (MBX) with beta-cyclodextrin (MBX-CD), a new gastro-intestinal function modulator, on the digestive system were studied in comparison with those of metoclopramide, domperidone and trimebutine. MBX-CD showed inhibitory effects that were approximately 1/4 times as potent as metoclopramide on both apomorphine- and copper sulfate-induced emesis and about 1/40 times as potent as domperidone on apomorphine-induced emesis in dogs. In rats, MBX-CD enhanced gastric emptying as potently as metoclopramide, and only MBX-CD showed a clear amelioration of the delayed gastric emptying induced by BaCl2. Similarly, only MBX-CD showed an ameliorative effect on small intestinal transport accelerated by BaCl2 in mice. Though both MBX and trimebutine inhibited spontaneous contractions of the isolated guinea pig stomach and rabbit intestine, it seemed that the properties of these effects were different from those of papaverine. On isolated guinea pig ileum, MBX inhibited contractions induced by various agonists equally to or more potently than trimebutine or papaverine. The results suggest that MBX-CD or MBX acts extensively on the gastro-intestinal system for the reason that it has not only the respective properties of the gastro-intestinal function modulators used as the standards, but also its own characteristic effects.
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PMID:[Pharmacological studies on the clathrate compound of mobenzoxamine with beta-cyclodextrin. (I). Effects on the digestive system]. 324 12

For 12 hours, excess hydrofluorosilicic acid was diverted to a 127-home community water supply. Fluoride levels peaked at 51 parts per million (ppm). Water acidification caused copper to leach from the domestic plumbing; raising copper levels to 25-41 ppm. Fifty-two (33 per cent) of those who drank hyperfluoridated water developed mild gastroenteritis. Vomiting was uncommon and symptom onsets usually occurred greater than 30 minutes after drinking water; suggesting that fluoride, rather than copper, caused illness. Skin contact with hyperfluoridated water caused itching and skin rashes.
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PMID:Community health effects of a municipal water supply hyperfluoridation accident. 336 8

Information from animal studies has demonstrated the harmful effects of zinc supplementation on copper transport. Although some studies have been carried out in humans, the effect on humans has not been as well documented as the effect on animals. Forty-seven healthy volunteers (26 women and 21 men) took part in a double-blind cross-over trial which lasted for 12 weeks. The subjects were asked to take 50 mg of elemental zinc (as 220 mg zinc sulphate) or placebo, three times a day for six weeks. Venous blood was collected for the analysis of plasma levels of copper and zinc. Symptoms, which included headaches, abdominal cramps, nausea, loss of appetite and vomiting, were registered from 84% of women and 18% of men. Six female volunteers discontinued the trial; five owing to gastric irritation and one owing to consistent headaches. Plasma zinc levels rose significantly in both men and women, the increase being 36% and 57%, respectively. Plasma copper levels did not change significantly. Our study suggests that the gastric discomfort that is associated with zinc supplementation may be related to body weight as symptoms were reported from the lower-weight volunteers. Our study also shows no detrimental effect of 150 mg of zinc a day on plasma copper levels in healthy volunteers over a period of six weeks.
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PMID:The effect of zinc supplements on plasma zinc and copper levels and the reported symptoms in healthy volunteers. 354 53


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