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)

The medical records for 174 patients who underwent cholecystectomy (n = 52) or hip/knee replacement (n = 122) at four community-based medical centers were retrospectively reviewed to determine if using a nonnarcotic alternative to morphine sulfate and/or meperidine as a primary postoperative analgesic could reduce resource costs per patient. Two cohorts were constructed: 87 patients received either morphine sulfate or meperidine as the primary postoperative analgesic, and 87 patients received ketorolac. Ketorolac patients undergoing cholecystectomy were associated with lower per case costs in inpatient care (length of stay), direct nursing labor, PRN (as required) procedures, and medications relating to emesis and to gastrointestinal distress. Higher per case costs were recorded for the primary analgesic (study drug) and for supplemental pain medications. In contrast to substantial differences in the acquisition cost of ketorolac versus morphine sulfate/meperidine, the ketorolac cholecystectomy group was associated with lower overall resource costs per patient. In joint replacement procedures, however, the ketorolac group was associated with higher overall resource costs per patient, attributable primarily to a slightly higher postoperative length of stay.
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PMID:Economic assessment of ketorolac versus narcotic analgesics in postoperative pain management. 826 60

The emetic effects of copper sulfate and cisplatin and the potential involvement of vagal afferent fibers and 5-HT3 receptors in the emesis were investigated in cynomolgus monkeys. Retching and vomiting induced by both oral (100 mg/kg) and intravenous (20 mg/kg) copper sulfate were inhibited markedly by abdominal vagotomy. Furthermore, the emetic response induced by oral copper sulfate was strongly inhibited by intravenous ICS 205-930 (0.1 mg/kg), a 5-HT3 receptor antagonist. Cisplatin (3 mg/kg, i.v.) caused severe retching and vomiting, and the number of emetic responses was much greater than that in other species. The emetic response induced by cisplatin was inhibited markedly by abdominal vagotomy or concurrent administration of ICS 205-930 (3 x 0.1 mg/kg, i.v.). These results suggest that the monkey is more sensitive to cisplatin than other species and that the vagal afferent terminals and 5-HT3 receptors play an important role in the emetic response induced by copper sulfate and cisplatin.
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PMID:Involvement of 5-HT3 receptors and vagal afferents in copper sulfate- and cisplatin-induced emesis in monkeys. 828 15

Mitchell et al. (1976, 1977) suggested that pica, eating of nonnutritive substances such as kaolin, is an illness-response behavior in rats. In the present study, we first confirmed their suggestion and then examined the effects of antiemetics on emetic-induced pica in rats. Intraperitoneal injection of apomorphine induced dose-dependent kaolin consumption. Pretreatment with domperidone inhibited apomorphine-induced kaolin intake. Oral administration of copper sulfate and intraperitoneal injection of cisplatin also induced dose-dependent kaolin consumption. Pretreatment with ondansetron inhibited cisplatin-induced kaolin intake. These findings suggest that pica in rats was induced through 1) dopamine D2 receptors in the chemoreceptor trigger zone, and 2) the stomach, partly via 5-HT3 receptors in the visceral afferents in the stomach wall. The present findings support the conclusion that pica in rats is analogous to vomiting in other species and suggest that pica in rats is mediated by the same mechanisms as vomiting in humans. Accordingly, we extended the utility of the animal model to pharmacological research of emesis with pica as an analogue to emesis.
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PMID:Pica in rats is analogous to emesis: an animal model in emesis research. 841 20

A 33 year-old man with undiagnosed neuropathy showing mental retardation and involuntary movements has been nourished for a long period by total parenteral nutrition (TPN) because of frequent vomiting and repeated aspiration pneumonitis. After ten months' TPN, macrocytic anemia and neutropenia developed and iron preparation was administered without hematological improvement. Bone marrow examination revealed normocellular marrow without features of megaloblastosis and dysplasia. In some erythroblasts and immature myeloid cells, vacuoles were observed and mature granulocytes were reduced in the bone marrow. Both serum copper and ceruloplasmin were very low (12 micrograms/dl and 7mg/dl, respectively). Thus, oral administration of copper sulfate resulted in marked increase of reticulocytes and subsequent improvement of anemia and neutropenia within two months. Copper deficiency is a rare condition, but during an unusual nutrition such as TNP, hematological abnormality due to copper deficiency must be noticed to occur.
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PMID:[Anemia and neutropenia due to copper deficiency during long-term total parenteral nutrition]. 849 15

We have shown previously that Suncus murinus, a species of the insectivore, can vomit in response to various emetogenic stimuli. In the present study we investigated whether or not Sorex unguiculatus, which belongs to different subfamily (Soricinae) of insectivore, vomits in response to emetogenic drugs. Subcutaneous injection of veratrine and oral administration of copper sulfate caused emesis in the animal. Histological study showed that bilateral structure of the area postrema was not important for the emetic reflex. Therefore, the capability of emesis may be common to the family of soricidae of the insectivore, and the Sorex unguiculatus is the smallest known mammal which can vomit.
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PMID:Emetic responses of Sorex unguiculatus. 851 99

The potent, selective, tachykinin NK1 receptor antagonist, CP-122,721 ([(+)-(2S,3S)-3-(2-methoxy-5-trifluoromethoxybenzyl)amino-2- phenylpiperidine]), at 0.01-1 mg/kg, s.c. reduced retching and vomiting elicited by loperamide, copper sulfate, ipecac syrup and cisplatin in a dose-dependent manner. ID50 values after subcutaneous administration ranged from 0.02 mg/kg (loperamide) to 0.08 mg/kg (ipecac). Oral CP-122,721 reduced cisplatin-induced emesis with an ID50 of approximately 0.08 mg/kg. The less active (2R, 3R)-enantiomer, CP-132.687, did not significantly suppress retching or vomiting induced by any of the emetogens. These data support the hypothesis that CP-122,721 blocks emesis by a specific action at tachykinin NK1 receptors. Its broad spectrum of antiemetic activity suggests a central site of action.
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PMID:Broad spectrum antiemetic effects of CP-122,721, a tachykinin NK1 receptor antagonist, in ferrets. 881 51

The pharmacological characteristics of DQ-2511, a substituted benzamide (3-[[[2-(3,4-dimethoxyphenyl)ethyl]carbamoyl]methyl] amino-N-methylbenzamide), as a prokinetic agent were studied. Cholecystokinin-octapeptide, dopamine, and alpha-calcitonin gene-related peptide, all suppressed gastric emptying in mice. Reversal of the depressed emptying occurred when DQ-2511 was administered by the oral or intraperitoneal route. When the action of eight proposed metabolites of DQ-2511 on the mouse cholecystokinin-octapeptide model was investigated, the main metabolite in plasma, MA-2, showed no effect, although two minor metabolites ameliorated or aggravated the delayed gastric emptying. This finding implies that DQ-2511, as the parent compound itself, exerts the ameliorative action. In dogs treated with cisplatin or copper sulfate, DQ-2511 had no antiemetic activity, as assessed by the number of vomiting episodes. The concern that the mechanism of action of DQ-2511 was blockade of receptors for cholecystokinin-octapeptide, dopamine, serotonin, alpha-calcitonin gene-related peptide, nicotine or muscarine, was resolved by results of radioligand binding studies showing the absence of a DQ-2511 binding to any of these receptor types. Evidence is accumulating that the mechanism of the prokinetic action of DQ-2511 involves the intrinsic and extrinsic autonomic innervation.
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PMID:Pharmacological characteristics of DQ-2511 as a prokinetic agent. 883 52

In Suncus murinus, various emetic responses and the anti-emetic activity of a new 5-hydroxytryptamine3 (5-HT3) receptor antagonist, GK-128 (2-[(2-methylimidazol-1-yl) methyl benzo[f]thiochromen-1-one monohydrochloride hemihydrate), were investigated. Cancer chemotherapeutic agents, cisplatin and cyclophosphamide, dose-dependently induced emesis of long-lasting duration. The 5-HT3 receptor agonist, 2-methyl-5-HT, and copper sulfate also induced emesis of short duration. However, another 5-HT3 receptor agonist, m-chlorophenylbiguanide, was not consistently emetic. GK-128 inhibited the emetic responses induced by chemotherapeutic agents and 2-methyl-5-HT with similar potency. The anti-emetic action of GK-128 was more potent than that of ondansetron, Y-25130, granisetron and metoclopramide. The order of potency of these drugs, except granisetron, was consistent with that of their 5-HT3 receptor binding affinity in rat cortex. GK-128 failed to inhibit copper sulfate-induced emesis. These data suggest that GK-128 has a potent inhibitory effect on emesis via the 5-HT3 receptor, and that the 5-HT3 receptor involved in emesis in Suncus murinus may be different from the classically defined 5-HT3 receptor in other animals such as rats, dogs and ferrets.
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PMID:The anti-emetic activity of GK-128 in Suncus murinus. 884 9

Some infants with hypertrophic pyloric stenosis (HPS) have responded to oral atropine treatment. To achieve sufficient effect of atropine, it must be administered intravenously (i.v.). Therefore, with ultrasonography, we studied the changes in the pyloric muscle in HPS during and after intravenous administration of atropine. Twenty-three infants were studied. Atropine sulfate was initially administered at a dose of 0.04 mg/kg day i.v., and the dose was increased by 0.01 mg/kg/day until vomiting ceased. When vomiting ceased after administration of intravenous atropine sulfate, the infants received oral atropine sulfate at twice the effective intravenous dose; this was continued for 2 weeks. Ultrasonography was repeated until pyloric muscles normalized. Twenty-two infants were free from vomiting after 1-8 days of intravenous atropine sulfate (dosages of 0.04-0.11 mg/kg/day). In 21 infants, weight gain continued after atropine treatment even though no change in thickness of the pyloric muscles was demonstrated ultrasonographically. Only 2 infants required pyloromyotomy because of prolonged treatment or a mistake in underdosing of oral atropine. All of the 21 infants who recovered after intravenous atropine without surgery had normalization of pyloric muscle caliber, as shown by ultrasonography 4-12 months after treatment. Atropine is an effective medicine for HPS. Regression of pyloric thickening after vomiting has been controlled implies that pyloric muscle hypertrophy could be worsened by the spasm that occurs in HPS.
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PMID:Management and ultrasonographic appearance of infantile hypertrophic pyloric stenosis with intravenous atropine sulfate. 885 85

Postoperative analgesia was assessed after intrathecal administration of morphine-6-glucuronide (M6G) 100 micrograms and 125 micrograms in 75 patients undergoing total hip replacement. Analgesia was excellent and was similar to that obtained after intrathecal administration of morphine sulfate 500 micrograms. Visual analog pain scores recorded postoperatively were low (median = 0) and were similar in all three groups. However, at 6 and 10 h after operation significantly more patients in the M6G 125 group recorded pain as 0 compared with patients in the morphine group (P < 0.04, P < 0.01) and significantly more patients in the M6G 100 group recorded pain as 0 at 24 h after operation compared with patients in the morphine group (P < 0.04). Postoperative meperidine consumption using a patient-controlled system was also similar in each of the three treatment groups. Nausea and emesis occurred frequently in all groups; morphine (nausea 88%, vomiting 76%), M6G 100 micrograms (nausea 76%, vomiting 64%), and M6G 125 micrograms (nausea 88%, vomiting 60%). Respiratory depression occurred in two and three patients, respectively, in the M6G 100-microgram and 125-microgram groups but did not occur in any patient who received morphine sulfate. The lack of statistical significance in the difference in incidence of respiratory depression between the groups may represent a type II error. However, the risk of late respiratory depression developing after administration of any intrathecal opioid necessitates careful postoperative observation of patients. As M6G is a potent intrathecal analgesic further investigation of this drug using small doses may be useful.
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PMID:A comparison of intrathecal morphine-6-glucuronide and intrathecal morphine sulfate as analgesics for total hip replacement. 889 85


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