Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Systemic administration of apomorphine, angiotensin II, neurotensin and leucine-enkephalin induces emesis in dogs in a dose-dependent fashion. Receptors for Leu-enkephalin and angiotensin II but not apomorphine show receptor desensitization, such that a second systemic administration 5 min after the first is ineffective. Domperidone blocked the emetic response to apomorphine but not to Leu-enkephalin or angiotensin II. Naloxone selectively blocked the Leu-enkephalin response, while saralasin blocked responses to both angiotensin II and Leu-enkephalin, but not apomorphine. Chlorpromazine prevented the emetic response to all agents, suggesting a dopamine receptor in the emetic pathway on the brain side of the blood-brain barrier. In dogs with ablation of the area postrema the emetic response to apomorphine and all peptides was prevented.
 ...
PMID:Peptide-induced emesis in dogs. 672 20

The analgesic agent butorphanol was evaluated for its ability to block cisplatin-induced emesis in ferrets and dogs. In ferrets, butorphanol (0.15, 0.3, or 0.45 mg/kg; expressed in terms of the tartrate salt) administered sc 30 minutes prior to cisplatin (8 mg/kg iv) reduced the number of emetic episodes but did not eliminate them. When these doses of butorphanol were administered 30 minutes before and 30 and 90 minutes after cisplatin, they caused a dose-related reduction in the number of emetic episodes; there was complete protection at a dose of 0.45 mg/kg/injection. In dogs, butorphanol (0.185 or 0.37 mg/kg/injection, expressed in terms of the tartrate salt) was administered sc on the same multiple-dose schedule used in the ferrets; this caused a nearly complete elimination of the emetic response to cisplatin (3 mg/kg iv). Butorphanol caused some sedation in both species at effective antiemetic doses but had no effect on the antitumor activity of cisplatin against murine L1210 leukemia. Naloxone blocked the antiemetic effect of butorphanol in ferrets, indicating the involvement of opiate receptors. The results of these studies suggest that butorphanol may be useful clinically in mitigating the emetic effects of cisplatin.
 ...
PMID:Antiemetic activity of butorphanol against cisplatin-induced emesis in ferrets and dogs. 688 14

Management of the acutely poisoned patient should start with decontamination of the skin and irrigation of the eyes, if necessary, and assessment of cardiorespiratory status, neurologic status, and pupils and eye movement. If a definable toxic syndrome is present, the specific "antidote" should be given. If no such syndrome is apparent and the patient is comatose, 50 ml of 50% glucose and 0.4 mg of naloxone (Narcan) intravenously should be tried. General measures, applicable in either situation, include induction of emesis or lavage and administration of charcoal and cathartics.
 ...
PMID:Acute poisoning: management protocol. 707 Oct 40

EEG, behavioral and autonomic effects of morphine and clonidine were compared in the unrestrained beagle dog placed in a dimly-lit, sound-attenuated chamber equipped with video monitors. Intravenous (i.v.) morphine (0.5, 1 and 2 mg/kg) and clonidine (11, 33 and 100 microgram/kg) caused parallel dose-related increases in NREM sleep with clonidine being 43 times more potent than morphine. Other similar effects were: an initial transient EEG-behavioral dissociation; increases in spectral power (8-16 Hz); decreases in temperature and heart and respiratory rates; emesis, miosis and salivation. Intraventricular (i.v.t.) morphine (33, 100 and 300 microgram) and clonidine (10 and 30 microgram) caused qualitatively similar EEG, sleep and behavioral effects. Naloxone (30 microgram/kg i.v.) prevented EEG synchrony and behavioral effects of i.v. morphine (1 mg/kg) but not those of i.v. clonidine (100 microgram/kg). Yohimbine pretreatment (0.1 mg/kg i.v.) was more effective in antagonizing clonidine than morphine. These results suggest that morphine and clonidine induce similar EEG, behavioral and autonomic effects through actions upon different receptors on the same or parallel neural pathways. The results further emphasize the importance of an alpha 2-adrenergic-opioid interaction to regulate sleep in the dog.
 ...
PMID:Morphine-like effects of clonidine on the EEG, slow wave sleep and behavior in the dog. 711 87

Apomorphine (0.03 mg . kg-1 s.c.) and morphine (0.5 mg . kg-1 s.c.) produced gastric relaxation and vomiting in the conscious dog. Domperidone (0.1-1 mg . kg-1 i.v.), haloperidol (0.1 mg . kg-1 i.v.) and pimozide (0.025 mg . kg-1 i.v.) selectively blocked the gastric relaxation as well as the vomiting caused by apomorphine. Naloxone (0.07 mg . kg-1 i.v.) selectively blocked the gastric relaxation and the vomiting caused by morphine; after naloxone, morphine produced a delayed gastric relaxation in 2 experiments out of 7. These results suggest that for gastric relaxation as well as for vomiting, apomorphine and morphine act on different receptors. Fentanyl elicited marked gastric relaxation, blocked by naloxone, but did not elicit vomiting. After fentanyl, morphine and apomorphine no longer produced gastric relaxation and vomiting. This observation shows that the known blocking effect of fentanyl at the vomiting center does not affect its gastric relaxing effect.
 ...
PMID:Gastric relaxation and vomiting by apomorphine, morphine and fentanyl in the conscious dog. 720 14

The house musk shrew Suncus murinus recently has been introduced for the study of emesis. We investigated the emetic effects of the opioids morphine (0.1-21.5 mg/kg i.p.) and loperamide (0.01-10 mg/kg i.p.) and found a complete lack of emetogenic potential. Nicotine, however, dose dependently induced vomiting in the Suncus with an ED50 of 8.8 mg/kg s.c. and a 100% incidence at 20 mg/kg. This drug-induced vomiting was reduced by morphine or loperamide: ED50 values obtained were 1.2 mg/kg i.p. for morphine and 0.7 mg/kg i.p. for loperamide. Naloxone (2 mg/kg s.c.) antagonised the inhibitory effect of morphine (2 mg/kg i.p.) or loperamide (10 mg/kg i.p.). Serotonin (20 mg/kg s.c.) had less reliable emetogenic potency than nicotine in the Suncus with incidences between 50 and 100%. However, the serotonin-induced vomiting was abolished by morphine and loperamide and this inhibition was antagonised by naloxone. These results suggest that systemically administered opioids are pure antiemetics in Suncus murinus in contrast to other animal models and man. Naloxone antagonism indicates that this antiemetic effect is mediated by opioid receptors.
 ...
PMID:Absence of emetic effects of morphine and loperamide in Suncus murinus. 804 73

There is interest in the development of antiemetics other than dopamine receptor antagonists for the treatment of postoperative nausea and vomiting. A ferret model of morphine-induced emesis may have wider application in evaluating newer agents than the apomorphine dog model. This study describes the conditions for morphine-induced emesis in ferrets and evaluates five antiemetics that are prototypical of three different mechanisms. The average numbers of vomiting and retching episodes induced by morphine (0.1-2.5 mg/kg s.c.) were distributed as a bell-shaped curve. Maximum number of vomits occurred at 0.3 mg/kg (11.8 +/- 2.1 vomits; 45 +/- 12.5 retches). Antiemetics or vehicle were given i.v. 5 min prior to morphine while each ferret was maintained under isoflurane-O2 anesthesia. Ondansetron, a 5-HT3 receptor antagonist, reduced vomiting episodes by 47% and 70% (3 and 10 mg/kg). Granisetron, a 5-HT3 receptor antagonist was inactive at doses of 0.1, 1.0, 3.0 and 10 mg/kg. Metoclopramide reduced vomiting episodes by 48% and 82% (3 and 10 mg/kg). Droperidol reduced vomiting episodes by 84% at 3 mg/kg. Naloxone reduced vomiting episodes by 91% and 43% at doses of 0.1 and 1.0 mg/kg. In most cases, prolonged latency times to the first episodes accompanied the reduction in total numbers of episodes. The significant reduction of morphine-induced emesis in the ferret by ondansetron, metoclopramide and droperidol is consistent with the reduction of postoperative emesis in man by these compounds when morphine was a component of the anesthetic regimen. These results suggested that the morphine ferret model may be useful for evaluating compounds having the potential for preventing and treating postoperative vomiting.
 ...
PMID:The effects of different antiemetic agents on morphine-induced emesis in ferrets. 822 24

Ingestion of sodium hypochlorite bleach is usually benign, leading most poison centers to advocate conservative, home management. We report a rare, fatal case of household bleach ingestion. A 66-y-old female ingested an unknown quantity of regular CLOROX bleach (5.25% sodium hypochlorite, pH = 11.4). Upon discovery, she was vomiting spontaneously, and had slurred speech and oral mucosal discoloration. On hospital arrival the patient became unresponsive with shallow respirations. Laboratory studies revealed hypernatremia (169 mEq Na/L), hyperchloremia (143 mEq Cl/L), and metabolic acidosis (5 mmol total CO2/L). Radiographic evaluation showed bilateral pneumothoraces and pneumoperitoneum. The patient was intubated and ventilated, hypotension was treated with fluid resuscitation, and metabolic acidosis corrected with sodium bicarbonate. Naloxone and flumazenil were given without effect, and thoracostomy tubes were placed. Rapid deterioration of vital signs and mental status ensued, with cardiorespiratory arrest from which she was resuscitated. A second cardiac arrest resulted in death. Autopsy revealed esophageal and gastric mucosal erosions, perforation at the gastroesophageal junction, and extensive necrosis of adjacent soft tissue. Stomach contents contained sodium hypochlorite, and pleural and peritoneal fluid had the aroma of bleach. Postmortem vitreous humor Na was 187 mEq/L and Cl was 169 mEq/L. Toxicologic analysis revealed meprobamate metabolites in the urine, and lidocaine in the blood. The literature regarding fatal bleach ingestion is reviewed.
 ...
PMID:Fatal ingestion of sodium hypochlorite bleach with associated hypernatremia and hyperchloremic metabolic acidosis. 1019 36

Naloxone is a non-selective, short-acting opioid receptor antagonist that has a long clinical history of successful use and is presently considered a safe drug over a wide dose range (up to 10 mg). In opioid-dependent patients, naloxone is used in the treatment of opioid-overdose-induced respiratory depression, in (ultra)rapid detoxification and in combination with buprenorphine for maintenance therapy (to prevent intravenous abuse). Risks related to naloxone use in opioid-dependent patients are: i) the induction of an acute withdrawal syndrome (the occurrence of vomiting and aspiration is potentially life threatening); ii) the effect of naloxone may wear off prematurely when used for treatment of opioid-induced respiratory depression; and iii) in patients treated for severe pain with an opioid, high-dose naloxone and/or rapidly infused naloxone may cause catecholamine release and consequently pulmonary edema and cardiac arrhythmias. These risks warrant the cautious use of naloxone and adequate monitoring of the cardiorespiratory status of the patient after naloxone administration where indicated.
 ...
PMID:Naloxone treatment in opioid addiction: the risks and benefits. 1736 58

It has been suggested that morphine has dual effects; emetic effects and anti-emetic effects. The chemoreceptor trigger zone, which is outside the BBB, mediates the emetic effect. In contrast, the vomiting center mediates the anti-emetic effect of opioids. Thus, naloxone methiodide, which does not cross the BBB, antagonizes emetic effects of opioids. We studied whether naloxone methiodide alters abnormal motility pattern induced by morphine in gastrointestinal (GI) tract. Strain gauge force transducers were sutured on the serosal surface of upper GI tract to record the circular muscle contractions in eight dogs. The ventricular access system was implanted to inject morphine intracerebroventricularly (icv). Effects of icv-injection of morphine (0.3-3.0 mug/kg, bolus) on GI motility were studied during intravenous infusion of naloxone hydrochloride or naloxone methiodide. Icv-injection of morphine (3.0 mug/kg) induced retching and vomiting in all dogs tested. Phasic contractions of the jejunum were observed after icv-injection of morphine. These contractions in the jejunum migrated orally to the antrum (retrograde peristaltic contractions; RPCs). Both naloxone hydrochloride and naloxone methiodide treatment virtually abolished the emetic effects of morphine. Naloxone hydrochloride completely abolished morphine-induced RPCs in all dogs, whereas naloxone methiodide converted morphine-induced RPCs to anterograde peristaltic contractions (APCs) in 6 of 8 dogs. Our current study suggests that central opioids may induce APCs and prevent emesis in conscious dogs. Naloxone methiodide may be useful to prevent the undesired side effects of morphine.
 ...
PMID:Central effects of morphine on GI motility in conscious dogs. 1766 72


<< Previous 1 2 3 Next >>