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)

Nicotine poisoning is a rarely reported toxicosis. The clinical signs and symptoms are complex and are mostly of central nervous system derangement. In addition, animals may have hypersalivation, vomiting, diarrhea, tachycardia, tachypnea, hypertension and hyperthermia. Some animals are presented in total collapse with slow and shallow respirations, hypotension, dilated pupils, and a weak, rapid and irregular pulse. Treatment is directed toward removing the unabsorbed poison and diluting, and counteracting or controlling the animal's signs. This report emphasises the comparative ease with which a dog would readily ingest chewing tobacco, which is sweet in taste, and come down with nicotine poisoning, as compared to cigarette tobacco which is nonpalatable and therefore less of a threat. The report further discusses clinical nicotine toxicosis, its incidence, clinical manifestations, diagnosis, prognosis and treatment.
 ...
PMID:Nicotine poisoning in a dog. 226 69

A prospective review of 51 cases of tobacco ingestion and 5 cases of nicotine resin chewing gum exposure was conducted to evaluate the incidence and degree of toxicity caused by these products in children. A dose-response relationship was observed for cigarette exposures. Nine of 10 children ingesting more than one cigarette or three cigarette butts developed signs or symptoms, while 12 of 24 ingesting lesser amounts became symptomatic (P less than 0.01). Severe symptoms (e.g. limb jerking and unresponsiveness) were only seen with the larger amounts. Nicotine resin gum produced toxicity in 4 of 5 children who chewed 1/2 to 4 pieces. Agitation, lethargy, tachycardia, hypotension, abdominal pain, and vomiting were seen within 30 min of exposure to the gum.
 ...
PMID:Cigarette and nicotine chewing gum toxicity in children. 334 35

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.
 ...
PMID:Further studies on nicotine-induced emesis: nicotinic mediation in area postrema. 360 20

1. The cardiovascular and behavioural effects of cholinomimetic drugs injected through a cannula chronically implanted into a lateral cerebral ventricle were examined in unanaesthetized dogs.2. Acetylcholine (ACh) (10-20 mug) produced an increase in arterial pressure and heart rate, the dogs became more alert, moved their heads, licked and swallowed and then became drowsy.3. The responses to ACh were potentiated by intraventricular physostigmine (5 mug), were abolished by intraventricular atropine (100 mug) but were unaffected by intraventricular mecamylamine (250 mug). The responses to ACh were reproducible on any one day if injections were given again after a 30 min interval but tolerance developed when ACh was injected repeatedly over periods of several days.4. Methacholine (40 mug) produced similar behavioural and cardiovascular effects to ACh but of a longer duration. The responses to methacholine were abolished by intraventricular atropine (100 mug).5. Nicotine (20-60 mug) produced a biphasic cardiovascular response of an initial brief pressor response and tachycardia followed by a secondary increase in arterial pressure and heart rate which was greater in magnitude and duration. The secondary cardiovascular effects were associated with restlessness and vomiting.6. The responses to nicotine were abolished by prior injection of mecamylamine (250 mug) but were unaffected by atropine (100 mug). The responses to nicotine were not reproducible if injections were repeated on the same day but could be again produced if a few days were allowed to elapse between injections.7. An increased heart rate occurred during the pressor response to the cholinomimetic drugs but when a comparable pressor response was produced by intravenous infusion of noradrenaline in the same unanaesthetized dogs pronounced reflex bradycardia resulted.8. The results indicate that the activation of both muscarinic and nicotinic cholinergic mechanisms leads to cardiovascular and behavioural effects in the conscious dog although the site of action and peripheral mechanisms have not been determined.
 ...
PMID:Cardiovascular responses to injections of cholinomimetic drugs into the cerebral ventricles of unanaesthetized dogs. 472 36

Nicotine produced a distinct reproducible syndrome in the conscious dog when injected intravenously or intracerebroventricularly. Intravenously administered nicotine (40 micrograms/kg/min for 20 minutes) increased cardiac and respiratory rates and produced analgesia, miosis, hypothermia, behavioral restlessness and emesis. When microinjected into the third cerebral ventricle, nicotine (100-200 micrograms) similarly increased cardiac and respiratory rates and pupillary diameter; and produced behavioral restlessness, emesis, erratic analgesia and maintained wakefulness and a desynchronized EEG. Microinjection of nicotine (5-25 micrograms) into the periaqueductal gray failed to alter any of the parameters studied. Intravenous pretreatment with the opioid antagonist naltrexone (2 mg/kg) influenced the action of intravenous nicotine on certain physiological systems. While naltrexone alone produced a significant degree of tachycardia, miosis, and analgesia, it potentiated the tachypnea and antagonized the miotic response evoked by nicotine. Methionine-enkephalin was detected in perfusates obtained from the lateral cerebral ventricles of conscious dogs. Nicotine produced a non-significant decrease in enkephalin levels. These observations suggest that there are interactions between endogenous opioid and nicotinic processes. However, they are complex and may differ from one functional system to another.
 ...
PMID:Interaction between nicotine and endogenous opioid mechanisms in the unanesthetized dog. 717 83

To evaluate potential adverse effects from inadvertent exposure to a nicotine transdermal system or "patch", three marketed products were administered topically and orally to dogs: Nicoderm (nicotine transdermal system), with a drug reservoir and a rate-controlling membrane; Nicotinell, with a nicotine solution dispersed in a cotton gauze pad between layers of adhesive; and Niconil, with a nicotine gel matrix. Nicotine doses during topical administration ranged from 1 to 2 mg/kg/24 h for all three products, with plasma nicotine concentrations as high as 43 ng/mL. Two of the 12 topical exposures (with Nicotinell and Niconil) were associated with clinical signs (excess salivation or emesis). The oral doses from the products ranged from 2.8 mg/kg (one patch) to 13.4 mg/kg (two patches) over 25-57 h, with mean maximal plasma levels of 73 ng/mL for two patches (mean maximal level 36 ng/mL). These doses are 2-9-fold higher than oral doses reported to produce severe toxicity in children and, at the highest dose, within the known lethal range for dogs. Oral dosing of Nicotinell and Niconil (two patches per dog) produced vomiting in 2 of 12 exposures. No clinical signs were observed with either topical or oral dosing of Nicodem. These data suggest that nicotine toxicity in dogs from nicotine transdermal patches may not be as severe as might be anticipated based on nicotine content alone.
 ...
PMID:Absorption and adverse effects following topical and oral administration of three transdermal nicotine products to dogs. 761 79

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

Accidental ingestion of cigarettes (and butts) is mainly seen in young children. Nicotine in tobacco products is easily absorbed by the oral mucosa and intestines; absorption depends on nicotine content and pH of tobacco. Symptoms are caused by the nicotine component and usually develop rapidly (< 4 hours). The most common symptom is vomiting. Although cigarettes are potentially toxic, their ingestion by children is generally benign. Decontamination of the mouth with water may be useful. Induction of emesis is not advised. Gastric lavage is not needed in asymptomatic patients (with an unreliable history) or after vomiting. Children who ingested cigarettes should receive medical observation for four hours after ingestion. Children with significant symptoms should be admitted and eventually treated by supportive care. In symptomatic children or children with a reliable history of ingestion of large quantities who have not vomited gastric lavage with administration of activated charcoal has to be performed. When after vomiting other symptoms persist activated charcoal can be given via a nasogastric tube.
 ...
PMID:[Accidental ingestion of cigarettes by children]. 1002 53

Nicotine, a rapid-acting poison, is present in environmental tobacco smoke and has been used as a greenhouse insecticide. Due to its toxicity, several health hazard evaluations (HHE) have resulted from potential nicotine exposures to casino workers, airline flight attendants, and greenhouse employees. Exposure to nicotine can occur by inhalation, skin adsorption, and ingestion, resulting in such adverse health effects as nausea, vomiting, headache, dizziness, tachycardia, hypertension, convulsions, and cardiac arrhythmia. The development of an improved sampling and analytical methodology for nicotine was required to accommodate the broad concentration of nicotine levels and varying sampling scenarios presented by the differing HHE requests. A XAD-4 sorbent tube was selected for the collection of airborne nicotine. Analytical methodology for the separation, identification, and quantitation of nicotine by both gas chromatography-flame ionization detection and gas chromatography-nitrogen/ phosphorous detection is described. The limit of detection for nicotine was 0.013 microg/sample. The desorption efficiency for nicotine was determined over the range of study and ranged from 90.9% (0.096 microg) to 93.7% (24.0 microg). Nicotine exhibited storage stability for 30 days at 5 degrees C and for 14 days at ambient temperature. Based on the results of this research study, the new method for nicotine was published in the NIOSH Manual of Analytical Methods (NMAM 2551).
 ...
PMID:Development of a versatile method for the detection of nicotine in air. 1176 27

The lack of a small animal model with an emetic reflex in which the relationship between conditioned food aversion and emesis could be investigated prompted a study of the insectivore, Suncus murinus (the house musk shrew). A novel food (either tuna or chicken cat food) was paired (C+) with a single exposure to either nicotine (4 mg/kg sc), motion (1 Hz, 4 cm, 10 min) or lithium chloride (100 mg/kg ip) or was paired (C-) with either saline or sham exposure to motion. Nicotine and motion both induced emesis (retching/vomiting) but lithium chloride did not. All three treatments produced a conditioned food aversion after a single pairing with consumption of C+ food. When given a choice between the two foods, S. murinus given lithium chloride, motion exposure and nicotine consumed, respectively, only 25%, 23% and 1% of their total intake from the C+ food. This study shows that a conditioned food aversion can be readily induced in S. murinus and that the induction of emesis can be uncoupled from food aversion. S. murinus provides a promising new model in which the relationship between emesis, nausea and conditioned food aversion can be investigated.
 ...
PMID:Conditioned food aversion in Suncus murinus (house musk shrew) - a new model for the study of nausea in a species with an emetic reflex. 1149 64


1 2 Next >>