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 effect on behavior of eight anticholinergic agents: atropine, scopolamine, trihexyphenidyl, biperiden, homatropine, eucatropine, hexocyclium and propantheline, injected into the cerebral ventricle (ICV) of the cat was investigated and compared. The anticholinergic agents evoked: (1) psychomotor stimulation such as miaowing, loud calling, restlessness, impelling locomotion, jumping, vacant staring, apprehension and loss of interest of the surroundings; (2) aggression, hissing, threat, attack, defense, fighting with paws and flight; (3) autonomic responses including mydriasis, tachypnea, dyspnea, licking, vomiting, salivation, micturition and defection; and (4) motor phenomena comprising scratching, ataxia, rigidity, tremor, weakness with adynamia or myoclonic jerks. Convulsions appeared only after ICV injections of atropine and homatropine. The most characteristic behavioral effect of anticholinergic agents was psychomotor stimulation accompanied by mild aggressive responses. The only exception was propantheline which caused a muscular weakness and adynamia. Atropine and scopolamine alone induced a dose-dependent impelling locomotion as well as fighting behavior. Carbachol and eserine injected intracerebroventricularly reversed the locomotion autonomic and motor phenomena produced by anticholinergic agents administered similarly. It is suggested that anticholinergic agents acting as partial agonists, can produce their behavioral effects through central cholinoceptive sites.
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PMID:Comparative behavioral effects of anticholinergic agents in cats: psychomotor stimulation and aggression. 370 93

Prior to vomiting, two gastrointestinal contractile events occur in succession: a giant contraction that propagates retrograde from mid-small intestine to the antrum (RGC) and a series of phasic contractions that occur at all levels of the gastrointestinal tract. We quantitatively examined the gastrointestinal myoelectric events associated with vomiting and correlated them with the previously defined contractile events. Twelve dogs of either sex were implanted with electrical or contractile recording devices implanted on the stomach and small intestine. After an overnight fast, gut activity was recorded before and after apomorphine administration (2.5-15 micrograms/kg, iv). We found that the RGC was correlated with two successive electrical events: disruption of electrical control activity (ECA) cycling and a potential change occurring at the upstroke of the RGC. However, the initial myoelectric event associated with vomiting was ECA frequency slowing of the antrum and lower half of the small intestine. The post-RGC phasic contractions were associated with ECA-dependent response activity and occurred during the period of ECA frequency slowing. Atropine (100 micrograms/kg iv) blocked the RGC and its associated electrical events but not the slowing of ECA frequency. Supradiaphragmatic vagotomy eliminated all gastrointestinal contractile and myoelectric events but antral ECA frequency slowing. Spontaneous occurrences of the myoelectric correlates of vomiting were not different from those activated by apomorphine. These results suggest that ECA disruption may be important for retrograde propagation of the RGC. The function of ECA frequency slowing, however, remains unknown.
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PMID:Gastrointestinal myoelectric correlates of vomiting in the dog. 378 49

Two cases of severe beta-blocker overdose are presented that were treated successfully with glucagon therapy. The effects of glucagon in reversing the cardiovascular depression of profound beta-blockade, including its mechanism of action, onset and duration of action, dosage and administration, cost and availability, and side effects are reviewed. Medical complications of beta-blocker overdose include hypotension, bradycardia, heart failure, impaired atrioventricular conduction, bronchospasm and, occasionally, seizures. Atropine and isoproterenol have been inconsistent in reversing the bradycardia and hypotension of beta-blocker overdose. Glucagon increases heart rate and myocardial contractility, and improves atrioventricular conduction. These effects are unchanged by the presence of beta-receptor blocking drugs. This suggests that glucagon's mechanism of action may bypass the beta-adrenergic receptor site. Because it may bypass the beta-receptor site, glucagon can be considered as an alternative therapy for profound beta-blocker intoxications. The doses of glucagon required to reverse severe beta-blockade are 50 micrograms/kg iv loading dose, followed by a continuous infusion of 1-15 mg/h, titrated to patient response. Glucagon-treated patients should be monitored for side effects of nausea, vomiting, hypokalemia, and hyperglycemia. The high cost and limited availability of glucagon may be the only factors precluding its future clinical acceptance.
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PMID:Glucagon therapy for beta-blocker overdose. 614 98

The parotid glands and skin of the toad contain toxic substances. Ingestion of toad or toad cake may result in intoxication. Clinically, it may be predominantly manifested by a digitalis-like cardioactive effect. During the last six years, the National Poison Center of Taiwan has collected four cases of toad or toad cake intoxication: two cases were toad intoxication and two cases were toad cake intoxication. All four cases manifested with general weakness; three cases showed bradycardia, vomiting and diarrhea; two cases had numbness of the oral cavity; one case had excessive salivation; and two cases showed a consciousness change. In one case, an EKG showed bradycardia, and a first and second degree A-V block; this patient died of ventricular fibrillation. The prognosis in two cases was good. We lost contact with the last patient. The treatment principles in toad or toad cake intoxication is life support. If ingested, treatment is directed at prevention of absorption, including emesis, gastric lavage, activated charcoal and cathartics. Atropine, a pacemaker and other antiarrhythmic agents may be helpful in treating cardiovascular toxicity.
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PMID:[Toad or toad cake intoxication in Taiwan: report of four cases]. 790 65

1. Erythromycin administration is associated with gastrointestinal problems, disturbed gastrointestinal motility and emesis. This study in the dog investigates the underlying mechanisms. 2. Intestinal myoelectrical activity and the occurrence and latency of emesis were recorded in eight conscious dogs. All drugs were administered intravenously. 3. Erythromycin (7 mg kg-1) increased contractions of the proximal small intestine, and caused emesis in all fasted dogs and in 5 dogs after food. Atropine (50 mg kg-1 min-1) and hexamethonium (10 mg kg-1 h-1) partially inhibited the GI motility effects but did not significantly reduce emesis. 4. Metoclopramide at a high dose (2 mg kg-1 h-1) reduced the incidence of emesis in the presence of increased intestinal motility, but a low dose (150 micrograms kg-1 h-1) was ineffective. 5. A 5-hydroxytryptamine3 (5-HT3) receptor antagonist, MDL 72222 (1 mg kg-1), reduced emesis when given alone and combined with metoclopramide (low dose). The 5-HT4 receptor agonist BRL24924 (Renzapride, 1 mg kg-1) had no effect on emesis either alone in combination with metoclopramide. 6. In conclusion, erythromycin-induced GI motility disturbances and emesis are not causally related. Whereas the increase in intestinal smooth muscle activity is possibly cholinergically mediated, emesis occurs at least in part via a 5-hydroxytryptaminergic mechanism, but does not involve the dopamine system.
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PMID:Effects of cholinoceptor and 5-hydroxytryptamine3 receptor antagonism on erythromycin-induced canine intestinal motility disruption and emesis. 809 27

Although droperidol is often used to prevent emesis, vomiting is still common in children undergoing strabismus surgery. METHODS. One hundred children aged 3 to 12 years admitted for strabismus surgery were enrolled in a randomised, double-blind study to investigate the influence of the timing of the administration of droperidol (75 micrograms/kg i.v.) and the effect of atropine (10 micrograms/kg i.v.) on postoperative vomiting and the occurrence of the oculocardiac reflex (OCR). Each child was prospectively assigned to one of the following groups: Group A: atropine and droperidol before the beginning of surgery (n = 25); Group B: atropine before the beginning, droperidol after completion of surgery (n = 25); Group C: no atropine, droperidol before the beginning of surgery (n = 25); Group D: no atropine, droperidol after completion of surgery (n = 25). After oral premedication with 0.4 mg/kg midazolam, anaesthesia was induced via a face mask by inhalation of halothane, nitrous oxide, and oxygen and 1 mg/kg succinylcholine was given to facilitate tracheal intubation. Gastric contents were aspirated by a gastric tube at the end of the operation. Vomiting and retching were recorded for 24 h; recovery from anaesthesia was assessed by a modified Steward score. RESULTS. The four groups were comparable regarding age, sex, body weight, duration of anaesthesia, and number of repaired eye muscles. Patients receiving droperidol before and after the end of surgery had a similar incidence of vomiting (groups A and C 60% vs. groups B and D 50%). There was no significant difference in the number of patients vomiting between groups A and B (58%) and groups C and D (52%). The incidence of the OCR was lower in the patients premedicated with atropine (18% vs. 60%, P < 0.01). There was no statistical relationship between the occurrence of the OCR and post-operative emesis. Younger children (3 to 6 years) vomited more often than older ones (7 to 12 years). The incidence of the OCR was higher in patients with more than two eye muscles repaired than in others. Recovery scores were slightly lower in patients with droperidol after completion of surgery; postoperative recovery times did not differ significantly between the study groups. CONCLUSIONS. The timing of the administration of droperidol (75 micrograms/kg) had no influence on postoperative vomiting. The application of atropine (10 micrograms/kg) prior to surgery did not influence vomiting after strabismus surgery. Atropine (10 micrograms/kg) reduced the incidence of the OCR significantly. There was no statistical relationship between the occurrence of the OCR and postoperative vomiting.
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PMID:[Emesis and the oculocardiac reflex. Drug prophylaxis with droperidol and atropine in children undergoing strabismus surgery]. 834 44

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

A poisoning from a Veratrum album infusion mistaken for Gentiana lutea is described. Confusion between these two plants can easily occur because they are very similar, although flowers and disposition of leaves allow their botanic determinat: V. album leaves are alternate and flowers are white, while G. lutea leaves are opposite and flowers yellow. The poisoning involves gastrointestinal (pyrosis, vomiting) and cardiocirculatory systems (bradyarrhy-thmias, A-V dissociation, vasodilatation) Atropine is the drug of choice.
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PMID:[A case of Veratrum poisoning]. 904 97

The aim of this study was to investigate the effect of several drug combinations (atropine, xylazine, romifidine, methotrimeprazine, midazolam, or fentanyl) with ketamine for short term anesthesia in cats. Twelve cats were anesthetized 6 times by using a cross-over Latin square protocol: methotrimeprazine was combined with midazolam, ketamine, and fentanyl; midazolam and ketamine; romifidine and ketamine; and xylazine and ketamine. Atropine was combined with romifidine and ketamine, and xylazine and ketamine. Temperature, heart rate, and respiratory rate decreased in all groups. Apnea occurred in 1 cat treated with methotrimeprazine, romifidine, and ketamine, suggesting that ventilatory support may be necessary when this protocol is used. Emesis occurred in some cats treated with alpha 2-adrenoceptor agonists, and this side effect should be considered when these drugs are used.
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PMID:A preliminary trial comparison of several anesthetic techniques in cats. 1085 32

Atropine, an anticholinergic agent commonly used in human and veterinary medicine, is reported to cause toxicity associated with its antimuscarinic action. A juvenile pygmy sperm whale, Kogia breviceps, was treated with atropine in an attempt to relieve symptoms similar to pyloric stenosis, as has been used in humans. Two doses of 0.01 mg/kg were given i.m., 12 hr apart, followed by three doses of 0.005 mg/kg i.m. s.i.d. over the next 3 days. Symptoms associated with atropine toxicity developed gradually and included hyperexcitability, a generalized ascending paralysis of body musculature, shallow, rapid respiration, vomiting, aspiration of seawater, and pulmonary edema. Treatment with physostigmine salicylate (two doses of 2 mg i.m., I hr apart) was effective in counteracting the paralysis, as well as other symptoms, beginning in as little as 17 min after the first dose, and the whale was back to swimming on its own after 8 hr. All overt symptoms of atropine toxicity were gone in about 24 hr, but there were other possible sequella that lasted much longer.
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PMID:Subacute atropine toxicity in a pygmy sperm whale, Kogia breviceps. 1221 96


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