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)

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

The gastrointestinal motor and myoelectric responses associated with vomiting induced by apomorphine (APO) and activated by cholecystokinin octapeptide (CCK-8) were compared as well as the mechanisms of initiation of these responses. Twelve dogs were surgically implanted with strain-gauge force transducers or bipolar electrodes for chronic recording of contractile or electrical activity. The responses to CCK-8 were determined in the fasted state and compared with the gastrointestinal motor and myoelectric correlates of vomiting activated by APO. After recording control responses, the effects of the following agents on these responses were determined: atropine, domperidone, and proglumide. In addition, the effects of supradiaphragmatic vagotomy or splanchnicectomy were determined. We found that CCK-8 activated contractile and myoelectric responses in the absence of vomiting, which were similar in most respects to those found in association with vomiting. These responses included 1) the retrograde giant contraction (RGC) and 2) the post-RGC phasic contractions. These RGCs were similar with respect to their activation in an all-or-none fashion, magnitude, duration, and position in the small intestine. The myoelectric correlates of these motor responses were similar qualitatively and quantitatively. The responses activated by APO and CCK-8 differed with respect to their coordination at different levels of the gastrointestinal tract. Whether activated by CCK-8 or APO, atropine blocked the RGC but not the post-RGC contractions. Domperidone blocked all responses to APO but not to CCK-8, and splanchnicectomy did not affect responses to either agent. Vagotomy blocked all gastrointestinal responses to APO but not to CCK-8. These results indicated that CCK-8 activates the gastrointestinal motor and myoelectric correlates of vomiting by a peripheral mechanism that does not include dopamine receptors.
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PMID:Comparison of gastrointestinal responses to CCK-8 and associated with vomiting. 334 77

This review examines the various clinical options used to elicit gastric emptying, viz. drug-induced emesis, mechanical pharyngeal stimulation, gastric lavage, and catharsis. Apomorphine and syrup of ipecac are the 2 drugs most frequently used for induction of emesis. Both agents act centrally and, in addition, syrup of ipecac has a peripheral action. Toxins ingested or foods previously eaten may inhibit or enhance emetic action by interfering with mediating and conducting mechanisms. Studies indicate that both syrup of ipecac and apomorphine are similarly effective in inducing emesis; however, apomorphine has a shorter reaction time compared with syrup of ipecac. There are more risks involved with the use of apomorphine, since it causes central nervous system and respiratory depression. Syrup of ipecac has been shown to be relatively safe when used in its recommended dosage for emesis. However, several toxicities have been reported with the use of the fluid extract of ipecac. Emesis is contraindicated in patients who are obtunded or comatose, and in patients who have ingested stimulants, some hydrocarbons, or corrosives. Mechanical pharyngeal stimulation is a simple method of inducing emesis; however, it is often unsuccessful and rarely recovers a significant portion of the gastric contents. Gastric lavage is a procedure which has been relied upon for over a century. Its effectiveness is dependent on the nature, form, and dosage of the poison, latency between time of ingestion and lavage, and technique. In clinical experiments studying gastric lavage, it has been noted that the procedure is most beneficial 1 to 2 hours postingestion for the majority of poison ingestions. Lavage also provides an excellent route for activated charcoal and selected antidotes. Gastric lavage may pose several risks to the patient, including obstruction and contamination of the airways and oesophageal damage. Contraindications for gastric lavage are similar to those for emesis except that it may be safer to use in obtunded, comatose, or uncooperative patients. Cathartics used during initial poisoning therapy are usually the saline cathartics. They elicit an osmotic reaction in the small intestine which results in increased intraluminal fluid bulk, hyperperistalsis, and subsequent propulsion of contents. Cathartics have also been shown to stimulate the secretion of cholecystokinin, which is thought to have similar effects on the intestine. Cathartics have not been shown to significantly enhance drug elimination from the gastrointestinal tract.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Gastric emptying. Risk versus benefit in the treatment of acute poisoning. 378 40

The purpose of the present study was to evaluate the effect of ovine corticotropin-releasing factor (CRF) on the gastric emptying of a saline meal in conscious dogs. Intravenous infusion of CRF (220-880 pmol . kg-1 . h-1), induced a significant linear dose dependent inhibition of gastric emptying (16-71%). CRF action was not modified by naloxone and not associated with vomiting or other side effects. Intravenous infusion of sulfated cholecystokinin octapeptide (CCK-8, 50-200 pmol . kg-1 . h-1) inhibited gastric emptying by 29-52%. The relative potency of CRF with respect to CCK-8 is 4 times less. These studies demonstrated that CRF given intravenously in picomolar amount inhibits gastric emptying of a liquid meal in dogs through a mechanism unrelated to opiates. The role of endogenous CRF in stress-induced inhibition of gastric emptying needs to be investigated.
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PMID:Corticotropin-releasing factor inhibits gastric emptying in dogs. 387 18

Short-latency emetic responses were induced in dogs by injecting angiotensin II (AII), arginine vasopressin (AVP), and neurotensin (NTN) into cerebroventricular (ICV) and cisternal (ICT) sites also responsive to the emetic effects of apomorphine (APO). Angiotensin III, bradykinin, bombesin, oxytocin, adrenocorticotropic hormone, substance P, gastrin-related peptide and cholecystokinin were ineffective. The results suggest a possible dopaminergic mediation of peptide-induced emesis by receptors in the area postrema (AP).
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PMID:Emetic effects of centrally administered angiotensin II, arginine vasopressin and neurotensin in the dog. 404 79

1. In the intact conscious dog, caerulein causes emesis and evacuation of the bowel. The mean effective dose by the intravenous route is 0.4-0.5 mug/kg, and by the subcutaneous route 3-4 mug/kg.2. The gall bladder in situ or as an isolated preparation is highly sensitive to caerulein. A few ng/kg injected intravenously are sufficient to stimulate the gall bladder in situ and less than 1 ng/kg per min is effective when infused intravenously. The isolated gall bladder is contracted by caerulein in concentrations as low as 0.03-2 ng/ml. Krebs solution. There is no tachyphylaxis but, generally, a good dose-response relationship. Hence the gall bladder, especially that of the guinea-pig, appears to be very suitable for the bioassay of caerulein and related peptides.3. In situ, the musculature of the gastrointestinal tract is also highly sensitive to caerulein. Doses as low as 1-5 ng/kg, administered intravenously, have a spasmogenic action on jejunal loops of the dog, and slightly larger doses contract the small intestine of the cat. The stomach and the large intestine seem to be somewhat less sensitive to the polypeptide. Caerulein has a considerable spasmogenic action on the rat pylorus but relaxes the sphincter of Oddi of the guinea-pig.4. Isolated preparations of the gastrointestinal tract are relatively insensitive to caerulein and tachyphylaxis occurs readily.5. Blockade with atropine produces different effects in different intestinal segments and in different animal species. The spasmogenic action of caerulein on the gall bladder is atropine-resistant.6. The effects of caerulein are similar to those of cholecystokinin-pancreozymin in the organs tested in situ or as isolated preparations. Caerulein, however, is always more potent than cholecystokinin-pancreozymin, even on a molar basis. Compared with caerulein, human gastrin I has negligible activity.7. The possible use of caerulein in cholecystography is discussed.
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PMID:The actions of caerulein on the smooth muscle of the gastrointestinal tract and the gall bladder. 568 88

The responses of 122 neurons in the area postrema of anesthetized dogs to 17 common transmitters and peptides were determined. Recordings were made from one barrel of a seven-barrel ionophoretic electrode. All neurons were silent at rest, but most could be detected and excited by the application of glutamate. The glutamate response was a brief, high-frequency response of less than 1-sec duration. Excitatory responses were also found to histamine, norepinephrine, serotonin, dopamine, apomorphine, angiotensin II, neurotensin, leucine enkephalin, vasoactive intestinal polypeptide, thyrotropin releasing hormone, gastrin, vasopressin, and substance P. While most neurons tested were excited by dopamine and apomorphine, approximately half of those studied were also excited by each of the other substances. Inhibitory responses were found to norepinephrine (6 of 15 cells) and histamine (3 of 45 cells). No responses were found to acetylcholine, somatostatin, or cholecystokinin. The responses to all 13 excitatory substances other than glutamate were similar. Typically these responses had a latency of 2-20 sec and lasted for 30 sec to 5 min on their first application. The frequency of discharge was usually low (approximately 0.5 Hz). Multiple applications of these agents often induced a maintained spontaneous discharge of low frequency. Each application also induced a transient incremental discharge at a frequency that rarely exceeded 2 Hz. The area postrema has been proposed to be the "chemoreceptor trigger zone" for emesis (Borison and Wang, 1953). All of the agents which excite area postrema neurons, with the exception of serotonin and norepinephrine, are emetic, while none of the three agents without excitatory effects is known to be emetic. Thus these results provide strong support for the central role of the area postrema in emesis. The similarity of response to so many substances on small neurons suggests a common ionic and/or metabolic mechanism underlying the response. The prolonged nature of the response to brief administration of these agents would seem to be appropriate for neurons which subserve a sensation and behavior such as nausea and vomiting.
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PMID:Responses of neurons of canine area postrema to neurotransmitters and peptides. 614 78

Although the incidence of obesity in the domesticated dog is high, few studies have investigated the regulation of food intake in this species. In the present study we investigated the response of the dog to a number of putative satiety agents including cholecystokinin (CCK), bombesin, calcitonin and naloxone. CCK significantly suppressed food intake during a scheduled fifteen minute meal in intact dogs and in dogs receiving total subdiaphragmatic vagotomies. Emesis occurred following injection of higher doses of CCK in most dogs. Bombesin and calcitonin reduced intake in both normal and vagotomized dogs, although higher doses of calcitonin were needed to significantly suppress feeding in vagotomized dogs compared with intact animals. Naloxone reduced feeding by as much as 60% in intact and vagotomized animals. Glucagon suppressed feeding in intact dogs, but not in vagotomized animals. Somatostatin and pancreatic polypeptide did not alter food intake. Thus the domesticated dog responds somewhat differently to some neuropeptides compared with the laboratory rat stressing the importance of examining the regulation of food intake across species.
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PMID:Peptidergic regulation of feeding in the dog (Canis familiaris). 614 23

Cholecystokinin octapeptide (CCK-8) appears to modulate appetitive behavior, and in rodents, anxiety-related behavior. The authors studied CCK-8 in patients with bulimia nervosa. CSF concentrations of CCK-8 were measured in 11 drug-free female patients with DSM-III-R-defined bulimia nervosa and in 16 normal subjects. The bulimic patients had significantly lower levels of CCK-8 than the comparison subjects. CCK-8 concentrations were inversely correlated with scores on the anger-hostility, anxiety, and interpersonal sensitivity subscales of the SCL-90-R. They were not significantly correlated with age, percentage of standardized average body weight, or mean weekly frequency of binge eating or vomiting. The results indicate that central CCK-8 abnormalities may play a role in the pathophysiology of bulimia nervosa.
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PMID:CSF cholecystokinin octapeptide in patients with bulimia nervosa and in normal comparison subjects. 801 Mar 76

There is evidence to suggest that the arginine vasopressin release observed in association with emesis after i.v. injection of cholecystokinin (CCK) and N-methyl-D-aspartate (NMDA) is mediated by stimulation of emetic centers in the brainstem. That the GnRH-releasing action of NMDA is also sometimes accompanied by emesis led to the suggestion that stimulation of this parvocellular system by the glutamate agonist may also be mediated in part via activation of brainstem pathways. If this is the case, then other nauseogenic agents, such as CCK, should similarly elicit GnRH release. The foregoing prediction was tested in the castrated juvenile male monkey, an experimental model characterized by the absence of spontaneous GnRH release. GnRH discharges were monitored indirectly by measuring changes in circulating LH concentrations after the responsivity of the gonadotroph had been heightened by a chronic intermittent i.v. infusion of the decapeptide. An i.v. bolus of CCK at 10 and 30 micrograms/kg BW led to a distinct discharge of GnRH accompanied by emesis or other behaviors suggestive of nausea. Lower doses of CCK (1 and 3 micrograms/kg BW) failed to significantly perturb GnRH release or cause emesis, although NMDA (5 mg/kg BW; racemic form) injected i.v. 3 h after the CCK challenge led to a robust rise in GnRH. In a parallel study, three repetitive i.v. CCK injections at 2h intervals maintained intermittent GnRH release. Pretreatment with a long-acting GnRH receptor antagonist ([AcD2Nal1,4ClPhe2,DTrp3,DArg6,DAla10]GnRH -HOAc) abolished the LH response to CCK, confirming that the action of this peptide was mediated by GnRH release. Although a direct hypothalamic site of action for these agents remains the most likely possibility, since both NMDA and CCK receptors are present in the infundibular region, the present data are consistent with the notion that CCK and, by inference, NMDA may activate GnRH release in part via the stimulation of brainstem emetic centers. Plasma GH, PRL, and cortisol concentrations were also monitored during the course of some of these experiments, and the release of these hormones was observed after the administration of either the 10 or 30 micrograms/kg BW dose of CCK.
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PMID:Cholecystokinin stimulates gonadotropin-releasing hormone release in the monkey (Macaca mulatta). 846 72


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