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 anterior hypothalamic preoptic area (AH/POA) was examined as a possible site of action of clonidine and other alpha noradrenergic receptor agonists which evoke motor and autonomic changes. Chronically indwelling guide cannulae were implanted stereotaxically in the diencephalon of the cat. Following post-operative recovery, a micro-injection into AH/POA was made in a volume of 1.0 microliter of one of the following compounds: 5.0-50.0 micrograms clonidine, 5.0-50.0 micrograms norepinephrine, 5.0-50.0 micrograms phenylephrine and 5.0-50.0 micrograms methoxamine. The smallest dose of 5.0 micrograms clonidine produced a brief period of restlessness, licking, retching and emesis but a much longer-lasting mydriasis. When the dose of clonidine was raised to 20 micrograms, the cat became behaviorally sedated, after a latency of about 15 min, for a period of up to 1.0-2.0 hr. This was accompanied by a prolonged period of mydriasis and preceded by a short interval of restlessness, licking, retching and emesis. After the highest dose of 50.0 micrograms clonidine was micro-injected in AH/POA, a profound impairment of motor activity, adynomia and restlessness developed within 15-20 min, persisted for 30 to 60 min and was accompanied also by mydriasis with maximal pupillary dilation lasting for up to six hr. When 5.0-50.0 micrograms phenylephrine or 5.0-50.0 micrograms norepinephrine were micro-injected at clonidine-reactive sites in AH/POA, only rarely were brief instances of restlessness, licking, retching and emesis observed; however, methoxamine at all doses tested failed to produce any visible signs of autonomic or motor disturbance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dissociation of locomotor impairment from mydriasis evoked by clonidine injected into cat's rostral hypothalamus. 287 57

The localized effect of noradrenergic agonists administered directly in the anterior hypothalamic preoptic area (AH/POA) in inducing emesis in the cat was investigated. Of the noradrenergic agonists tested, which included norepinephrine, clonidine, phenylephrine and methoxamine, only clonidine in doses of 5.0-50.0 micrograms was found to evoke emesis consistently when micro-injected in a volume of 1.0 microliter into AH/POA of the unrestrained cat. The emetic response to clonidine was short-lasting, generally dose-dependent in terms of latency and frequency, and occurred in bouts of one to three episodes. The sequence of the vomiting response, beginning with licking and retching, functionally resembled a normal pattern of an emetic response. The clonidine-induced emesis was not antagonized by the following antagonists micro-injected in AH/POA just prior to clonidine: alpha-adrenergic blocking agents, yohimbine, RX 781094 and phentolamine; the antimuscarinic drug, atropine; the serotonin antagonist, methysergide; the opioid antagonist, naloxone; and the dopamine antagonist, chlorpromazine. Therefore, it would appear that clonidine-induced emesis is not mediated by alpha noradrenergic, serotonergic, dopaminergic, muscarinic and opiate receptor systems within the AH/POA of the cat. Finally, the obtained results show that apart from the area postrema and a circumscribed zone of the brain-stem reticular formation, the hypothalamus is now implicated as a neuroanatomical site in the central nervous system mechanism underlying neurochemically-induced emesis.
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PMID:Rostral hypothalamus: a new neuroanatomical site of neurochemically-induced emesis in the cat. 288 12