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Sida 1 från 26 resultat
Xylazine emesis, yohimbine and motion sickness susceptibility in the cat.
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The possible role of the alpha-2 adrenoceptors in xylazine-induced vomiting and in motion sickness was investigated. Cats were divided into two groups according to motion sickness susceptibility and were observed after s.c. injections of xylazine. The incidence of vomiting increased with the dose,
Xylazine-induced vomiting in dogs: elimination by ablation of the area postrema and blockade by yohimbine.
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The role of adrenergic receptors in the initiation of vomiting and its gastrointestinal motor correlates.
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We investigated the role of adrenergic receptors in the mechanisms of initiation of vomiting and its gastrointestinal (GI) motor correlates. The effects of clonidine, UK-14304, St-91, naphazoline, phenylephrine and isoproterenol were examined for their ability to initiate vomiting and its GI motor
Rostral hypothalamus: a new neuroanatomical site of neurochemically-induced emesis in the cat.
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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
The role of alpha-adrenergic mechanisms within the area postrema in dopamine-induced emesis.
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Intracerebroventricular injection of dopamine (0.5-4.0 mg) produced dose-dependent and short-lasting emesis (1-8 min) in cats, which was abolished after ablation of the area postrema. Relatively selective alpha 2-adrenoceptor antagonists (yohimbine and idazoxan) and a mixed alpha 1- and alpha
Clonidine-induced emesis: a multitransmitter pathway concept.
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The emetic effect of clonidine injected into the cerebral ventricles through chronically implanted cannulae was investigated in unanaesthetized cats. Clonidine (0.1-300 micrograms) induced dose-dependent and shortlasting emesis. The emesis induced by the supramaximal dose of clonidine (100
Noradrenaline-induced emesis. Alpha-2 adrenoceptor mediation in the area postrema.
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The emetic action of noradrenaline was investigated in unanesthetized cats, after it was injected into the cerebral ventricles through chronically implanted cannulae. Intracerebroventricular injection of noradrenaline produced dose-dependent and shortlasting emesis, which was abolished after
The comparative efficacy of yohimbine and atipamezole to treat amitraz intoxication in dogs.
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This study compared the efficacy of yohimbine with atipamezole, a new alpha2 adrenergic antagonist, to treat canine amitraz intoxication. Thirty dogs were divided equally into 3 groups (A, AY, and AA). Group A received 2.5% amitraz iv at 1 mg/kg; Group AY received the same dose of amitraz followed
RU 24969-induced emesis in the cat: 5-HT1 sites other than 5-HT1A, 5-HT1B or 5-HT1C implicated.
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RU 24969 was administered s.c. to cats and found to elicit emesis with a maximally effective dose of 1.0 mg/kg. 5-Methoxytryptamine was found to have lower efficacy and to produce a higher incidence of non-specific effects while trifluoromethylphenylpiperizine (TFMPP) was devoid of emetic effects.
Acute neurotoxicity after yohimbine ingestion by a body builder.
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Yohimbine is an alkaloid obtained from the Corynanthe yohimbe tree and other biological sources. Yohimbine is currently approved in the United States for erectile dysfunction and has undergone resurgence in street use as an aphrodisiac and mild hallucinogen. In recent years yohimbine use has become
PDE4 inhibitors induce emesis in ferrets via a noradrenergic pathway.
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The objective of this work was to assess the role of alpha(2)-adrenoceptors in emesis induced by inhibitors of type 4 phosphodiesterase (PDE4) in ferrets. Pre-treatment with yohimbine, MK-912 or MK-467 (alpha(2)-adrenoceptor antagonists) caused sudden and unexpected vomiting. In contrast, clonidine
Central alpha-adrenoceptor subtypes involved in the emetic pathway in cats.
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The intracerebroventricular (i.c.v.) injection of clonidine, xylazine, adrenaline and methoxamine elicited dose-dependent vomiting in cats in that order of potency. The vomiting induced by clonidine, xylazine and adrenaline was antagonized by i.c.v. yohimbine and phentolamine possessing alpha
Modification of reserpine-induced emetic response in pigeons by alpha 2-adrenoceptors.
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In the present study, an attempt has been made to elucidate the role of alpha 2-adrenoceptors in reserpine-induced emesis in pigeons. Reserpine was found to induce dose-dependent emesis and a 500 micrograms kg-1 dose was found to be the 100% emetic dose. alpha 2-adrenoceptor agonists clonidine and
Antagonism of apomorphine-induced pecking in pigeons.
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Central nervous system stimulants, tranquillizers and other central nervous system depressants, antiemetics, antihistamine drugs and autonomic blocking agents were examined for their ability to prevent the pecking response in pigeons induced by apomorphine (250 mug/kg intramuscularly). Reduction in
Alpha adrenoceptor subtypes involved in the emetic action in dogs.
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In order to assess the involvement of alpha-1 and alpha-2 adrenoceptors in emesis, the emetic effect of eight alpha agonists was studied in dogs. The i.m. administration of each agonist elicited dose-dependent emesis. The order of potency in inducing emesis was: clonidine greater than oxymetazoline
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