ROLE OF CATECHOLAMINES IN THE CENTRAL MECHANISM OF EMETIC RESPONSE INDUCED BY PERUVOSIDE AND OUABAIN IN CATS

Open Access
Publisher Website
Google Scholar
Abstract
Peruvoside, (a glycoside obtained from the plant, Thevetia neriifolia Juss) and ouabain produce emesis in cats. Vomiting is not produced by these drugs in animals pretreated with catecholamine depleting drugs like reserpine, tetrabenazine or syrosingopine. Chloropromazine hydrochloride, mepyramine maleate, or BOL‐148 administered intravenously or intracerebroventricularly do not afford protection. Phenoxybenzamine produces partial protection against peruvoside‐induced emesis. Haloperidol (1 mg/kg i.v.) prevents vomiting induced by peruvoside or ouabain. Intracerebroventricularly administered haloperidol is ineffective. Cats pretreated with SKF‐525‐A, are not protected by haloperidol. Animals pretreated with phenobarbitone in a dose of 25 mg/kg for a week were protected by haloperidol, 250 μg/kg i.e. one quarter of the effective antiemetic dose in normal cats. It is postulated that catecholamines are involved in the mechanism of vomiting induced by cardiac gycosides. Further, a metabolite of haloperidol seems to be responsible for its effective antiemetic action.