Effects of Dexamethasone, Metoclopramide or Acepromazine on Emesis in Cats Sedated with Xylazine Hydrochloride

This study was designed to determine antiemetic efficacy of prophylactic administration of dexamethasone, metoclopramide or acepromazine and their influence on sedation in cats sedated with xylazine hydrochloride. Ten healthy adult cats (5 males and 5 females) were used. The prophylactic antiemetic effects of dexamethasone (4 mg/kg of body weight, IM), metoclopramide (0.4 mg/kg of body weight, IM), acepromazine (0.1 mg/kg of body weight, IM) or saline (0.9% NaCI) solution (0.1 ml/kg, IM) administered 1 hour before administration of xylazine hydrochloride (2 mg/kg, IM) was evaluated. Initially, the cats were given saline treatment (day 0); sequentially they were given dexamethasone, metoclopramide or acepromazine at 1 week intervals. After a xylazine injection, all cats were observed for 90 minutes for the assesment of frequency of emesis, and the time until the onset of the first emetic episode, and the determination of xylazine-induced sedation time. Prior treatment with 4 mg/kg of dexamethasone significantly reduced the frequency of emetic episodes but no alteration was observed in the time until the onset of the first emetic episode after the xylazine injection. Metoclopramide and acepromazine did not alter the frequency of emetic episodes but metoclopramide significantly prolonged the onset of the first emetic episode. Dexamethasone (4 mg/kg, IM) significantly decreased the frequency of emetic episodes without affecting the time until the onset of the first emetic episode, xylazine-induced sedation in cats.

Surgical and pharmacological dissociation of cardiovascular and emetic responses to intragastric CuSO4

Under control (intact and laparotomized) conditions, arterial pressure of urethan-anesthetized ferrets rose significantly in response to intragastric copper sulfate (CuSO4; 10 ml of 5 mg/ml). CuSO4 was emetic 75-90% of the time, and a cardiovascular response always immediately preceded and accompanied emetic responses. The cardiovascular response was significantly reduced or abolished by hexamethonium (0.35 mg/kg) pretreatment combined with atropine methyl bromide (1 mg/kg). Addition of the alpha 2-receptor antagonist 2,3-dichloro-alpha-methylbenzylamine HCl (DCMB, 10 mg/kg) and the beta-receptor antagonist propranolol (3 mg/kg) to the hexamethonium and atropine combination prevented its reduction of the cardiovascular response. Given individually, these agents did not alter cardiovascular response, nor did yohimbine (0.30 mg/kg), RS(+/-)-zacopride (0.30 mg/kg), or granisetron (0.50 mg/kg). Only RS(+/-)-zacopride significantly reduced incidence of emesis. Atropine methyl bromide alone, with hexamethonium, or with hexamethonium, propranolol, and DCMB significantly delayed the first emetic episode. Conversely, bilateral abdominal vagotomy significantly reduced the number of vomiting animals without affecting cardiovascular response. These results suggest that the neural pathways mediating the two events are not identical. In another series of experiments, a significantly greater proportion of animals vomited in response to intragastric CuSO4 than to intraduodenal CuSO4, suggesting that the primary site of CuSO4 action in the ferret is the stomach.