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Papers and Articles |
1 Departamento de Cirurgia e Anestesiologia Veterinária, Faculdade de Medicina Veterinária e Zootecnia, Universidade Estadual Paulista, Botucatu, São Paulo, CEP 18618-000, Brazil
Correspondence: Correspondence to Dr Teixeira Neto
To test the hypothesis that acepromazine could potentiate the sedative
actions and attenuate the pressor response induced by dexmedetomidine, the
effects of acepromazine or atropine were compared in six healthy adult dogs
treated with this 
2-agonist. In a randomised block design,
the dogs received intravenous doses of either physiological saline,
0·05 mg/kg acepromazine or 0·04 mg/kg atropine, 15 minutes
before an intravenous dose of 5 µg/kg dexmedetomidine. The dogs' heart rate
was reduced by 50 to 63 per cent from baseline and their mean arterial blood
pressure was increased transiently from baseline for 20 minutes after the
dexmedetomidine. Atropine prevented the 2-agonist-induced
bradycardia and increased the severity and duration of the hypertension, but
acepromazine did not substantially modify the cardiovascular effects of the
2-agonist, except for a slight reduction in the magnitude
and duration of its pressor effects. The dexmedetomidine induced moderate to
intense sedation in all the treatments, but the dogs' sedation scores did not
differ among treatments. The combination of acepromazine with dexmedetomidine
had no obvious advantages in comparison with dexmedetomidine alone, but the
administration of atropine before dexmedetomidine is contraindicated because
of a severe hypertensive response.
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