No abstract

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 alpha2-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 microg/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 alpha2-agonist-induced bradycardia and increased the severity and duration of the hypertension, but acepromazine did not substantially modify the cardiovascular effects of the alpha2-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.

No abstract

Remifentanil decreased ISO(MAC) in a dose-related fashion; the reduction in ISO(MAC) was stable over the course of a prolonged CRI (6 hours). A dose of 0.30 microg of remifentanil/kg/min resulted in nearly maximal isoflurane-sparing effect in dogs; a ceiling effect was observed at higher infusion rates.

Anesthesia maintained with remifentanil-isoflurane may decrease tissue perfusion as a result of a decrease in Cl. However, hypotension may not develop because of systemic vasoconstriction. An increase in plasma vasopressin concentration was associated with the vasoconstriction observed in dogs anesthetized with remifentanil-isoflurane.