LAUSR

OBJECTIVE To evaluate the effects of progressively increasing doses of acepromazine on cardiopulmonary variables and sedation in conscious dogs. STUDY DESIGN Prospective, experimental study. ANIMALS A group of six healthy, adult, mixed-breed dogs weighing 16.5 ± 5.0 kg (mean ± standard deviation). METHODS Dogs were instrumented with thermodilution and arterial catheters for evaluation of hemodynamics and arterial blood gases. On a single occasion, acepromazine was administered intravenously to each dog at 10, 15, 25 and 50 μg kg-1 at 20 minute intervals, resulting in cumulative acepromazine doses of 10 μg kg-1 (ACP10), 25 μg kg-1 (ACP25), 50 μg kg-1 (ACP50) and 100 μg kg-1 (ACP100). Hemodynamic data and sedation scores were recorded before (baseline) and 20 minutes after each acepromazine dose. RESULTS Compared with baseline, all acepromazine doses significantly decreased stroke index (SI), mean arterial pressure (MAP) and arterial oxygen content (CaO2) with maximum decreases of 16%, 17% and 21%, respectively. Cardiac index (CI) decreased by up to 19% but not significantly. Decreases of 26-38% were recorded for oxygen delivery index (DO2I), with significant differences for ACP50 and ACP100. Systemic vascular resistance index (SVRI) and heart rate did not change significantly. No significant difference was found among acepromazine doses for hemodynamic data. After ACP10, mild sedation was observed in five/six dogs and moderate sedation in one/six dogs, whereas after ACP25, ACP50 and ACP100, moderate sedation was observed in five/six or six/six dogs. CONCLUSIONS AND CLINICAL RELEVANCE In conscious dogs, acepromazine decreased MAP, SI, CaO2 and DO2I, but no significant dose effect was detected. SVRI was not significantly changed, suggesting that the reduction in MAP resulted from decreased CI. The ACP25, ACP50 and ACP100 doses resulted in moderate sedation in most dogs; ACP10 resulted in only mild sedation.