Cardiorespiratory effects of acepromazine maleate and buprenorphine hydrochloride in clinically normal dogs

Cardiorespiratory effects of the combination of acepromazine maleate (ACP) and buprenorphine hydrochloride (BPN) were studied in 11 healthy, conscious dogs. Values for systemic and pulmonary artery blood pressure, cardiac output, arterial and venous pH and blood gas tensions, and invasive and noninvasive estimates of ventricular systolic function, preload, and afterload were obtained before sedation and after administration of each drug. Acepromazine maleate (0.1 mg/kg, IV) depressed cardiac function, compared with baseline values for unsedated dogs. Cardiac output decreased from a mean (+/- SD) value of 4.2 (+/- 1.5) L/min to 3.1 (+/- 0.8) L/min (P < 0.001), a change not attributed to heart rate. Pulmonary capillary wedge pressure decreased from 8.3 (+/- 4.2) mm of Hg to 6.5 (+/- 4.3) mm of Hg (P < 0.01), but mean right atrial pressure did not change. Left ventricular measurement of the maximal positive rate of pressure change (dP/dtmax) decreased from 2,668 (+/- 356)/mm of Hg/s to 2,145 (+/- 463) mm of Hg/s (P < 0.001), and ventricular stroke volume decreased from 43.2 (+/- 15.2) ml/beat to 32.3 (/- 8.6) ml/beat. Noninvasive indices of left ventricular function, ventricular shortening fraction, peak aortic velocity, and aortic average acceleration were decreased after ACP administration, but were not statistically different from baseline values. Mean systemic arterial blood pressure decreased from 121 +/- 12 mm of Hg to 96 +/- 13 mm of Hg 15 minutes after ACP administration (P < 0.001). Total systemic vascular resistance was not significantly different from the baseline value. Sequential administration of cumulative doses of BPN (0.005, 0.01, and 0.1 mg/kg of body weight, IV), initiated 15 minutes after administration of ACP, did not cause statistically significant depression of hemodynamic variables, except for heart rate, which decreased after BPN, and left ventricular dP/dtmax, which decreased slightly at the highest dose of BPN. Small, clinically insignificant changes in blood pH, venous bicarbonate concentration, and PaCO2 were observed after administration of ACP and BPN. Respiratory rate decreased from 60 +/- 48 breaths/min to 24 +/- 12 breaths/min, and sedation level was significantly (P < 0.05) increased from baseline values by administration of ACP. Sedation level was further increased by administration of BPN at the lowest dose (P < 0.05). The combination of ACP and BPN resulted in good to excellent sedation, but depressed ventricular function; however, most of the hemodynamic effects could be attributed to administration of ACP and withdrawal of sympathetic activity.