Evaluation of the impact of acepromazine on tissue oxygenation in horses sedated with detomidine.

Sedation with α₂-agonists can impair microcirculation and oxygen delivery. This prospective randomized crossover study investigated whether administering acepromazine maleate before detomidine hydrochloride maintains higher peripheral tissue oxygen saturation (StO₂) in sedated horses. Eight healthy adult horses randomly received intravenous detomidine (10 μg/kg) either alone (D) or in combination with acepromazine (20 μg/kg; DA), with a one-week washout. Hemoglobin concentration and central venous oxygen saturation (ScvO₂) were measured at baseline. Tissue oxygen saturation, tissue hemoglobin index (THI), sedation depth, heart rate (HR), respiratory rate (fR), mean arterial pressure (MAP), gastrointestinal motility, and serum lactate concentrations were recorded at baseline, 5, 15, 30, 60, and 120 min after injection. Mixed-effects linear models were used to assess time and treatment effects, and correlations were analyzed using the Bland-Altman Repeated Measures correlation. Across both treatment groups, StO₂ (p < 0.011), HR (p ≤ 0.007), fR (p < 0.0001), MAP (p ≤ 0.024), and gastrointestinal motility (p < 0.0001) declined significantly over time with no significant difference between groups. A negative correlation between StO₂ and serum lactate was found (r = -0.37, p = 0.0004); however, no correlation with ScvO₂ was observed. Sedation scores increased from 5 to 60 min (p < 0.001), ranging between 5 and 8 regardless of group allocation and were overall higher in the DA group (p = 0.02). These findings suggest that acepromazine enhances the sedative effect of detomidine but may not fully counteract its adverse impact on peripheral tissue oxygenation.