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

Objective Overview

• This study evaluated whether administering acepromazine before detomidine improves peripheral tissue oxygen levels in sedated horses.
• The research also assessed the combined effects on sedation depth and various physiological parameters.

Background and Context

• Detomidine is an α₂-agonist sedative commonly used in horses.
• α₂-agonists can impair microcirculation, potentially reducing oxygen delivery to tissues (microcirculation and tissue oxygenation).
• Acepromazine is another sedative that might modify the effects of detomidine, possibly improving tissue oxygen delivery.

Study Design and Methods

• The study was prospective, randomized, and used a crossover design with eight healthy adult horses.
• Each horse received two treatments with a one-week washout between: detomidine alone (D) and acepromazine plus detomidine (DA).
• Dosing: 10 μg/kg detomidine; acepromazine at 20 μg/kg administered IV before detomidine in the DA group.
• Measurements taken at baseline, 5, 15, 30, 60, and 120 minutes post-injection:
• Peripheral tissue oxygen saturation (StO₂)
• Tissue hemoglobin index (THI)
• Heart rate (HR)
• Respiratory rate (fR)
• Mean arterial pressure (MAP)
• Gastrointestinal motility
• Serum lactate concentration
• Central venous oxygen saturation (ScvO₂) and hemoglobin concentration (measured only at baseline)
• Sedation depth, scored clinically
• Statistical analyses involved mixed-effects linear models to evaluate time and treatment effect and Bland-Altman repeated measures correlation for relationships between variables.

Key Findings

• Peripheral tissue oxygen saturation (StO₂) declined significantly over time in both groups, indicating reduced tissue oxygenation during sedation.
• Heart rate (HR), respiratory rate (fR), mean arterial pressure (MAP), and gastrointestinal motility also declined significantly over time, consistent with sedative effects.
• There was no significant difference between the detomidine alone and the acepromazine plus detomidine groups in these declines, indicating acepromazine did not prevent decreases in tissue oxygenation or cardiovascular/respiratory parameters.
• Serum lactate and StO₂ showed a negative correlation (r = -0.37), meaning higher lactate levels were associated with lower tissue oxygenation, a marker of impaired oxygen delivery or utilization.
• No correlation was found between StO₂ and ScvO₂, suggesting peripheral tissue saturation may not directly reflect central venous oxygen levels during sedation.
• Sedation scores increased over time for both groups, with higher overall sedation intensity in the acepromazine plus detomidine group, showing acepromazine enhances sedation depth.

Interpretation and Implications

• Although acepromazine increased the sedative effect of detomidine, it did not prevent the decline in peripheral tissue oxygen saturation caused by detomidine sedation.
• Declining tissue oxygenation signals that detomidine impairs peripheral microcirculation oxygen delivery despite combined sedation.
• The negative correlation between StO₂ and serum lactate supports that tissue hypoxia is occurring during sedation with α₂-agonists.
• The unchanged cardiovascular and respiratory parameters between groups imply acepromazine does not mitigate detomidine’s adverse effects on these measures under conditions studied.
• This suggests careful monitoring of tissue oxygenation is warranted in horses sedated with detomidine, whether or not acepromazine is used.

Limitations and Future Directions

• Small sample size of eight horses; larger studies needed to confirm findings.
• Study involved healthy adult horses; results may differ in diseased or geriatric populations.
• Only a single dose of acepromazine was tested; different doses or timing might influence outcomes.
• Future studies could explore alternative methods to improve tissue oxygenation during sedation and evaluate clinical relevance during surgery or transport.