Acepromazine Reduces Airway Contraction in a Murine Model of Asthma.

Abstract

Acepromazine (ACP) is one of the most used sedatives in veterinary medicine, and its cardiovascular effects are well documented. In contrast, its effects on the respiratory system remain less well understood, particularly in the context of assessment of respiratory mechanics in murine models of asthma, where its use has become more common in recent years. This study aims to investigate the effect of ACP on respiratory mechanics in BALB/c mice, specifically in an ovalbumin (OVA)-induced model of allergic asthma. Mice received ACP (2.5 mg/kg) in combination with standard ketamine (100 mg/kg) and xylazine (10 mg/kg) anaesthesia. Respiratory mechanics were assessed in vivo using forced oscillation technique (FOT) following methacholine (MCh) challenge. Additionally, tracheal rings and lung strips were evaluated in vitro for airway smooth muscle (ASM) responsiveness to MCh. ACP administration significantly reduced Newtonian resistance (Rn) in OVA-sensitised mice following MCh challenge, suggesting an inhibitory effect on ASM contractility. Furthermore, ACP mitigated increases in tissue damping (G) and hysteresivity (η), particularly in the inflamed lungs of OVA-treated mice. In vitro, ACP induced a rightward shift in MCh concentration-response curves in non-inflamed ASM and lung strips. These findings highlight the potential confounding effects of ACP in studies assessing airway hyperresponsiveness and offer insights into how sedative choice can shape the scientific validity of studies involving assessment of respiratory mechanics.