一项初步研究表明,冰水浸泡不会激活镇静或麻醉犬(Canis familiaris)脊髓反射的弥漫性有害抑制控制。

IF 2.5 Q2 CLINICAL NEUROLOGY
Frontiers in pain research (Lausanne, Switzerland) Pub Date : 2025-03-10 eCollection Date: 2025-01-01 DOI:10.3389/fpain.2025.1505064
J R Hunt, D Knazovicky, J Harris, S Kelly, T G Knowles, J C Murrell, B D X Lascelles
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引用次数: 0

摘要

导言:人类骨关节炎(OA)疼痛患者的弥漫性毒性抑制控制(DNIC)可能会受损。狗自发性 OA 被认为是人类 OA 的宝贵模型;然而,评估狗 DNIC 的方法尚未完全开发出来。本研究的目的是利用冰水浸泡法开发一种合适的 DNIC 方案,类似于人类使用的方案:本研究的目的是制定一个实验方案,用于诱导镇静或麻醉犬的 DNIC,以确保其在未来涉及自发性犬 OA 模型的研究中对 DNIC 的评估具有表面有效性。我们假设,诱导健康犬的 DNIC 会导致其对特定痛觉刺激的肌电图(EMG)反应减弱:方法:在对远端前肢进行持续 20 分钟的条件冰水浸泡之前和期间,记录七只健康犬的颅胫肌对测试电刺激和趾间皮肤温度的肌电图(EMG)反应。每只狗在三种不同的状态下重复该实验:使用阿司丙嗪或阿法沙酮镇静,或使用阿法沙酮麻醉:结果:冰水浸泡导致所有三组狗的趾间皮肤温度下降,最低温度(4.9-13.6°C)出现在浸泡后 10 分钟。阿法沙酮镇静剂犬的皮肤温度明显高于阿司咪唑镇静剂犬(p = 0.018),而且阿法沙酮镇静剂犬比阿司咪唑镇静剂犬更快恢复到基线温度。与阿法沙酮治疗犬相比,乙酰丙嗪镇静犬的肌电图反应幅度(p p = 0.07)或晚期反应(p = 0.27)明显更大,而且在时间和麻醉状态与肌电图幅度之间没有观察到明显的交互作用:我们的数据表明,冷调节刺激未能诱发 DNIC。结论:我们的数据表明,冷调节刺激未能引起 DNIC,可能是调节刺激的幅度不足以引起狗的 DNIC。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Ice water immersion does not activate diffuse noxious inhibitory controls of spinal reflexes in sedated or anaesthetised dogs (Canis familiaris): a pilot study.

Introduction: Diffuse noxious inhibitory controls (DNIC) may be impaired in human subjects with osteoarthritis (OA) pain. Spontaneously occurring OA in dogs is considered a valuable model of human OA; however, methodology for assessing DNIC in dogs has not been fully developed. The aim of this study was to develop a suitable DNIC protocol using ice water immersion, similar to protocols used in humans.

Objective: This study objective was to create an experimental protocol for inducing DNIC in sedated or anesthetized dogs, ensuring it has face validity for future assessments of DNIC in studies involving the spontaneous canine OA model. We hypothesized that inducing DNIC in healthy dogs would result in a reduced electromyographic (EMG) response to a specific nociceptive stimulus.

Methods: Electromyographic (EMG) responses of the cranial tibial muscle to test electrical stimuli and interdigital skin temperature were recorded in seven healthy dogs before and during a 20-min duration conditioning ice water immersion of the distal forelimb. The protocol was repeated for each dog using three different states: sedation with acepromazine or alfaxalone or anaesthesia with alfaxalone.

Results: Ice water immersion caused a decrease of interdigital skin temperature in dogs in all three groups with the nadir (4.9-13.6°C) at 10 min following immersion. Skin temperatures remained significantly higher (p = 0.018) in alfaxalone sedated compared to acepromazine sedated dogs and returned to baseline more quickly than in acepromazine sedated dogs. Magnitudes of EMG responses were significantly larger in acepromazine sedated dogs compared to alfaxalone treated dogs (p < 0.001). DNIC was not induced, as the EMG magnitude did not significantly change over time for either the early (p = 0.07) or late responses (p = 0.27), and no significant interactions were observed between time and anaesthetic state in relation to EMG magnitude.

Conclusion: Our data suggest that a cold conditioning stimulus failed to elicit DNIC. It is possible that the magnitude of the conditioning stimulus was not sufficient to recruit DNIC in dogs.

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