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冰水冷敷不能激活镇静或麻醉犬脊髓反射的弥散性伤害性抑制控制:一项初步研究。

Ice water immersion does not activate diffuse noxious inhibitory controls of spinal reflexes in sedated or anaesthetised dogs (): a pilot study.

作者信息

Hunt J R, Knazovicky D, Harris J, Kelly S, Knowles T G, Murrell J C, Lascelles B D X

机构信息

School of Veterinary Sciences, University of Bristol, Bristol, United Kingdom.

Comparative Pain Research Laboratory, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, United States.

出版信息

Front Pain Res (Lausanne). 2025 Mar 10;6:1505064. doi: 10.3389/fpain.2025.1505064. eCollection 2025.

Abstract

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 ( = 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 ( < 0.001). DNIC was not induced, as the EMG magnitude did not significantly change over time for either the early ( = 0.07) or late responses ( = 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.

摘要

引言

在患有骨关节炎(OA)疼痛的人类受试者中,弥漫性伤害性抑制控制(DNIC)可能受损。犬类自发发生的OA被认为是人类OA的一种有价值的模型;然而,评估犬类DNIC的方法尚未完全开发出来。本研究的目的是开发一种合适的使用冰水浸泡的DNIC方案,类似于人类使用的方案。

目的

本研究的目的是创建一种在镇静或麻醉犬中诱导DNIC的实验方案,确保其在涉及自发犬OA模型的研究中对未来DNIC评估具有表面效度。我们假设在健康犬中诱导DNIC会导致对特定伤害性刺激的肌电图(EMG)反应降低。

方法

在七只健康犬的远端前肢进行20分钟的冰水浸泡预处理之前和期间,记录胫骨前肌对测试电刺激的肌电图(EMG)反应和指间皮肤温度。对每只犬使用三种不同状态重复该方案:用乙酰丙嗪或阿法沙龙镇静或用阿法沙龙麻醉。

结果

在所有三组犬中,冰水浸泡导致指间皮肤温度下降,浸泡后10分钟达到最低点(4.9 - 13.6°C)。与乙酰丙嗪镇静的犬相比,阿法沙龙镇静的犬皮肤温度显著更高(= 0.018),并且比乙酰丙嗪镇静的犬更快恢复到基线。与阿法沙龙处理的犬相比,乙酰丙嗪镇静的犬的EMG反应幅度显著更大(< 0.001)。未诱导出DNIC,因为早期(= 0.07)或晚期反应(= 0.27)的EMG幅度均未随时间显著变化,并且在与EMG幅度相关的时间和麻醉状态之间未观察到显著相互作用。

结论

我们的数据表明冷预处理刺激未能引发DNIC。有可能预处理刺激的强度不足以在犬中诱发DNIC。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc83/11931054/9b422f85e57f/fpain-06-1505064-g001.jpg

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