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使用肠电图评估右美托咪定对马肌电活动的影响。

Evaluation of the Effects of Detomidine on Equine Myoelectrical Activity Using Electrointestinography.

作者信息

Munsterman Amelia S, Dias Moreira Ana S, Kottwitz Jack

机构信息

Department of Large Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing, Michigan, USA.

Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan, USA.

出版信息

J Vet Emerg Crit Care (San Antonio). 2025 Mar-Apr;35(2):120-130. doi: 10.1111/vec.13464. Epub 2025 Apr 20.


DOI:10.1111/vec.13464
PMID:40254911
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12065429/
Abstract

OBJECTIVE: To evaluate the effects of detomidine on equine intestinal slow-wave activity and frequency distribution measured by electrointestinography (EIG). DESIGN: Prospective, experimental study. SETTING: University teaching hospital. ANIMALS: A convenience sample of twelve 7- to 21-year-old clinically normal horses. INTERVENTIONS: Horses were randomly assigned to saline control (four horses) or detomidine treatment (eight). After obtaining a 30-min baseline EIG, a saline or detomidine bolus was administered, followed by a constant rate infusion, and another EIG was recorded. Ultrasonographic examinations monitored cecal and left ventral colon contractions. Spectral analysis was performed to evaluate changes in dominant frequency, dominant power, total power, percent frequency distribution, and changes in slow-wave rhythmic activity. MEASUREMENTS AND MAIN RESULTS: Median (interquartile range [IQR]) dominant frequency in cycles per minute (cpm) was similar for the cecum (2.4 cpm; IQR: 0.51 cpm) and left ventral colon (2.13 cpm; IQR: 0.16 cpm) and unchanged by either treatment (P > 0.074). Compared with saline, which was unchanged, detomidine reduced dominant power ratios for both cecum (0.45; IQR: 0.18) and left ventral colon (0.63; IQR: 0.35; P = 0.002). Detomidine decreased total power for the cecum in the 2-4 cpm frequency range from 55.0% (IQR: 4.4%) to 43.1% (IQR: 6.7%) and for the left ventral colon from 54.4% (IQR: 5.5%) to 27.3% (IQR: 9.3%; P < 0.087). Total power for the cecum was increased in the 8-12 cpm frequency range from 9.6% (IQR: 1.9%) to 18.5% (IQR: 6.6%; P = 0.0044) with detomidine. No change in frequency distribution was noted in controls (P > 0.08). Dominant power correlated with the rate of contractions measured ultrasonographically (P < 0.001). CONCLUSIONS: Detomidine decreased dominant power ratios for both the cecum and left ventral colon and produced tachyarrhythmias in cecal slow-wave activity. The correlation of dominant power with intestinal contractions supports the clinical development of EIG to diagnose equine motility disorders.

摘要

目的:评估右美托咪定对通过肠电图(EIG)测量的马肠道慢波活动及频率分布的影响。 设计:前瞻性实验研究。 地点:大学教学医院。 动物:选取12匹7至21岁临床健康马作为便利样本。 干预措施:将马随机分为生理盐水对照组(4匹)和右美托咪定治疗组(8匹)。在获取30分钟的基线EIG后,给予生理盐水或右美托咪定推注,随后进行恒速输注,并记录另一次EIG。超声检查监测盲肠和左腹结肠的收缩情况。进行频谱分析以评估主导频率、主导功率、总功率、频率分布百分比的变化以及慢波节律活动的变化。 测量指标及主要结果:盲肠(2.4次/分钟;四分位间距[IQR]:0.51次/分钟)和左腹结肠(2.13次/分钟;IQR:0.16次/分钟)的每分钟周期数的中位数(IQR)主导频率在两种治疗中均相似(P > 0.074)。与未改变的生理盐水相比,右美托咪定降低了盲肠(0.45;IQR:0.18)和左腹结肠(0.63;IQR:0.35;P = 0.002)的主导功率比。右美托咪定使盲肠在2 - 4次/分钟频率范围内的总功率从55.0%(IQR:4.4%)降至43.1%(IQR:6.7%),左腹结肠从54.4%(IQR:5.5%)降至27.3%(IQR:9.3%;P < 0.087)。右美托咪定使盲肠在8 - 12次/分钟频率范围内的总功率从9.6%(IQR:1.9%)增加至18.5%(IQR:6.6%;P = 0.0044)。对照组的频率分布无变化(P > 0.08)。主导功率与超声测量的收缩速率相关(P < 0.001)。 结论:右美托咪定降低了盲肠和左腹结肠的主导功率比,并使盲肠慢波活动出现快速心律失常。主导功率与肠道收缩的相关性支持了EIG在诊断马运动障碍方面的临床开发。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/121b/12065429/98632821adca/VEC-35-120-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/121b/12065429/64943cf9ba72/VEC-35-120-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/121b/12065429/064cb151c31a/VEC-35-120-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/121b/12065429/89ccc8a9e1db/VEC-35-120-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/121b/12065429/ea80541d98dd/VEC-35-120-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/121b/12065429/98632821adca/VEC-35-120-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/121b/12065429/64943cf9ba72/VEC-35-120-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/121b/12065429/064cb151c31a/VEC-35-120-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/121b/12065429/89ccc8a9e1db/VEC-35-120-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/121b/12065429/ea80541d98dd/VEC-35-120-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/121b/12065429/98632821adca/VEC-35-120-g001.jpg

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