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麻醉大鼠中液体超负荷导致颏舌肌活动减少。

Reduced genioglossus muscle activity caused by fluid overload in anesthetized rats.

机构信息

Institute of Biomaterials and Biomedical Engineering, University of Toronto, Toronto, ON, Canada.

Toronto Rehabilitation Institute, University Health Network, University of Toronto, Toronto, ON, Canada.

出版信息

Physiol Rep. 2020 Jul;8(13):e14445. doi: 10.14814/phy2.14445.

DOI:10.14814/phy2.14445
PMID:32633469
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7339833/
Abstract

INTRODUCTION

Although the precise cause of obstructive sleep apnea (OSA) remains unknown, various anatomical or structural factors are thought to influence upper airway patency. Recent clinical studies show that OSA is frequently observed among patients with fluid-retaining states, such as heart/renal failure and postsurgery. It is important to note that a cause-effect relationship is not yet established, and our understanding of the effects of fluid overload is limited. The goal of this study was to investigate an animal model that can characterize the physiological changes that occur in response to fluid overload.

METHOD

Acute nonsurvival experiments were conducted in 16 Sprague-Dawley rats. Rats were initially anesthetized by inhaled isoflurane, while the femoral vein was cannulated and urethane (1.2-1.5 g/Kg body weight) was gradually delivered intravenously to induce anesthesia. Additional doses of urethane were delivered as necessary to maintain a surgical plane of anesthesia. A surgical incision was made on the cervical area to catheterize carotid artery to measure blood pressure. A pair of stainless-steel wires was injected into the tongue to measure genioglossus muscle activity (GGEMG). All physiological measurements were recorded as intravenous infusion of saline was provided to the rat (infusion rate = 22 ml/kg over 30 min).

RESULTS

Acute saline overloading resulted in a 33% decrease in GGEMG, when compared to baseline. There was also a gradual drop in the respiratory rate (13% decrease) that reached statistical significance at 10 min after infusion was stopped. The blood pressure exhibited a 14% increase which subsequently returned to baseline within 40 min stopping infusion. There were no significant changes in the heart rate.

CONCLUSION

The results of this study indicate that systemic fluid overload can affect significant changes in different physiological systems including reduction in genioglossus muscle activity, increase in blood pressure, and change autonomic nervous system function.

摘要

简介

尽管阻塞性睡眠呼吸暂停(OSA)的确切原因仍不清楚,但各种解剖或结构因素被认为会影响上呼吸道通畅。最近的临床研究表明,OSA 常发生于液体潴留状态的患者中,如心力衰竭、肾衰竭和手术后。需要注意的是,目前尚未建立因果关系,我们对液体超负荷的影响的了解也有限。本研究的目的是研究一种可以描述对液体超负荷反应的生理变化的动物模型。

方法

16 只 Sprague-Dawley 大鼠进行急性非生存实验。大鼠首先通过吸入异氟烷麻醉,同时经股静脉置管,并逐渐静脉内给予尿嘧啶(1.2-1.5 g/Kg 体重)以诱导麻醉。必要时给予额外剂量的尿嘧啶以维持手术麻醉平面。在颈部区域进行手术切口以插入颈动脉导管以测量血压。将一对不锈钢丝注入舌中以测量颏舌肌肌电图(GGEMG)。在向大鼠静脉内输注生理盐水(30 分钟内输注 22 ml/kg)时,记录所有生理测量值。

结果

与基线相比,急性盐水超负荷导致 GGEMG 降低 33%。呼吸频率也逐渐下降(下降 13%),在停止输注 10 分钟后达到统计学意义。血压升高 14%,停止输注 40 分钟后恢复基线。心率无明显变化。

结论

本研究结果表明,全身液体超负荷会影响包括颏舌肌活动减少、血压升高和自主神经系统功能改变在内的不同生理系统的显著变化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd1/7339833/518be3bb8c44/PHY2-8-e14445-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd1/7339833/090635ccf952/PHY2-8-e14445-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd1/7339833/e4eb8bb86124/PHY2-8-e14445-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd1/7339833/8bace931d439/PHY2-8-e14445-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd1/7339833/64d7a4d71b14/PHY2-8-e14445-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd1/7339833/1f0871ae04c7/PHY2-8-e14445-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd1/7339833/518be3bb8c44/PHY2-8-e14445-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd1/7339833/090635ccf952/PHY2-8-e14445-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd1/7339833/e4eb8bb86124/PHY2-8-e14445-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd1/7339833/8bace931d439/PHY2-8-e14445-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd1/7339833/64d7a4d71b14/PHY2-8-e14445-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd1/7339833/1f0871ae04c7/PHY2-8-e14445-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd1/7339833/518be3bb8c44/PHY2-8-e14445-g006.jpg

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