As an inhibitor of norepinephrine release, dexmedetomidine provides no improvement on stroke-associated pneumonia in mice

Background: Dexmedetomidine (DEX) is commonly employed as a sedative agent to attenuate sympathetic tone and reduce norepinephrine (NE) levels. In the context of stroke-associated pneumonia (SAP), which is believed to arise from heightened sympathetic nervous system activity and elevated NE release,...

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Main Authors: Miaomiao Zhou, Qiong Luo, Younian Xu
Format: Article
Language:English
Published: Frontiers Media S.A. 2023-08-01
Series:Frontiers in Pharmacology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fphar.2023.1203646/full
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author Miaomiao Zhou
Qiong Luo
Younian Xu
Younian Xu
author_facet Miaomiao Zhou
Qiong Luo
Younian Xu
Younian Xu
author_sort Miaomiao Zhou
collection DOAJ
description Background: Dexmedetomidine (DEX) is commonly employed as a sedative agent to attenuate sympathetic tone and reduce norepinephrine (NE) levels. In the context of stroke-associated pneumonia (SAP), which is believed to arise from heightened sympathetic nervous system activity and elevated NE release, the precise influence of DEX remains uncertain.Methods: In this study, we generated an SAP model using middle cerebral artery occlusion (MCAO) and examined NE levels, immunological statuses in the brain and periphery, pneumonia symptoms, and extent of infarction. We aimed to determine the effects of DEX on SAP and explore the underlying. Despite its potential to reduce NE levels, DEX did not alleviate SAP symptoms or decrease the infarct area. Interestingly, DEX led to an increase in spleen size and spleen index. Furthermore, we observed a decrease in the CD3+ T cell population in both the blood and brain, but an increase in the spleen following DEX administration. The precise mechanism linking decreased CD3+ T cells and DEX’s role in SAP requires further investigation.Conclusion: The clinical use of DEX in stroke patients should be approached with caution, considering its inability to alleviate SAP symptoms and reduce the infarct area. Further research is necessary to fully understand the relationship between decreased CD3+ T cells and DEX’s influence on SAP.
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spelling doaj.art-1070c4819a654f6eb4c1e6ed4134cf152023-08-02T10:03:56ZengFrontiers Media S.A.Frontiers in Pharmacology1663-98122023-08-011410.3389/fphar.2023.12036461203646As an inhibitor of norepinephrine release, dexmedetomidine provides no improvement on stroke-associated pneumonia in miceMiaomiao Zhou0Qiong Luo1Younian Xu2Younian Xu3Anesthesiology Department, Zhongnan Hospital of Wuhan University, Wuhan, ChinaAnesthesiology Department, Zhongnan Hospital of Wuhan University, Wuhan, ChinaAnesthesiology Department, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaInstitute of Anesthesia and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaBackground: Dexmedetomidine (DEX) is commonly employed as a sedative agent to attenuate sympathetic tone and reduce norepinephrine (NE) levels. In the context of stroke-associated pneumonia (SAP), which is believed to arise from heightened sympathetic nervous system activity and elevated NE release, the precise influence of DEX remains uncertain.Methods: In this study, we generated an SAP model using middle cerebral artery occlusion (MCAO) and examined NE levels, immunological statuses in the brain and periphery, pneumonia symptoms, and extent of infarction. We aimed to determine the effects of DEX on SAP and explore the underlying. Despite its potential to reduce NE levels, DEX did not alleviate SAP symptoms or decrease the infarct area. Interestingly, DEX led to an increase in spleen size and spleen index. Furthermore, we observed a decrease in the CD3+ T cell population in both the blood and brain, but an increase in the spleen following DEX administration. The precise mechanism linking decreased CD3+ T cells and DEX’s role in SAP requires further investigation.Conclusion: The clinical use of DEX in stroke patients should be approached with caution, considering its inability to alleviate SAP symptoms and reduce the infarct area. Further research is necessary to fully understand the relationship between decreased CD3+ T cells and DEX’s influence on SAP.https://www.frontiersin.org/articles/10.3389/fphar.2023.1203646/fullischemic strokestroke-associated pneumoniadexmedetomidinenorepinephrineimmunity
spellingShingle Miaomiao Zhou
Qiong Luo
Younian Xu
Younian Xu
As an inhibitor of norepinephrine release, dexmedetomidine provides no improvement on stroke-associated pneumonia in mice
Frontiers in Pharmacology
ischemic stroke
stroke-associated pneumonia
dexmedetomidine
norepinephrine
immunity
title As an inhibitor of norepinephrine release, dexmedetomidine provides no improvement on stroke-associated pneumonia in mice
title_full As an inhibitor of norepinephrine release, dexmedetomidine provides no improvement on stroke-associated pneumonia in mice
title_fullStr As an inhibitor of norepinephrine release, dexmedetomidine provides no improvement on stroke-associated pneumonia in mice
title_full_unstemmed As an inhibitor of norepinephrine release, dexmedetomidine provides no improvement on stroke-associated pneumonia in mice
title_short As an inhibitor of norepinephrine release, dexmedetomidine provides no improvement on stroke-associated pneumonia in mice
title_sort as an inhibitor of norepinephrine release dexmedetomidine provides no improvement on stroke associated pneumonia in mice
topic ischemic stroke
stroke-associated pneumonia
dexmedetomidine
norepinephrine
immunity
url https://www.frontiersin.org/articles/10.3389/fphar.2023.1203646/full
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