{"title":"右美托咪定对止血带所致骨骼肌损伤的影响。","authors":"Wenjie Cheng, Zhe Wu, Jizheng Zhang, Wanlu Ren","doi":"10.1590/1806-9282.20220865","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>The aim of this study was to investigate whether dexmedetomidine could reduce tourniquet-induced skeletal muscle injury.</p><p><strong>Methods: </strong>C57BL6 male mice were randomly assigned to sham, ischemia/reperfusion, and dexmedetomidine groups. Mice in the ischemia/reperfusion and dexmedetomidine groups received normal saline solution and dexmedetomidine intraperitoneally, respectively. The sham group underwent the same procedure as the ischemia/reperfusion group, with the exception of tourniquet application. Subsequently, the ultrastructure of the gastrocnemius muscle was observed, and its contractile force was examined. In addition, Toll-like receptor 4 and nuclear factor-κB expression within muscles was detected by Western blot.</p><p><strong>Results: </strong>Dexmedetomidine alleviated myocyte damage and increased the contractility of skeletal muscles. Moreover, dexmedetomidine significantly inhibited the expression of Toll-like receptor 4/nuclear factor-κB in the gastrocnemius muscle.</p><p><strong>Conclusion: </strong>Taken together, these results demonstrate that dexmedetomidine administration attenuated tourniquet-induced structural and functional impairment of the skeletal muscle, partly through inactivation of the Toll-like receptor 4/nuclear factor-κB pathway.</p>","PeriodicalId":21234,"journal":{"name":"Revista da Associacao Medica Brasileira","volume":null,"pages":null},"PeriodicalIF":1.2000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/70/c7/1806-9282-ramb-69-02-0228.PMC9983473.pdf","citationCount":"1","resultStr":"{\"title\":\"Effect of dexmedetomidine on tourniquet-induced skeletal muscle injury.\",\"authors\":\"Wenjie Cheng, Zhe Wu, Jizheng Zhang, Wanlu Ren\",\"doi\":\"10.1590/1806-9282.20220865\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>The aim of this study was to investigate whether dexmedetomidine could reduce tourniquet-induced skeletal muscle injury.</p><p><strong>Methods: </strong>C57BL6 male mice were randomly assigned to sham, ischemia/reperfusion, and dexmedetomidine groups. Mice in the ischemia/reperfusion and dexmedetomidine groups received normal saline solution and dexmedetomidine intraperitoneally, respectively. The sham group underwent the same procedure as the ischemia/reperfusion group, with the exception of tourniquet application. Subsequently, the ultrastructure of the gastrocnemius muscle was observed, and its contractile force was examined. In addition, Toll-like receptor 4 and nuclear factor-κB expression within muscles was detected by Western blot.</p><p><strong>Results: </strong>Dexmedetomidine alleviated myocyte damage and increased the contractility of skeletal muscles. Moreover, dexmedetomidine significantly inhibited the expression of Toll-like receptor 4/nuclear factor-κB in the gastrocnemius muscle.</p><p><strong>Conclusion: </strong>Taken together, these results demonstrate that dexmedetomidine administration attenuated tourniquet-induced structural and functional impairment of the skeletal muscle, partly through inactivation of the Toll-like receptor 4/nuclear factor-κB pathway.</p>\",\"PeriodicalId\":21234,\"journal\":{\"name\":\"Revista da Associacao Medica Brasileira\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.2000,\"publicationDate\":\"2023-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/70/c7/1806-9282-ramb-69-02-0228.PMC9983473.pdf\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Revista da Associacao Medica Brasileira\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1590/1806-9282.20220865\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"MEDICINE, GENERAL & INTERNAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Revista da Associacao Medica Brasileira","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1590/1806-9282.20220865","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
Effect of dexmedetomidine on tourniquet-induced skeletal muscle injury.
Objective: The aim of this study was to investigate whether dexmedetomidine could reduce tourniquet-induced skeletal muscle injury.
Methods: C57BL6 male mice were randomly assigned to sham, ischemia/reperfusion, and dexmedetomidine groups. Mice in the ischemia/reperfusion and dexmedetomidine groups received normal saline solution and dexmedetomidine intraperitoneally, respectively. The sham group underwent the same procedure as the ischemia/reperfusion group, with the exception of tourniquet application. Subsequently, the ultrastructure of the gastrocnemius muscle was observed, and its contractile force was examined. In addition, Toll-like receptor 4 and nuclear factor-κB expression within muscles was detected by Western blot.
Results: Dexmedetomidine alleviated myocyte damage and increased the contractility of skeletal muscles. Moreover, dexmedetomidine significantly inhibited the expression of Toll-like receptor 4/nuclear factor-κB in the gastrocnemius muscle.
Conclusion: Taken together, these results demonstrate that dexmedetomidine administration attenuated tourniquet-induced structural and functional impairment of the skeletal muscle, partly through inactivation of the Toll-like receptor 4/nuclear factor-κB pathway.
期刊介绍:
A Revista da Associação Médica Brasileira (RAMB), editada pela Associação Médica Brasileira, desde 1954, tem por objetivo publicar artigos que contribuam para o conhecimento médico.