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Rocuronium Bromide Inhibits Inflammation and Pain by Suppressing Nitric Oxide Production and Enhancing Prostaglandin E(2) Synthesis in Endothelial Cells

PURPOSE: Rocuronium bromide is a nondepolarizing neuromuscular blocking drug and has been used as an adjunct for relaxation or paralysis of the skeletal muscles, facilitation of endotracheal intubation, and improving surgical conditions during general anesthesia. However, intravenous injection of ro...

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Autores principales: Baek, Sang Bin, Shin, Mal Soon, Han, Jin Hee, Moon, Sang Woong, Chang, Boksoon, Jeon, Jung Won, Yi, Jae Woo, Chung, Jun Young
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Korean Continence Society 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5209582/
https://www.ncbi.nlm.nih.gov/pubmed/28043117
http://dx.doi.org/10.5213/inj.1632796.398
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author Baek, Sang Bin
Shin, Mal Soon
Han, Jin Hee
Moon, Sang Woong
Chang, Boksoon
Jeon, Jung Won
Yi, Jae Woo
Chung, Jun Young
author_facet Baek, Sang Bin
Shin, Mal Soon
Han, Jin Hee
Moon, Sang Woong
Chang, Boksoon
Jeon, Jung Won
Yi, Jae Woo
Chung, Jun Young
author_sort Baek, Sang Bin
collection PubMed
description PURPOSE: Rocuronium bromide is a nondepolarizing neuromuscular blocking drug and has been used as an adjunct for relaxation or paralysis of the skeletal muscles, facilitation of endotracheal intubation, and improving surgical conditions during general anesthesia. However, intravenous injection of rocuronium bromide induces injection pain or withdrawal movement. The exact mechanism of rocuronium bromide-induced injection pain or withdrawal movement is not yet understood. We investigated whether rocuronium bromide treatment is involved in the induction of inflammation and pain in vascular endothelial cells. METHODS: For this study, calf pulmonary artery endothelial (CPAE) cells were used, and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, Western blot, nitric oxide detection, and prostaglandin E(2) immunoassay were conducted. RESULTS: Rocuronium bromide treatment inhibited endothelial nitric oxide synthase and suppressed nitric oxide production in CPAE cells. Rocuronium bromide activated cyclooxygenase-2, inducible nitric oxide synthase and increased prostaglandin E(2) synthesis in CPAE cells. CONCLUSIONS: Rocuronium bromide induced inflammation and pain in CPAE cells. Suppressing nitric oxide production and enhancing prostaglandin E(2) synthesis might be associated with rocuronium bromide-induced injection pain or withdrawal movement.
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spelling pubmed-52095822017-01-04 Rocuronium Bromide Inhibits Inflammation and Pain by Suppressing Nitric Oxide Production and Enhancing Prostaglandin E(2) Synthesis in Endothelial Cells Baek, Sang Bin Shin, Mal Soon Han, Jin Hee Moon, Sang Woong Chang, Boksoon Jeon, Jung Won Yi, Jae Woo Chung, Jun Young Int Neurourol J Original Article PURPOSE: Rocuronium bromide is a nondepolarizing neuromuscular blocking drug and has been used as an adjunct for relaxation or paralysis of the skeletal muscles, facilitation of endotracheal intubation, and improving surgical conditions during general anesthesia. However, intravenous injection of rocuronium bromide induces injection pain or withdrawal movement. The exact mechanism of rocuronium bromide-induced injection pain or withdrawal movement is not yet understood. We investigated whether rocuronium bromide treatment is involved in the induction of inflammation and pain in vascular endothelial cells. METHODS: For this study, calf pulmonary artery endothelial (CPAE) cells were used, and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, Western blot, nitric oxide detection, and prostaglandin E(2) immunoassay were conducted. RESULTS: Rocuronium bromide treatment inhibited endothelial nitric oxide synthase and suppressed nitric oxide production in CPAE cells. Rocuronium bromide activated cyclooxygenase-2, inducible nitric oxide synthase and increased prostaglandin E(2) synthesis in CPAE cells. CONCLUSIONS: Rocuronium bromide induced inflammation and pain in CPAE cells. Suppressing nitric oxide production and enhancing prostaglandin E(2) synthesis might be associated with rocuronium bromide-induced injection pain or withdrawal movement. Korean Continence Society 2016-12 2016-12-26 /pmc/articles/PMC5209582/ /pubmed/28043117 http://dx.doi.org/10.5213/inj.1632796.398 Text en Copyright © 2016 Korean Continence Society This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Baek, Sang Bin
Shin, Mal Soon
Han, Jin Hee
Moon, Sang Woong
Chang, Boksoon
Jeon, Jung Won
Yi, Jae Woo
Chung, Jun Young
Rocuronium Bromide Inhibits Inflammation and Pain by Suppressing Nitric Oxide Production and Enhancing Prostaglandin E(2) Synthesis in Endothelial Cells
title Rocuronium Bromide Inhibits Inflammation and Pain by Suppressing Nitric Oxide Production and Enhancing Prostaglandin E(2) Synthesis in Endothelial Cells
title_full Rocuronium Bromide Inhibits Inflammation and Pain by Suppressing Nitric Oxide Production and Enhancing Prostaglandin E(2) Synthesis in Endothelial Cells
title_fullStr Rocuronium Bromide Inhibits Inflammation and Pain by Suppressing Nitric Oxide Production and Enhancing Prostaglandin E(2) Synthesis in Endothelial Cells
title_full_unstemmed Rocuronium Bromide Inhibits Inflammation and Pain by Suppressing Nitric Oxide Production and Enhancing Prostaglandin E(2) Synthesis in Endothelial Cells
title_short Rocuronium Bromide Inhibits Inflammation and Pain by Suppressing Nitric Oxide Production and Enhancing Prostaglandin E(2) Synthesis in Endothelial Cells
title_sort rocuronium bromide inhibits inflammation and pain by suppressing nitric oxide production and enhancing prostaglandin e(2) synthesis in endothelial cells
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5209582/
https://www.ncbi.nlm.nih.gov/pubmed/28043117
http://dx.doi.org/10.5213/inj.1632796.398
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