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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...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Korean Continence Society
2016
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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. |
format | Online Article Text |
id | pubmed-5209582 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Korean Continence Society |
record_format | MEDLINE/PubMed |
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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