Int Neurourol J.
2016 Dec;20(4):296-303. 10.5213/inj.1632796.398.
Rocuronium Bromide Inhibits Inflammation and Pain by Suppressing Nitric Oxide Production and Enhancing Prostaglandin E2 Synthesis in Endothelial Cells
- Affiliations
-
- 1Department of Psychiatry, Ulsan University Gangneung Asan Hospital, College of Medicine, Ulsan University, Gangneung, Korea.
- 2School of Global Sport Studies, Korea University, Sejong, Korea.
- 3Department of Anesthesiology and Pain Medicine, Kyung Hee University Medical Center, College of Medicine, Kyung Hee University, Seoul, Korea.
- 4Department of Ophthalmology, Kyung Hee University Hospital at Gangdong, College of Medicine, Kyung Hee University , Seoul, Korea.
- 5Department of Internal Medicine, Kyung Hee University Hospital at Gangdong, College of Medicine, Kyung Hee University, Seoul, Korea.
- 6Department of Anesthesiology and Pain Medicine, Kyung Hee University Hospital at Gangdong, College of Medicine, Kyung Hee University, Seoul, Korea. madsleep@gmail.com
- KMID: 2365693
- DOI: http://doi.org/10.5213/inj.1632796.398
Abstract
- 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 E2 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 E2 synthesis in CPAE cells.
CONCLUSIONS
Rocuronium bromide induced inflammation and pain in CPAE cells. Suppressing nitric oxide production and enhancing prostaglandin E2 synthesis might be associated with rocuronium bromide-induced injection pain or withdrawal movement.
MeSH Terms
-
Anesthesia, General
Blotting, Western
Cyclooxygenase 2
Dinoprostone*
Endothelial Cells*
Immunoassay
Inflammation*
Injections, Intravenous
Intubation, Intratracheal
Muscle, Skeletal
Neuromuscular Blockade
Nitric Oxide Synthase Type II
Nitric Oxide Synthase Type III
Nitric Oxide*
Paralysis
Pulmonary Artery
Relaxation
Cyclooxygenase 2
Dinoprostone
Nitric Oxide
Nitric Oxide Synthase Type II
Nitric Oxide Synthase Type III
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