Rocuronium Bromide Inhibits Inflammation and Pain by Suppressing Nitric Oxide Production and Enhancing Prostaglandin E2 Synthesis in Endothelial Cells.
- Author:
Sang Bin BAEK
1
;
Mal Soon SHIN
;
Jin Hee HAN
;
Sang Woong MOON
;
Boksoon CHANG
;
Jung Won JEON
;
Jae Woo YI
;
Jun Young CHUNG
Author Information
- Publication Type:Original Article
- Keywords: Rocuronium; Endothelial Cells; Cyclooxygenase 2; Nitric Oxide; Prostaglandin E2
- MeSH: 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
- From:International Neurourology Journal 2016;20(4):296-303
- CountryRepublic of Korea
- Language:English
- 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.
