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Int. J. Mol. Sci. 2017, 18(2), 394; doi:10.3390/ijms18020394

A Lipid Emulsion Reverses Toxic-Dose Bupivacaine-Induced Vasodilation during Tyrosine Phosphorylation-Evoked Contraction in Isolated Rat Aortae

1
Department of Anesthesiology and Pain Medicine, Gyeongsang National University School of Medicine, Gyeongsang National University Hospital, 79 Gangnam-ro, Jinju 52727, Korea
2
Department of Physiology, Institute of Clinical and Translational Research, Catholic Kwandong University, College of Medicine, Gangneung 25601, Korea
3
Department of Anesthesiology and Pain Medicine, Gyeongsang National University Changwon Hospital, Changwon 51472, Korea
4
Department of Anesthesia and Pain Medicine, School of Medicine, Pusan National University, Biomedical Research Institute, Pusan National University Hospital, Busan 49241, Korea
5
Institute of Health Sciences, Gyeongsang National University, Jinju 52727, Korea
*
Author to whom correspondence should be addressed.
Academic Editor: Guido R.M.M. Haenen
Received: 11 January 2017 / Revised: 3 February 2017 / Accepted: 7 February 2017 / Published: 13 February 2017
(This article belongs to the Section Molecular Toxicology)
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Abstract

The goal of this in vitro study was to examine the effect of a lipid emulsion on toxic-dose bupivacaine-induced vasodilation in a model of tyrosine phosphatase inhibitor sodium orthovanadate-induced contraction in endothelium-denuded rat aortae and to elucidate the associated cellular mechanism. The effect of a lipid emulsion on vasodilation induced by a toxic dose of a local anesthetic during sodium orthovanadate-induced contraction was examined. In addition, the effects of various inhibitors, either bupivacaine alone or a lipid emulsion plus bupivacaine, on protein kinase phosphorylation induced by sodium orthovanadate in rat aortic vascular smooth muscle cells was examined. A lipid emulsion reversed the vasodilation induced by bupivacaine during sodium orthovanadate-induced contraction. The lipid emulsion attenuated the bupivacaine-mediated inhibition of the sodium orthovanadate-induced phosphorylation of protein tyrosine, c-Jun NH2-terminal kinase (JNK), myosin phosphatase target subunit 1 (MYPT1), phospholipase C (PLC) γ-1 and extracellular signal-regulated kinase (ERK). These results suggest that a lipid emulsion reverses toxic-dose bupivacaine-induced vasodilation during sodium orthovanadate-induced contraction via the activation of a pathway involving either tyrosine kinase, JNK, Rho-kinase and MYPT1 or tyrosine kinase, PLC γ-1 and ERK, and this reversal is associated with the lipid solubility of the local anesthetic and the induction of calcium sensitization. View Full-Text
Keywords: lipid emulsion; bupivacaine; vasodilation; sodium orthovanadate; tyrosine kinase; myosin phosphatase target subunit; aorta lipid emulsion; bupivacaine; vasodilation; sodium orthovanadate; tyrosine kinase; myosin phosphatase target subunit; aorta
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MDPI and ACS Style

Ok, S.-H.; Lee, S.H.; Kwon, S.-C.; Choi, M.H.; Shin, I.-W.; Kang, S.; Park, M.; Hong, J.-M.; Sohn, J.-T. A Lipid Emulsion Reverses Toxic-Dose Bupivacaine-Induced Vasodilation during Tyrosine Phosphorylation-Evoked Contraction in Isolated Rat Aortae. Int. J. Mol. Sci. 2017, 18, 394.

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