Effects of Acidification and Alkalinization on the Lipid Emulsion-Mediated Reversal of Toxic Dose Levobupivacaine-Induced Vasodilation in the Isolated Rat Aortaopen access
- Authors
- Ok S.-H.[Ok S.-H.]; Kim W.H.[Kim W.H.]; Yu J.[Yu J.]; Lee Y.[Lee Y.]; Choi M.-J.[Choi M.-J.]; Lim D.H.[Lim D.H.]; Hwang Y.[Hwang Y.]; Kim Y.A.[Kim Y.A.]; Sohn J.-T.[Sohn J.-T.]
- Issue Date
- 2016
- Publisher
- IVYSPRING INT PUBL
- Keywords
- Lipid emulsion; Pre-acidification; Levobupivacaine; Nitric oxide; Aorta
- Citation
- INTERNATIONAL JOURNAL OF MEDICAL SCIENCES, v.13, no.1, pp.68 - 76
- Indexed
- SCIE
SCOPUS
- Journal Title
- INTERNATIONAL JOURNAL OF MEDICAL SCIENCES
- Volume
- 13
- Number
- 1
- Start Page
- 68
- End Page
- 76
- URI
- https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/41525
- DOI
- 10.7150/ijms.13016
- ISSN
- 1449-1907
- Abstract
- The goal of this in vitro study was to examine the effects of pre-acidification and pre-akalinization on the lipid emulsion-mediated reversal of toxic dose levobupivacaine-induced vasodilation in isolated rat aorta. Isolated aortic rings with and without the nitric oxide synthase inhibitor N.-nitro-L-arginine methyl ester (L-NAME) were exposed to four types of Krebs solution (pH 7.0, 7.2, 7.4, and 7.6), followed by the addition of 60 mM potassium chloride. When the toxic dose of levobupivacaine (3 x 10(-4) M) produced a stable and sustained vasodilation in the isolated aortic rings that were precontracted with 60 mM potassium chloride, increasing lipid emulsion concentrations (SMOFlipid (R) : 0.24, 0.48, 0.95 and 1.39%) were added to generate concentration-response curves. The effects of mild pre-acidification alone and mild pre-acidification in combination with a lipid emulsion on endothelial nitric oxide synthase (eNOS) phosphorylation in human umbilical vein endothelial cells were investigated by Western blotting. Mild pre-acidification caused by the pH 7.2 Krebs solution enhanced the lipid emulsion-mediated reversal of levobupivacaine-induced vasodilation in isolated endothelium-intact aortic rings, whereas mild pre-acidification caused by the pH 7.2 Krebs solution did not significantly alter the lipid emulsion-mediated reversal of the levobupivacaine-induced vasodilation in isolated endothelium-denuded aortic rings or endothelium-intact aortic rings with L-NAME. A lipid emulsion attenuated the increased eNOS phosphorylation induced by the pH 7.2 Krebs solution. Taken together, these results suggest that mild pre-acidification enhances the lipid emulsion-mediated reversal of toxic dose levobupivacaine-induced vasodilation in the endothelium-intact aorta via the inhibition of nitric oxide.
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Collections - Medicine > Department of Medicine > 1. Journal Articles
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