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Levobupivacaine-induced contraction of isolated rat aorta is calcium dependent

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Levobupivacaine is a long-acting local anesthetic that intrinsically produces vasoconstriction in isolated vessels. The goals of this study were to investigate the calcium-dependent mechanism underlying levobupivacaine-induced contraction of isolated rat aorta in vitro and to elucidate the pathway responsible for the endothelium-dependent attenuation of levobupivacaine-induced contraction. Isolated rat aortic rings were suspended to record isometric tension. Cumulative levobupivacaine concentration–response curves were generated in either the presence or absence of the antagonists verapamil, nifedipine, SKF-96365, 2-aminoethoxydiphenylborate, Gd3+, N W -nitro-l-arginine methyl ester (L-NAME), 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), and methylene blue, either alone or in combination. Verapamil, nifedipine, SKF-96365, 2-aminoethoxydiphenylborate, low calcium concentrations, and calcium-free Krebs solution attenuated levobupivacaine-induced contraction. Gd3+ had no effect on levobupivacaine-induced contraction. Levobupivacaine increased intracellular calcium levels in vascular smooth muscle cells. L-NAME, ODQ, and methylene blue increased levobupivacaine-induced contraction in endothelium-intact aorta. SKF-96365 attenuated calcium-induced contraction in a previously calcium-free isotonic depolarizing solution containing 100 mmol/L KCl. Levobupivacaine-induced contraction of rat aortic smooth muscle is mediated primarily by calcium influx from the extracellular space mainly via voltage-operated calcium channels and, in part, by inositol 1,4,5-trisphosphate receptor-mediated release of calcium from the sarcoplasmic reticulum. The nitric oxide – cyclic guanosine monophosphate pathway is involved in the endothelium-dependent attenuation of levobupivacaine-induced contraction.
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Keywords: aorta; aorte; calcium; contraction; endothelium; endothélium; levobupivacaine; lévobupivacaïne; monoxyde d’azote; nitric oxide; verapamil; vérapamil

Document Type: Research Article

Affiliations: 1: Department of Anesthesiology and Pain Medicine, Gyeongsang National University Hospital, Jinju, 660-702, Korea. 2: Department of Anesthesiology and Pain Medicine, Institute of Health Sciences, Gyeongsang National University School of Medicine, Jinju, 660-702, Korea. 3: Department of Physiology, Gyeongsang National University School of Medicine, Jinju, 660-702, Korea. 4: Center for Functional Connectomics, Korea Institute of Science and Technology, Seoul, 136-791, Korea. 5: Department of Anesthesiology and Pain Medicine, Gyeongsang National University School of Medicine, Jinju, 660-702, Korea.

Publication date: July 27, 2011

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