This study investigated endothelium-derived vasodilators and potassium channels involved in the modulation of ropivacaine-induced contraction. In endothelium-intact rat aortae, ropivacaine concentration-response curves were generated in the presence or absence of the following inhibitors: the nonspecific nitric oxide synthase (NOS) inhibitor N (ω) -nitro-L-arginine methyl ester (L-NAME), the neuronal NOS inhibitor N (ω) -propyl-L-arginine hydrochloride, the inducible NOS inhibitor 1400W dihydrochloride, the nitric oxide-sensitive guanylyl cyclase (GC) inhibitor ODQ, the NOS and GC inhibitor methylene blue, the phosphoinositide-3 kinase inhibitor wortmannin, the cytochrome p450 epoxygenase inhibitor fluconazole, the voltage-dependent potassium channel inhibitor 4-aminopyridine (4-AP), the calcium-activated potassium channel inhibitor tetraethylammonium (TEA), the inward-rectifying potassium channel inhibitor barium chloride, and the ATP-sensitive potassium channel inhibitor glibenclamide. The effect of ropivacaine on endothelial nitric oxide synthase (eNOS) phosphorylation in human umbilical vein endothelial cells was examined by western blotting.
View Article and Find Full Text PDFThe goals of this study were to determine which lipid emulsion (Intralipid(®) and Lipofundin MCT/LCT(®)) is more effective in reversing high-dose levobupivacaine-induced reduced vasoconstriction in isolated rat aortas and to examine the associated cellular mechanisms with a particular focus on the endothelium. Two lipid emulsion concentration-response curves were generated using high-dose levobupivacaine-induced reduced vasoconstriction and vasodilation of isolated aortas pretreated with or without 60 mM KCl. Endothelial nitric oxide synthase (eNOS) and caveolin-1 phosphorylation were measured in rat aortic tissue treated with levobupivacaine in the presence or absence of lipid emulsion.
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