Lipofundin MCT/LCT Inhibits Levcromakalim-Induced Vasodilation by Inhibiting Endothelial Nitric Oxide Release.

作者: Soo Hee Lee , Dawon Kang , Seong-Ho Ok , Ji-Yoon Kim , Sung Il Bae

DOI: 10.3390/IJMS21051763

关键词:

摘要: The goal of this study was to examine the effect lipid emulsion on vasodilation induced by ATP-sensitive potassium (KATP) channels in isolated rat aortae and underlying mechanism. effects Intralipid, containing 100% long-chain fatty acids, Lipofundin MCT/LCT, 50% acids plus medium-chain levcromakalim endothelium-intact aorta with or without NW-nitro-L-arginine methyl ester (L-NAME) endothelium-denuded were examined. L-arginine, L-NAME, glibenclamide, alone combined, levcromakalim-induced MCT/LCT inhibited aortae, whereas Intralipid did not. In addition, had no L-NAME. L-arginine produced more than alone. Glibenclamide vasodilation. Levcromakalim not significantly alter endothelial nitric oxide synthase phosphorylation, decreased cyclic guanosine monophosphate. membrane hyperpolarization. Taken together, these results suggest that inhibits inhibiting basally released oxide, which seems occur through acids.

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