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BioMed Research International
Volume 2015 (2015), Article ID 871545, 9 pages
http://dx.doi.org/10.1155/2015/871545
Research Article

Lipid Emulsion Attenuates Acetylcholine-Induced Relaxation in Isolated Rat Aorta

1Department of Anesthesiology and Pain Medicine, Gyeongsang National University Hospital, Gyeongsang National University School of Medicine, Jinju 660-715, Republic of Korea
2Department of Anesthesiology and Pain Medicine, Gyeongsang National University Hospital, Jinju 660-702, Republic of Korea
3Department of Oral and Maxillofacial Surgery, Gyeongsang National University Hospital, Jinju 660-702, Republic of Korea
4Department of Anesthesiology and Pain Medicine, Pusan National University Hospital, Biomed Research Institute, Pusan National University School of Medicine, Pusan 602-739, Republic of Korea
5Institute of Health Sciences, Gyeongsang National University School of Medicine, Jinju 660-715, Republic of Korea

Received 7 April 2015; Revised 20 June 2015; Accepted 8 July 2015

Academic Editor: Jean C. Bopassa

Copyright © 2015 Seong-Ho Ok et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

We investigated the effect of Lipofundin MCT/LCT and Intralipid on acetylcholine-induced nitric oxide- (NO-) mediated relaxation in rat aorta to determine which lipid emulsion (LE) is more potent in terms of inhibition of NO-induced relaxation. Dose-response curves of responses induced by acetylcholine, the calcium ionophore A23187, and sodium nitroprusside were generated using isolated rat aorta with or without LE. The effect of Lipofundin MCT/LCT on acetylcholine-induced endothelial nitric oxide synthase (eNOS) phosphorylation in human umbilical vein endothelial cells (HUVECs) was investigated using western blotting. Lipofundin MCT/LCT (0.1 and 0.2%) attenuated acetylcholine-induced relaxation in endothelium-intact aorta with or without tiron, whereas 0.2% Intralipid only inhibited relaxation. Lipofundin MCT/LCT inhibited relaxation induced by the calcium ionophore A23187 and sodium nitroprusside in endothelium-intact aorta, but Lipofundin MCT/LCT had no effect on sodium nitroprusside-induced relaxation in the endothelium-denuded aorta. Combined pretreatment with l-arginine plus Lipofundin MCT/LCT increased acetylcholine-induced maximal relaxation in endothelium-intact aorta compared with Lipofundin MCT/LCT alone. l-Arginine attenuated Lipofundin MCT/LCT-mediated inhibition of acetylcholine-induced eNOS phosphorylation in HUVECs. Taken together, Lipofundin MCT/LCT attenuated acetylcholine-induced NO-mediated relaxation via an inhibitory effect on the endothelium including eNOS, which is proximal to activation of guanylyl cyclase.