Lipid Emulsion Attenuates Acetylcholine-Induced Relaxation in Isolated Rat Aorta.

Seong-Ho Ok,Youngju Lee,Jeong Yeol Han,Young-Kyun Chung,Il-Woo Shin,Jeong-Min Hong,Hyunhoo Cho,Jungchul Park,Jongsun Yu,Ju-Tae Sohn,Mun-Jeoung Choi,Soo Hee Lee,Jiseok Baik,Heon Keun Lee

doi:10.1155/2015/871545

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.

Highlights

Intravenous lipid emulsion (LE) has been used for parenteral nutrition when the oral and enteral route is not available
This study suggests that the magnitude of LE-mediated inhibition of acetylcholine-induced nitric oxide- (NO-)mediated relaxation in the isolated rat aorta appears to be dependent on the fatty acid components of LE
Considering previous reports, in our current study, Lipofundin MCT/LCT-mediated enhanced inhibition of acetylcholine-induced nitric oxide (NO)-mediated relaxation may be associated with differences in fatty acid components that are contained in LE such as increased medium-chain fatty acids and decreased long-chain fatty acids [8, 10, 11, 17, 20, 27, 28]

Summary

Introduction

Intravenous lipid emulsion (LE) has been used for parenteral nutrition when the oral and enteral route is not available. LEs such as either Intralipid 20% containing 100% long-chain triglycerides or Lipofundin MCT/LCT 20% containing 50% long-chain triglycerides and 50% medium-chain triglycerides are effective for treatment of cardiovascular collapse induced by a toxic dose of local anesthetics including bupivacaine, levobupivacaine, ropivacaine, mepivacaine, and lidocaine [1,2,3,4,5,6,7]. LE containing only longchain triglycerides has no effect on blood pressure, whereas LE containing both medium-chain triglycerides and longchain triglycerides causes an increase in blood pressure [12]. Intralipid increases blood pressure and inhibits acetylcholine-induced NO-mediated vasorelaxation [13,14,15,16,17]. Intravenous administration of LE produces increased left ventricular systolic pressure, and pretreatment

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Conclusion