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

Ok SH, Lee SH, Yu J, Park J, Shin IW, Lee Y, Cho H, Choi MJ, Baik J, Hong JM, Han JY, Lee HK, Chung YK, Sohn JT - Biomed Res Int (2015)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology and Pain Medicine, Gyeongsang National University Hospital, Gyeongsang National University School of Medicine, Jinju 660-715, Republic of Korea.

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.

No MeSH data available.


Related in: MedlinePlus

Effect of Lipofundin MCT/LCT (0.1 or 0.2%) on the phenylephrine dose-response curves in isolated endothelium-intact aorta. Data (N = 8) are the mean ± SD and are expressed as the percentage of maximal precontraction induced by isotonic 60 mM KCl. N indicates the number of descending thoracic aortic rings. ∗P < 0.001, †P < 0.01, and #P < 0.05 versus control.
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fig5: Effect of Lipofundin MCT/LCT (0.1 or 0.2%) on the phenylephrine dose-response curves in isolated endothelium-intact aorta. Data (N = 8) are the mean ± SD and are expressed as the percentage of maximal precontraction induced by isotonic 60 mM KCl. N indicates the number of descending thoracic aortic rings. ∗P < 0.001, †P < 0.01, and #P < 0.05 versus control.

Mentions: Lipofundin MCT/LCT (0.1 and 0.2%) increased phenylephrine-induced maximal contraction in isolated endothelium-intact aorta (P < 0.01 versus control; Figure 5).


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

Ok SH, Lee SH, Yu J, Park J, Shin IW, Lee Y, Cho H, Choi MJ, Baik J, Hong JM, Han JY, Lee HK, Chung YK, Sohn JT - Biomed Res Int (2015)

Effect of Lipofundin MCT/LCT (0.1 or 0.2%) on the phenylephrine dose-response curves in isolated endothelium-intact aorta. Data (N = 8) are the mean ± SD and are expressed as the percentage of maximal precontraction induced by isotonic 60 mM KCl. N indicates the number of descending thoracic aortic rings. ∗P < 0.001, †P < 0.01, and #P < 0.05 versus control.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4530220&req=5

fig5: Effect of Lipofundin MCT/LCT (0.1 or 0.2%) on the phenylephrine dose-response curves in isolated endothelium-intact aorta. Data (N = 8) are the mean ± SD and are expressed as the percentage of maximal precontraction induced by isotonic 60 mM KCl. N indicates the number of descending thoracic aortic rings. ∗P < 0.001, †P < 0.01, and #P < 0.05 versus control.
Mentions: Lipofundin MCT/LCT (0.1 and 0.2%) increased phenylephrine-induced maximal contraction in isolated endothelium-intact aorta (P < 0.01 versus control; Figure 5).

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology and Pain Medicine, Gyeongsang National University Hospital, Gyeongsang National University School of Medicine, Jinju 660-715, Republic of Korea.

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.

No MeSH data available.


Related in: MedlinePlus