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Int J Biol Sci 2014; 10(4):367-376. doi:10.7150/ijbs.8048

Research Paper

Systemic Blockage of Nitric Oxide Synthase by L-NAME Increases Left Ventricular Systolic Pressure, Which Is Not Augmented Further by Intralipid®

Il-Woo Shin1, Young-Sool Hah2, Cheol Kim3, Jungchul Park4, Heewon Shin5, Kyeong-Eon Park4, Seong-Ho Ok1, Heon-Keun Lee1, Young-Kyun Chung1, Haeng Seon Shim6, Dong Hoon Lim7, Ju-Tae Sohn1✉

1. Department of Anesthesiology and Pain Medicine, Gyeongsang National University Hospital, Institute of Health Sciences, Gyeongsang National University School of Medicine, Jinju, Korea;
2. Clinical Research Institute, Gyeongsang National University Hospital, Jinju, Korea;
3. Department of Anesthesiology and Pain Medicine, Gyeongsang National University School of Medicine, Jinju, Korea;
4. Department of Anesthesiology and Pain Medicine, Gyeongsang National University Hospital, Jinju, Korea;
5. Department of Biological Sciences, California State University, Long Beach, California, USA;
6. Department of Anesthesiology and Pain Medicine, Samsung Changwon Hospital, Sungkyunkwan University School of Medicine, Changwon, Korea;
7. Department of Information Statistics and RINS, Gyeongsang National University, Jinju, 660-701, Korea.

Abstract

Intravenous lipid emulsions (LEs) are effective in the treatment of toxicity associated with various drugs such as local anesthetics and other lipid soluble agents. The goals of this study were to examine the effect of LE on left ventricular hemodynamic variables and systemic blood pressure in an in vivo rat model, and to determine the associated cellular mechanism with a particular focus on nitric oxide. Two LEs (Intralipid® 20% and Lipofundin® MCT/LCT 20%) or normal saline were administered intravenously in an in vivo rat model following induction of anesthesia by intramuscular injection of tiletamine/zolazepam and xylazine. Left ventricular systolic pressure (LVSP), blood pressure, heart rate, maximum rate of intraventricular pressure increase, and maximum rate of intraventricular pressure decrease were measured before and after intravenous administration of various doses of LEs or normal saline to an in vivo rat with or without pretreatment with the non-specific nitric oxide synthase inhibitor Nω-nitro-L-arginine-methyl ester (L-NAME). Administration of Intralipid® (3 and 10 ml/kg) increased LVSP and decreased heart rate. Pretreatment with L-NAME (10 mg/kg) increased LSVP and decreased heart rate, whereas subsequent treatment with Intralipid® did not significantly alter LVSP. Intralipid® (10 ml/kg) increased mean blood pressure and decreased heart rate. The increase in LVSP induced by Lipofundin® MCT/LCT was greater than that induced by Intralipid®. Intralipid® (1%) did not significantly alter nitric oxide donor sodium nitroprusside-induced relaxation in endothelium-denuded rat aorta. Taken together, systemic blockage of nitric oxide synthase by L-NAME increases LVSP, which is not augmented further by intralipid®.

Keywords: lipid emulsion, left ventricular systolic pressure, blood pressure, nitric oxide, L-NAME.

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How to cite this article:
Shin IW, Hah YS, Kim C, Park J, Shin H, Park KE, Ok SH, Lee HK, Chung YK, Shim HS, Lim DH, Sohn JT. Systemic Blockage of Nitric Oxide Synthase by L-NAME Increases Left Ventricular Systolic Pressure, Which Is Not Augmented Further by Intralipid®. Int J Biol Sci 2014; 10(4):367-376. doi:10.7150/ijbs.8048. Available from http://www.ijbs.com/v10p0367.htm