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Lipid emulsion, but not propofol, induces skeletal muscle damage and lipid peroxidation

PURPOSE: Prolonged propofol infusion induces skeletal muscle damage. However, it is well known that the lipid emulsion that is the solvent of propofol causes various types of tissue damage via lipid peroxidation, and that propofol, conversely, has an anti-lipid peroxidative effect. The purpose of th...

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Autores principales: Chaki, Tomohiro, Hirata, Naoyuki, Yoshikawa, Yusuke, Tachibana, Shunsuke, Tokinaga, Yasuyuki, Yamakage, Michiaki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Japan 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6874638/
https://www.ncbi.nlm.nih.gov/pubmed/31473808
http://dx.doi.org/10.1007/s00540-019-02676-8
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author Chaki, Tomohiro
Hirata, Naoyuki
Yoshikawa, Yusuke
Tachibana, Shunsuke
Tokinaga, Yasuyuki
Yamakage, Michiaki
author_facet Chaki, Tomohiro
Hirata, Naoyuki
Yoshikawa, Yusuke
Tachibana, Shunsuke
Tokinaga, Yasuyuki
Yamakage, Michiaki
author_sort Chaki, Tomohiro
collection PubMed
description PURPOSE: Prolonged propofol infusion induces skeletal muscle damage. However, it is well known that the lipid emulsion that is the solvent of propofol causes various types of tissue damage via lipid peroxidation, and that propofol, conversely, has an anti-lipid peroxidative effect. The purpose of this study was to determine whether propofol or the lipid emulsion is the cause of muscle damage following prolonged administration. METHODS: Rats were divided into four groups: NI group (no intervention), Cath group (venous catheter insertion only), Prop group (1% propofol (Maruishi) intravenous infusion at 10 mg/kg/h), and Lipid group (10% Lipofundin® intravenous infusion at 100 mg/kg/h) (n = 10, each group). 1% Propofol (Maruishi) or Lipofundin was infused at 1 mL/kg/h for 72 h. The solvent of 1% propofol (Maruishi) is a 10% lipid emulsion. Lipofundin consists of 50% long-chain triacylglycerols and 50% medium-chain triacylglycerols, similar to the propofol solvent. Plasma concentrations of creatine kinase and myoglobin, superoxide production level, and 4-hydroxynonenal and malondialdehyde expression in the gastrocnemius muscle were evaluated 72 h after the interventions. RESULTS: Plasma concentrations of creatine kinase and myoglobin in the Lipid group were significantly higher than those in the other three groups. The superoxide production level, and 4-hydroxynonenal and malondialdehyde expression in the Lipid group were also significantly higher than in the other three groups. CONCLUSION: Lipofundin induces skeletal muscle damage via lipid peroxidation, and 1% propofol (Maruishi) conversely suppresses the muscle damage via antioxidant effects.
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spelling pubmed-68746382019-12-06 Lipid emulsion, but not propofol, induces skeletal muscle damage and lipid peroxidation Chaki, Tomohiro Hirata, Naoyuki Yoshikawa, Yusuke Tachibana, Shunsuke Tokinaga, Yasuyuki Yamakage, Michiaki J Anesth Original Article PURPOSE: Prolonged propofol infusion induces skeletal muscle damage. However, it is well known that the lipid emulsion that is the solvent of propofol causes various types of tissue damage via lipid peroxidation, and that propofol, conversely, has an anti-lipid peroxidative effect. The purpose of this study was to determine whether propofol or the lipid emulsion is the cause of muscle damage following prolonged administration. METHODS: Rats were divided into four groups: NI group (no intervention), Cath group (venous catheter insertion only), Prop group (1% propofol (Maruishi) intravenous infusion at 10 mg/kg/h), and Lipid group (10% Lipofundin® intravenous infusion at 100 mg/kg/h) (n = 10, each group). 1% Propofol (Maruishi) or Lipofundin was infused at 1 mL/kg/h for 72 h. The solvent of 1% propofol (Maruishi) is a 10% lipid emulsion. Lipofundin consists of 50% long-chain triacylglycerols and 50% medium-chain triacylglycerols, similar to the propofol solvent. Plasma concentrations of creatine kinase and myoglobin, superoxide production level, and 4-hydroxynonenal and malondialdehyde expression in the gastrocnemius muscle were evaluated 72 h after the interventions. RESULTS: Plasma concentrations of creatine kinase and myoglobin in the Lipid group were significantly higher than those in the other three groups. The superoxide production level, and 4-hydroxynonenal and malondialdehyde expression in the Lipid group were also significantly higher than in the other three groups. CONCLUSION: Lipofundin induces skeletal muscle damage via lipid peroxidation, and 1% propofol (Maruishi) conversely suppresses the muscle damage via antioxidant effects. Springer Japan 2019-08-31 2019 /pmc/articles/PMC6874638/ /pubmed/31473808 http://dx.doi.org/10.1007/s00540-019-02676-8 Text en © The Author(s) 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Original Article
Chaki, Tomohiro
Hirata, Naoyuki
Yoshikawa, Yusuke
Tachibana, Shunsuke
Tokinaga, Yasuyuki
Yamakage, Michiaki
Lipid emulsion, but not propofol, induces skeletal muscle damage and lipid peroxidation
title Lipid emulsion, but not propofol, induces skeletal muscle damage and lipid peroxidation
title_full Lipid emulsion, but not propofol, induces skeletal muscle damage and lipid peroxidation
title_fullStr Lipid emulsion, but not propofol, induces skeletal muscle damage and lipid peroxidation
title_full_unstemmed Lipid emulsion, but not propofol, induces skeletal muscle damage and lipid peroxidation
title_short Lipid emulsion, but not propofol, induces skeletal muscle damage and lipid peroxidation
title_sort lipid emulsion, but not propofol, induces skeletal muscle damage and lipid peroxidation
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6874638/
https://www.ncbi.nlm.nih.gov/pubmed/31473808
http://dx.doi.org/10.1007/s00540-019-02676-8
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