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脂肪乳剂而非丙泊酚可诱导骨骼肌损伤和脂质过氧化。

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

机构信息

Department of Anesthesiology, Sapporo Medical University School of Medicine, 291, South 1, West 16, Chuo-ku, Sapporo, Hokkaido, Japan.

出版信息

J Anesth. 2019 Dec;33(6):628-635. doi: 10.1007/s00540-019-02676-8. Epub 2019 Aug 31.

Abstract

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.

摘要

目的

持续输注丙泊酚会导致骨骼肌损伤。然而,众所周知,丙泊酚的溶剂——脂乳剂,会通过脂质过氧化导致各种类型的组织损伤,而丙泊酚则具有抗脂质过氧化作用。本研究旨在确定是丙泊酚还是脂乳剂是导致长时间输注后肌肉损伤的原因。

方法

将大鼠分为四组:NI 组(无干预)、Cath 组(仅静脉导管插入)、Prop 组(1%丙泊酚(Maruishi)静脉输注,剂量为 10mg/kg/h)和 Lipid 组(10%脂肪乳剂(Lipofundin®)静脉输注,剂量为 100mg/kg/h)(n=10,每组)。1%丙泊酚(Maruishi)或脂肪乳剂以 1mL/kg/h 的速度输注 72h。1%丙泊酚(Maruishi)的溶剂为 10%脂乳剂。脂肪乳剂由 50%长链三酰甘油和 50%中链三酰甘油组成,与丙泊酚溶剂相似。干预 72h 后,评估血浆肌酸激酶和肌红蛋白浓度、超氧化物产生水平以及腓肠肌中 4-羟基壬烯醛和丙二醛的表达。

结果

脂质组的血浆肌酸激酶和肌红蛋白浓度明显高于其他三组。脂质组的超氧化物产生水平以及 4-羟基壬烯醛和丙二醛的表达也明显高于其他三组。

结论

脂肪乳剂通过脂质过氧化导致骨骼肌损伤,而 1%丙泊酚(Maruishi)则通过抗氧化作用抑制肌肉损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b900/6874638/48842d6d65cb/540_2019_2676_Fig1_HTML.jpg

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