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脂质乳剂可逆转毒性剂量布比卡因在离体大鼠主动脉酪氨酸磷酸化诱发收缩过程中引起的血管舒张。

A Lipid Emulsion Reverses Toxic-Dose Bupivacaine-Induced Vasodilation during Tyrosine Phosphorylation-Evoked Contraction in Isolated Rat Aortae.

作者信息

Ok Seong-Ho, Lee Soo Hee, Kwon Seong-Chun, Choi Mun Hwan, Shin Il-Woo, Kang Sebin, Park Miyeong, Hong Jeong-Min, Sohn Ju-Tae

机构信息

Department of Anesthesiology and Pain Medicine, Gyeongsang National University School of Medicine, Gyeongsang National University Hospital, 79 Gangnam-ro, Jinju 52727, Korea.

Department of Physiology, Institute of Clinical and Translational Research, Catholic Kwandong University, College of Medicine, Gangneung 25601, Korea.

出版信息

Int J Mol Sci. 2017 Feb 13;18(2):394. doi: 10.3390/ijms18020394.

DOI:10.3390/ijms18020394
PMID:28208809
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5343929/
Abstract

The goal of this in vitro study was to examine the effect of a lipid emulsion on toxic-dose bupivacaine-induced vasodilation in a model of tyrosine phosphatase inhibitor sodium orthovanadate-induced contraction in endothelium-denuded rat aortae and to elucidate the associated cellular mechanism. The effect of a lipid emulsion on vasodilation induced by a toxic dose of a local anesthetic during sodium orthovanadate-induced contraction was examined. In addition, the effects of various inhibitors, either bupivacaine alone or a lipid emulsion plus bupivacaine, on protein kinase phosphorylation induced by sodium orthovanadate in rat aortic vascular smooth muscle cells was examined. A lipid emulsion reversed the vasodilation induced by bupivacaine during sodium orthovanadate-induced contraction. The lipid emulsion attenuated the bupivacaine-mediated inhibition of the sodium orthovanadate-induced phosphorylation of protein tyrosine, c-Jun NH₂-terminal kinase (JNK), myosin phosphatase target subunit 1 (MYPT1), phospholipase C (PLC) γ-1 and extracellular signal-regulated kinase (ERK). These results suggest that a lipid emulsion reverses toxic-dose bupivacaine-induced vasodilation during sodium orthovanadate-induced contraction via the activation of a pathway involving either tyrosine kinase, JNK, Rho-kinase and MYPT1 or tyrosine kinase, PLC γ-1 and ERK, and this reversal is associated with the lipid solubility of the local anesthetic and the induction of calcium sensitization.

摘要

本体外研究的目的是在原钒酸钠诱导去内皮大鼠主动脉收缩的模型中，研究脂质乳剂对毒性剂量布比卡因诱导的血管舒张的影响，并阐明相关的细胞机制。研究了脂质乳剂对原钒酸钠诱导收缩过程中由毒性剂量局部麻醉药诱导的血管舒张的影响。此外，还研究了各种抑制剂，单独使用布比卡因或脂质乳剂加布比卡因，对原钒酸钠诱导的大鼠主动脉血管平滑肌细胞蛋白激酶磷酸化的影响。脂质乳剂可逆转原钒酸钠诱导收缩过程中布比卡因诱导的血管舒张。脂质乳剂减弱了布比卡因介导的对原钒酸钠诱导的蛋白酪氨酸、c-Jun氨基末端激酶（JNK）、肌球蛋白磷酸酶靶向亚基1（MYPT1）、磷脂酶C（PLC）γ-1和细胞外信号调节激酶（ERK）磷酸化的抑制作用。这些结果表明，脂质乳剂通过激活涉及酪氨酸激酶、JNK、Rho激酶和MYPT1或酪氨酸激酶、PLCγ-1和ERK的途径，逆转原钒酸钠诱导收缩过程中毒性剂量布比卡因诱导的血管舒张，并且这种逆转与局部麻醉药的脂溶性和钙敏化的诱导有关。

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