体外脂肪乳剂呈浓度和时间依赖性恢复布比卡因诱导停博心脏的收缩功能
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Intralipid Restoration of Myocardial Contractions Following Bupivacaine-Induced Asystole: Concentration- and Time-Dependence In Vitro.
背景与目的
脂肪乳剂（LE）呈浓度和时间性恢复布比卡因（BPV）诱导停博心脏的收缩功能的关系有待验证。
方 法
观察500uM BPV诱发心脏骤停后1.2 HZ 刺激频率时，不同浓度LE处理下豚鼠心肌的收缩反应和收缩恢复情况。所有涉及LE的实验均采用持续60min的循环（2%-16%）处理模型或非循环（0.05%-12%）处理模型。本实验检测了单纯LE制剂（0.05%-12%）对心脏的影响，并通过检测羟苯甘氨酸水平评价LE恢复停博心脏代谢反应的作用，同时也检测了溶液和心肌组织中BPV的浓度.
结 果
持续60min LE循环（2%-16%）处理时，应用4%和8%以及12% 浓度的LE均能部分恢复停博豚鼠心脏的收缩力，而相同的心肌应用16%浓度LE能出现肌痉挛。在非循环（0.05%-12%）处理模型实验结果显示LE（0.05%-12%）并不影响停博心肌首次恢复心脏收缩和完全恢复心脏收缩的时间。此外，本研究结果显示LE（0.1%-8%）处理45min后能完全恢复停博心脏的初始收缩能力，低浓度（0.05%）和高浓度（12%）的LE处理均能部分恢复停博心脏的收缩能力；羟苯甘氨酸水平并未影响停博心脏收缩能力的恢复；单纯的12% LE处理能削弱心脏的收缩能力；LE循环（2%-16%）处理模型中LE呈剂量依赖性的减少了心肌组织中BPV的浓度。
结 论
LE呈时间依赖性和浓度依赖性的恢复BPV诱发的停博心脏收缩力。脂质的再摄取作用和LE其它的不清楚机制可能与其恢复停博心脏收缩功能有关，但似乎LE可能并不影响500uM BPV剂量诱发的停博心肌代谢。
原始文献摘要
Park W K, Kim H S, Kim S H, et al. Intralipid Restoration of Myocardial Contractions Following Bupivacaine-Induced Asystole: Concentration- and Time-Dependence In Vitro.[J]. Anesthesia and analgesia, 2017,125(1):91-100. DOI:10.1213/ANE.0000000000002124
BACKGROUND: The concentration- and time-response relationships of lipid emulsion (LE; Intralipid) on the recovery of myocardial contractility following bupivacaine (BPV)-induced asystole are poorly defined.
METHODS: After achieving asystole by 500-muM BPV, varied concentrations of LE were applied to determine the recovery of stimulated contractile responses and contractions in the cardiac tissues of guinea pigs at a 1.2-Hz stimulation rate. These experiments were performed with LE in either a recirculating (2%-16%) or washout (nonrecirculating) condition (0.05%-12%) for 60 minutes. The effect of LE itself (0.05%-12%) was examined. Oxfenicine was used to evaluate the metabolic action of LE to reverse asystole. BPV concentrations in solution and myocardial tissues were measured.
RESULTS: In the recirculation condition, partial recovery of contractile forces was observed for 60 minutes at 4%, 8%, and 12% LE. A contracture followed after exposure to 16% LE in some asystolic muscles. In the washout experiments, following asystole, LE (0.05%-12%) had no effect on the recovery time of the first and regular contractile responses. LE (0.1%-8%) restored contractility to baseline levels after 45 minutes; partial recovery was shown with lower (0.05%) and higher (12%) concentrations. Oxfenicine did not alter the recovery of contractile forces. Contractile depression was observed with 12% LE alone. Concentration-related reduction of tissue BPV concentration by LE was observed in both circulating conditions.
CONCLUSIONS: LE induced time- and concentration-dependent recovery of stimulated myocardial contractions from BPV-induced asystole. The lipid uptake effect, along with other undefined mechanisms of LE, seems to contribute to the recovery of contractile function; however, the LE effect on myocardial metabolism is less likely involved at this concentration (500 muM) of BPV.
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