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作 者:York A. Zausig, MD, DEAA Wolfgang Zink, MD, DEAA Meike Keil, MS Barbara Sinner, MD, DEAA Juergen Barwing, MD, DEAA Christoph H. R. Wiese, MD Bernhard M. Graf, MD, MSc 周全红(译)
机构地区:[1]Department of Anaesthesiology, University of Regensburg, Regensburg [2]Department of Anaesthesiology, Emergency and Intensive Care Medicine, University of Goettingen, Goettingen, Germany [3]不详
出 处:《麻醉与镇痛》2011年第5期15-19,共5页Anesthesia & Analgesia
摘 要:背景局麻药(10calanesthetics,LAs)的心肌毒性与其亲脂性有显著的相关性。近来的临床报道发现输注脂肪乳剂是治疗局麻药引起的心跳骤停的一种好方法。人们假设其作用机制是“脂肪库”(1ipidsink)效应,该效应的强度可能取决于局麻药的亲脂性。本研究探讨是否脂肪效应与所使用的局麻药有关。方法用等效剂量的布比卡因、罗哌卡因和甲哌卡因使离体鼠心脏骤停,之后给予或不给予心脏灌注脂肪乳剂(0.25ml·k^-1·min^-1)进行复苏。监测指标包括从开始输注脂肪乳剂到心肌活动出现的时间、心率恢复的时间和心率一压力乘积恢复到基础值90%的时间。结果输注脂肪乳剂对各组的心肌活动恢复时间均没有作用。但是,输注脂肪乳剂可以显著缩短布比卡因组中心率恢复时间和心率-压力乘积恢复到基础值90%的时间,而在罗哌卡因和甲哌卡因组中却没有这个结果。结论以上的数据表明脂肪乳剂解救局麻药引起的心跳骤停的效果取决于不同的局麻药。我们认为局麻药的亲脂性对使用脂肪乳剂治疗因局麻药引起的心跳骤停的效果有显著影响。BACKGROUND: Cardiac toxicity significantly correlates with the lipophilicity of local anesthetics (LAs). Recently, the infusion of lipid emulsions has been shown to be a promising approach to treat LA-induced cardiac arrest. As the postulated mechanism of action, the so-called "lipid sink" effect may depend on the lipophilicity of LAs. In this study, we investigated whether lipid effects differ with regard to the administered LAs. METHODS: In the isolated rat heart, cardiac arrest was induced by administration of equipotent doses of bupivacaine, ropivacaine, and mepivacaine, respectively, followed by cardiac perfusion with or without lipid emulsion (0. 25 ml· kg^-1 · min^-1 ). Subsequently, the times from the start of perfusion to return of first heart activity and to recovery of heart rate and rate-pressure product ( to 90% of baseline values) were assessed. RESULTS: In all groups, lipid infusion had no effects on the time to the return of any cardiac activi- ty. However, recovery times of heart rate and rate-pressure product (to 90% of baseline values) were significantly shorter with the administration of llpids in bupivacaine-induced cardiac toxicity, but not in ropivacaine-or mepivacaine-induced car- diac toxicity. CONCLUSIONS: These data show that the effects of lipid infusion on LA-induced cardiac arrest are strongly dependent on the administered LAs itself. We conclude that lipophilicity of LAs has a marked impact on the efficacy of lipid infusions to treat cardiac arrest induced by these drugs.
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