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利多卡因消除了七氟醚后处理的心肌保护作用。

Lidocaine abolishes the myocardial protective effect of sevoflurane post-conditioning.

作者信息

Yan M, Chen C, Zhang F, Chen G

机构信息

Department of Anesthesiology, Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.

出版信息

Acta Anaesthesiol Scand. 2008 Jan;52(1):111-6. doi: 10.1111/j.1399-6576.2007.01487.x. Epub 2007 Nov 8.

Abstract

BACKGROUND

Post-ischemic administration of volatile anesthetics activates ischemia-reperfusion injury salvage process and decreases myocardial damage. However, the mechanisms underlying anesthetic post-conditioning and effects of lidocaine on it remain unclear. Here we report the cardioprotection of sevoflurane-induced post-conditioning and the effects of lidocaine on it.

METHODS

Isolated perfused rat hearts were exposed to 40 min of ischemia followed by 1 h of reperfusion. Volatile anesthetic post-conditioning was induced by 15 min of 3 vol% sevourane (1.5 minimum alveolar concentration) administered at the onset of reperfusion. In some experiments, lidocaine was coadministered with sevoflurane in different concentrations (2, 10 and 20 microg/ml). Infarct size was determined by dividing the total necrotic area of the left ventricle by the total left ventricular slice area (percent necrotic area).

RESULTS

Sevoflurane-induced post-conditioning signicantly improved post-ischemia functional recovery and decreased infarct size (47.3+/-5.6% in unprotected hearts vs. 18.6+/-3.1% in anesthetic post-conditioning, P<0.05). Sevourane-mediated cardioprotection was abolished by 20 microg/ml lidocaine.

CONCLUSIONS

Sevourane-induced post-conditioning effectively protected myocardium against reperfusion damage and its cytoprotection was reversed by 20 microg/ml lidocaine.

摘要

背景

挥发性麻醉剂在缺血后给药可激活缺血再灌注损伤挽救过程并减少心肌损伤。然而,麻醉后处理的潜在机制以及利多卡因对其的影响仍不清楚。在此,我们报告七氟烷诱导的后处理的心脏保护作用以及利多卡因对其的影响。

方法

将离体灌注的大鼠心脏暴露于40分钟缺血,随后再灌注1小时。在再灌注开始时给予15分钟的3%七氟烷(1.5最低肺泡浓度)诱导挥发性麻醉剂后处理。在一些实验中,将不同浓度(2、10和20微克/毫升)的利多卡因与七氟烷共同给药。通过将左心室的总坏死面积除以左心室切片总面积(坏死面积百分比)来确定梗死面积。

结果

七氟烷诱导的后处理显著改善缺血后功能恢复并减小梗死面积(未保护心脏中为47.3±5.6%,麻醉后处理中为18.6±3.1%,P<0.05)。20微克/毫升的利多卡因消除了七氟烷介导的心脏保护作用。

结论

七氟烷诱导的后处理有效保护心肌免受再灌注损伤,其细胞保护作用被20微克/毫升的利多卡因逆转。

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