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本文引用的文献

1
Emulsified isoflurane induces postconditioning against myocardial infarction via JAK-STAT pathway.乳化异氟醚通过 JAK-STAT 通路诱导心肌梗死后适应。
J Surg Res. 2012 Dec;178(2):578-85. doi: 10.1016/j.jss.2012.06.007. Epub 2012 Jun 21.
2
Phosphorylation of GSK-3β mediates intralipid-induced cardioprotection against ischemia/reperfusion injury.GSK-3β 的磷酸化介导脂肪乳剂诱导的缺血/再灌注损伤心肌保护作用。
Anesthesiology. 2011 Aug;115(2):242-53. doi: 10.1097/ALN.0b013e318223b8b9.
3
[The sedative and hypnotic effects and safety of oral emulsified isoflurane in rats].[大鼠口服乳化异氟烷的镇静催眠作用及安全性]
Sichuan Da Xue Xue Bao Yi Xue Ban. 2010 Sep;41(5):862-4, 887.
4
Cardioprotection afforded by St Thomas solution is enhanced by emulsified isoflurane in an isolated heart ischemia reperfusion injury model in rats.在大鼠离体心脏缺血再灌注损伤模型中,圣托马斯溶液提供的心脏保护作用通过乳化异氟醚得到增强。
J Cardiothorac Vasc Anesth. 2010 Feb;24(1):99-103. doi: 10.1053/j.jvca.2009.10.016.
5
[The optimal concentration for the protective effect of emulsified isoflurane on the neonatal rat cardiac myocytes hypoxia/reoxygenation injury of primary culture].[乳化异氟醚对原代培养新生大鼠心肌细胞缺氧/复氧损伤保护作用的最佳浓度]
Sichuan Da Xue Xue Bao Yi Xue Ban. 2009 Nov;40(6):1075-7, 1090.
6
Isoflurane postconditioning protects against reperfusion injury by preventing mitochondrial permeability transition by an endothelial nitric oxide synthase-dependent mechanism.异氟烷后处理通过内皮型一氧化氮合酶依赖性机制防止线粒体通透性转换,从而防止再灌注损伤。
Anesthesiology. 2010 Jan;112(1):73-85. doi: 10.1097/ALN.0b013e3181c4a607.
7
Mechanism of cardiac preconditioning with volatile anaesthetics.挥发性麻醉药心脏预处理的机制
Anaesth Intensive Care. 2009 Jul;37(4):532-8. doi: 10.1177/0310057X0903700402.
8
The protective effects of emulsified isoflurane on myocardial ischemia and reperfusion injury in rats.乳化异氟醚对大鼠心肌缺血再灌注损伤的保护作用。
Can J Anaesth. 2009 Feb;56(2):115-25. doi: 10.1007/s12630-008-9016-3. Epub 2008 Dec 31.
9
Effects of emulsified isoflurane on haemodynamics and cardiomyocyte apoptosis in rats with myocardial ischaemia.乳化异氟醚对心肌缺血大鼠血液动力学和心肌细胞凋亡的影响。
Clin Exp Pharmacol Physiol. 2009 Aug;36(8):776-83. doi: 10.1111/j.1440-1681.2009.05138.x. Epub 2009 Jan 17.
10
Postconditioning by volatile anesthetics: salvaging ischemic myocardium at reperfusion by activation of prosurvival signaling.挥发性麻醉药后处理:通过激活生存信号通路挽救再灌注时的缺血心肌。
J Cardiothorac Vasc Anesth. 2008 Oct;22(5):753-65. doi: 10.1053/j.jvca.2008.03.005. Epub 2008 May 27.

乳化异氟醚后处理对大鼠心肌缺血再灌注损伤产生心脏保护作用。

Emulsified isoflurane postconditioning produces cardioprotection against myocardial ischemia-reperfusion injury in rats.

机构信息

Department of Anesthesiology and Translational Neuroscience Center, West China Hospital, Sichuan University, Chengdu 610041, People's Republic of China.

出版信息

J Physiol Sci. 2013 Jul;63(4):251-61. doi: 10.1007/s12576-013-0261-z. Epub 2013 Apr 27.

DOI:10.1007/s12576-013-0261-z
PMID:23625523
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10717228/
Abstract

Emulsified isoflurane (EIso) preconditioning can induce cardioprotection. We investigated whether EIso application after ischemia protects hearts against reperfusion injury and whether it is mediated by the inhibition of apoptosis. Rats were subjected to 30-min coronary occlusion followed by 180-min reperfusion. At the onset of reperfusion, rats were intravenously administered saline (sham, control group), 30 % intralipid (IL group) or 2 ml kg(-1) EIso (EIso group) for 30 min. After reperfusion, infarct sizes, myocardial apoptosis and expression of Bcl-2, Bax and caspase-3 proteins were determined. Hemodynamic parameters were not different among groups. Compared with control and intralipid group, EIso limited infarct size, inhibited apoptosis, increased the expression of Bcl-2, decreased the expression of Bax, cleaved caspase-3, and enhanced Bcl-2/Bax ratio. EIso protects hearts against reperfusion injury when administered at the onset of reperfusion, which may be mediated by the inhibition of apoptosis via modulation of the expression of pro- and anti-apoptotic proteins.

摘要

乳化异氟醚(EIso)预处理可诱导心脏保护。我们研究了缺血后应用 EIso 是否能保护心脏免受再灌注损伤,以及它是否通过抑制细胞凋亡来介导。大鼠进行 30 分钟的冠状动脉闭塞,然后进行 180 分钟的再灌注。在再灌注开始时,大鼠静脉注射生理盐水(假手术,对照组)、30%脂肪乳剂(IL 组)或 2mlkg(-1)EIso(EIso 组)30 分钟。再灌注后,测定梗死面积、心肌凋亡以及 Bcl-2、Bax 和 caspase-3 蛋白的表达。各组血流动力学参数无差异。与对照组和脂肪乳剂组相比,EIso 可限制梗死面积、抑制凋亡、增加 Bcl-2 表达、降低 Bax 表达、切割 caspase-3,并增强 Bcl-2/Bax 比值。EIso 在再灌注开始时给药可保护心脏免受再灌注损伤,这可能是通过调节促凋亡和抗凋亡蛋白的表达来抑制细胞凋亡介导的。