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七氟醚后处理对兔缺血再灌注损伤心肌保护作用的研究。

The effect of sevoflurane postconditioning on cardioprotection against ischemia-reperfusion injury in rabbits.

机构信息

Department of Anesthesiology, FuWai Cardiovascular Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beilishi Road, Xicheng District, Beijing, 100037, People's Republic of China.

出版信息

Mol Biol Rep. 2012 May;39(5):6049-57. doi: 10.1007/s11033-011-1419-5. Epub 2012 Jan 7.

DOI:10.1007/s11033-011-1419-5
PMID:22228087
Abstract

Sevoflurane postconditioning is a potential clinical measure to protect myocardial. This experiment was designed to investigate the efficacy of sevoflurane postconditioning against ischemia-reperfusion injury. A total of 132 Japanese White Rabbits were enrolled into this study. They were underwent 15-, 30-, or 60-min left anterior descending coronary (LAD) artery occlusion, respectively. At the end of LAD artery occlusion, they randomly received a 5-min inhalation of air (control group), 1% sevoflurane (1% sev group), 2% sevoflurane (2% sev group), 4% sevoflurane (4% sev group) or an IV bolus injection of 5 mg/kg of NIM811 [a specific inhibitor of mitochondrial permeability transition pores (mPTP)]. Infarct size was determined after 2 h of reperfusion (triphenyltetrazolium chloride straining, percentage of risk area). The infarct sizes were significantly (P < 0.05) reduced after 15 min ischemia (5.5 ± 3.3%, 5.8 ± 3.6% vs. 20.3 ± 6.9% for 2% sev, 4% sev vs. control, respectively) and 30 min ischemia (23.5 ± 5.0%, 20.7 ± 5.9% vs. 50.9 ± 10.2%, for 2% sev, 4% sev vs. control, respectively; P < 0.05). However, it had no effect on infarct size after 60 min ischemia (64.1 ± 5.9%, 62.3 ± 7.6% vs. 72.7 ± 9.2% for 2% sev, 4% sev vs. control, respectively, P > 0.05).The efficacy of sevoflurane postconditioning gradually weakened with increasing ischemia duration and disappears after 60 min ischemia in rabbits in vivo.

摘要

七氟醚后处理是一种保护心肌的潜在临床措施。本实验旨在研究七氟醚后处理对缺血再灌注损伤的疗效。共纳入 132 只日本大白兔,分别行 15、30 或 60min 左前降支(LAD)动脉闭塞。在 LAD 动脉闭塞结束时,它们随机接受 5min 空气吸入(对照组)、1%七氟醚(1% sev 组)、2%七氟醚(2% sev 组)、4%七氟醚(4% sev 组)或 5mg/kg NIM811(一种线粒体通透性转换孔(mPTP)的特异性抑制剂)静脉推注。再灌注 2h 后测定梗死面积(氯化三苯基四氮唑染色,危险区百分比)。15min 缺血后(2% sev、4% sev 组与对照组相比分别为 5.5±3.3%、5.8±3.6%和 20.3±6.9%)和 30min 缺血后(2% sev、4% sev 组与对照组相比分别为 23.5±5.0%、20.7±5.9%和 50.9±10.2%)梗死面积明显减少(P<0.05)。然而,60min 缺血后,它对梗死面积没有影响(2% sev、4% sev 组与对照组相比分别为 64.1±5.9%、62.3±7.6%和 72.7±9.2%)(P>0.05)。七氟醚后处理的疗效随缺血时间的延长而逐渐减弱,在兔体内 60min 缺血后消失。

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Enhanced glucose uptake via GLUT4 fuels recovery from calcium overload after ischaemia-reperfusion injury in sevoflurane- but not propofol-treated hearts.通过 GLUT4 增强葡萄糖摄取可促进七氟醚而非丙泊酚处理的心脏在缺血再灌注损伤后从钙过载中恢复。
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Cytoprotective effects of the volatile anesthetic sevoflurane are highly dependent on timing and duration of sevoflurane conditioning: findings from a human, in-vitro hypoxia model.挥发性麻醉剂七氟醚的细胞保护作用高度依赖于七氟醚预处理的时间和持续时间:来自人体体外缺氧模型的研究结果。
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七氟醚后处理通过蛋白激酶 B 和糖原合成酶激酶 3β的激活减轻缺血再灌注损伤。
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Sevoflurane postconditioning prevents activation of caspase 3 and 9 through antiapoptotic signaling after myocardial ischemia-reperfusion.七氟醚后处理通过抗凋亡信号转导防止心肌缺血再灌注后 caspase 3 和 9 的激活。
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Sevoflurane preconditioning at 1 MAC only provides limited protection in patients undergoing coronary artery bypass surgery: a randomized bi-centre trial.仅1个最低肺泡有效浓度的七氟醚预处理对接受冠状动脉搭桥手术的患者仅提供有限的保护:一项随机双中心试验。
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