异氟烷对心肌损伤的作用  

Isoflurane and Myocardial Injury

作　　者：张彬[1] 单士强[1] 

机构地区：[1]沧州市中心医院麻醉科,河北沧州061001

出　　处：《医学综述》2013年第4期650-652,共3页Medical Recapitulate

摘　　要：异氟烷可作用于KATP通道,舒张冠状动脉血管,增加冠状动脉血流速率和流量。细胞膜是心肌抵御损伤的第一道防线,异氟烷可与L型钙通道结合,减少钙内流,降低氧自由基对细胞骨架结构的破坏。异氟烷还可有效抑制线粒体膜通透转换孔道开放,抑制凋亡蛋白的表达,从而减少心肌细胞的凋亡。现探讨异氟烷降低心肌损伤,改善心功能的机制。Isoflurane can act on the KATP channel, dialate coronary artery and increase coronary blood rate and flow. Membrane is the first line of defense against injury of myocardium. Isoflurane could bind with the L type calcium channel of myocardium, reducing calcium influx, and oxygen free radicals on cytoskeletal structure damage. Isoflurane can also effectively inhibit mitochondrlal membrane permeability transition pore opening, inhibit the expression of apoptosis proteins, thereby reducing the myocardial cell apoptosis. Here is to explore the mechanism of isoflurane reducing myocardial injury and improving myocardium function.

关 键 词：异氟烷 心肌损伤 ATP敏感钾通道 膜通透转换孔道 凋亡 

分 类 号：R969[医药卫生—药理学]