中文摘要：

本文旨在研究线粒体ATP敏感性钾（mitochondrial ATP-sensitive potassium channel，mitoKAav）通道开放剂二氮嗪（diazoxide，DE）对离体长时程低温保存的大鼠心脏促凋亡蛋白Fas和FasL表达的影响。利用Langendorff离体大鼠心脏灌注法，观察心脏在4℃含或不含（对照组）DE的Celsior保存液保存8h后，复灌期心脏作功量（rate-pressure product，RPP）变化情况，采用原位末端标记（TdT-mediated dUTP nick end labeling，TUNEL）染色法检测心肌细胞凋亡和免疫组织化学方法检测Fas和FasL蛋白表达情况。结果显示，在Celsior保存液中加入DE（30μmol／L），复灌期RPP的恢复率在多个复灌时间点上优于对照组；同时可降低长时程低温保存心脏心肌细胞凋亡指数，减少Fas和FasL蛋白的表达。DE的上述作用可被mitoKATP通道特异性阻断剂5-羟基葵酸盐（5-hydroxydecanoate，5-HD）所取消。以上结果提示，DE可能通过激活mitoKATP通道来减少Fas和FasL蛋白表达，从而减轻大鼠心肌缺血，再灌注损伤后的心肌细胞凋亡。

英文摘要：

The purpose of this study was to investigate the effect of a mitochondrial ATP-sensitive potassium channel （mitoKATP） opener, diazoxide （DE）, on Fas/FasL protein expressions in rat heart suffered from long-term hypothermic preservation. The Langendorff isolated rat heart model was used. The hearts were stored in 4℃ Celsior solution with or without （control） DE for 8 h followed by 60 min of reperfusion. The recovery of rate-pressure product （RPP） was observed. Apoptotic cardiomyocytes were detected by TdTmediated dUTP nick end labeling （TUNEL） technique. The expressions of Fas/FasL proteins were also analyzed by immunohistochemical method. The results showed that compared with the control group, DE （30 mmol/L） increased the recovery of RPP during reperfusion, reduced the percentage of apoptotic cells and the expressions of Fas and FasL proteins in rat hearts suffered from 8 h of hypothermic preservation. The above effects of DE were attenuated by a mitoKATP channel inhibitor 5-hydroxydecanoate （5-HD）. These results indicate that DE could alleviate rat myocardial injury induced by ischemia-repeffusion through reducing the expressions of Fas and FasL proteins via opening of mitoKATP channel.