中文摘要：

目的研究七氟烷后处理对离体大鼠心肌细胞凋亡蛋白表达的影响。方法雄性SD大鼠30只，体重230—250g，使用随机数字表法将实验动物随机分为3组（n=10）：假手术组，缺血再灌注组（I／R组），七氟烷后处理组（SPC组）。采用Langendroff离体心脏灌注模型，除假手术组外其余两组平衡灌注30min，全心缺血40min，再灌注120min。SPC组在再灌注即刻给予2．5％（约1．0MAC）七氟烷10min后改用普通Krebs-Henseleit（K—H）液灌注。记录平衡灌注末，再灌注30、60、90、120min时左室收缩压（LVSP）、左室舒张末压（LVEDP）、左室发展压（LVDP）、左室内压上升最大速率（＋dp／dt）、左室内压下降最大速率（-dp／dt）、心率（HR）以及冠脉流量（CF）。分光光度法测量肌酸激酶（CK）和乳酸脱氢酶（LDH）。再灌注末1Trc染色法测定心肌梗死面积。Western印迹法测定凋亡蛋白Bcl-2、Bax表达情况。结果SPC组LVSP、LVDP、±dp／dt和CF在再灌注30rain后各时点均高于I／R组（均P〈0．05），LVEDP均低于I／R组（均P〈0．05）；HR较I／R组高，但差异无统计学意义（P〉0．05）。SPC组LDH和CK释放量均低于I／R组（均P〈0．05），梗死面积低于I／R组（22．2％±2．8％比44．9％±6．6％，P〈0．05）。与I／R组比较，SPC组Bcl-2表达高，Bax表达低（均P〈0．05）。结论七氟烷后处理可改善心功能，降低心肌梗死面积，通过调节凋亡蛋白表达减轻离体大鼠心肌细胞凋亡。

英文摘要：

Objective To explore the effects of sevoflurane postconditioning on ischemic/reperfused myocardial apoptosis. Methods Isolated perfused rat hearts were randomly assigned into 3 groups： shamoperation （sham）, ischemia/reperfusion （I/R） and sevoflurane postconditioning （SPC）. Except for the sham group, the hearts were subjected to 40 mix global myocardial ischemia and 120 mix reperfusion. Left ventricular systolic pressure （LVSP） , left ventricular developed pressure （LVDP） , left ventrieular end- diastolic pressure （LVEDP） , maximum increase rate of LVDP （ ＋ dp/dt） , maximum decrease rate of LVDP （ -dp/dt）, heart rate （HR） and coronary flow （CF） were measured at baseline, R （reperfusion） 30 mix, R60 mix, Rgo mix and R120 mix. Creatine kinase （CK） and lactate dehydrogenase （LDH） were measured at 5 mix and 10 min post-reperfusion. Infarct size was determined by triphenyltetrazolium chloride staining at the end of reperfusion. The expressions of Bcl-2 and Bax were determined by Western blot. Results The values of LVSP, LVDP, ＋ dp/dt and CF were higher while that of LVEDP was lower in the SPC group than the L/R group at all time points of reperfusion （ P 〈 0. 05 ）. The releases of CK and LDH and infarct size were significantly reduced in the SPC group versus the I/R group （22. 2% ±2. 8% vs I/R： 44.9% 6. 6%, P 〈 0.05 ）. The expression of Bcl-2 increased significantly while that of Bax decreased in the SPC group verus the I/R group. Conclusion Sevoflurane postconditioning may improve myocardial functions, reduce infarct size and attenuate myocardial apoptosis. And the modulated expression of apoptotic proteins plays an important role in sevoflurane-indueed myocardial protection.