大鼠心脏缺血预适应延迟保护模型的建立

Establishment of the Delayed Preconditioning Model Induced by Cardiac Ischemia in Rats

目的建立、评价大鼠在体心脏缺血预适应延迟保护模型。方法将24只雄性SD大鼠按随机数字表法分为3组,每组8只。缺血-再灌注组:大鼠结扎冠脉左前降支,缺血45 min后剪断结扎线再灌注3 h;假手术组:缺血-再灌注前24 h给大鼠行开胸手术,但不阻断冠脉血流;缺血预适应组:缺血-再灌注前24 h给大鼠行心脏缺血预适应,阻断冠脉左前降支造成心脏缺血3 min,再灌注5 min,反复4次。测定3组大鼠心肌梗死面积及血清肌酸激酶(CK)活性以评价心肌损伤的程度。结果缺血-再灌注组心肌梗死区面积为(0.18±0.03)cm2;缺血预适应组心肌梗死区面积为(0.11±0.02)cm2,2组比较差异有统计学意义(P<0.01),假手术则对心肌梗死面积则无显著影响。与缺血-再灌组比较,缺血预适应组能显著减少血清CK的释放(P<0.01),假手术则对血清CK水平无显著影响。结论已建立的大鼠心脏缺血预适应延迟保护模型具有显著的心肌保护作用,可为缺血预适应的研究提供稳定的在体模型。

Objective To establish and evaluate the delayed preconditioning model induced by cardiac ischemia in rats.Methods Twenty-four male Sprague-Dawley rats were divided into 3 groups,with 8 rats in each group.Rats in ischemia-reperfusion（I/R） group were subjected to 45 minutes of left anterior descending coronary artery ligation followed by 3 hours of reperfusion.Rats in sham operation group underwent the same procedure but without occlusion of coronary artery 24 hours before I/R.Rats in ischemic preconditioning（IPC） group were subjected to 4 cycles of 3 minutes of left coronary artery occlusion followed by 5 minutes of reperfusion 24 hours before I/R.Myocardial injury degree was evaluated by measurement of infarct size and serum creatine kinase（CK） activity.Results Compared with I/R,IPC significantly reduced infarct size（0.11±0.22 cm2 vs 0.18±0.03 cm2） and CK release during reperfusion（P0.01）.Sham operation had no significant effect on infarct size and CK levels.Conclusion The established rat model of delayed preconditioning has significant cardiac protection.