缺血后适应对再灌注小鼠心肌梗死面积、心肌酶以及血流动力学的影响

The influence on myocardial infarct size, plasma myocardial enzyme and hemodynamics of ischemia postconditioning in mice model

目的:探讨缺血后适应对小鼠心肌缺血再灌注(I/R)损伤的影响,为临床急性心肌缺血事件发生后的心肌保护措施提供可靠的实验依据。方法:成年60只雄性KM小鼠随机分为缺血后适应、I/R、假手术3组,每组20只。后适应组采用开胸手术结扎左冠状动脉缺血45min,建立急性心肌梗死模型,在完全再灌注早期给予反复短暂再通/闭塞的后适应;I/R组为同期开胸完成I/R,在结扎冠状动脉前后不做任何特殊处理;假手术组开胸不结扎冠状动脉。采用伊文思蓝(Evans blue)和三苯基氯化四氮唑(TTC)染色的方法确定缺血心肌范围[缺血心肌重量(AI)/左室重量(LV)]以及梗死心肌范围[梗死心肌重量(AN)/AI],并测定血清磷酸肌酸激酶(CK)、乳酸脱氢酶(LDH)、天冬氨酸转氨酶(AST)水平以及血流动力学指标主动脉平均动脉压(MAP)、左心室收缩压(LVSP)、左心室舒张末压(LVEDP)及左心室压力变化最大、最小速率(dp/dtmax、dp/dtmin)。结果:缺血后适应组与I/R组小鼠AI/LV、AN/AI均大于假手术组(P<0.05),缺血后适应组AN/AI明显小于I/R组(P<0.05);缺血后适应组血清CK、LDH、AST水平均明显低于I/R组(P<0.05);与I/R组比较,缺血后适应组MAP、LVSP、dp/dtmax、dp/dtmin明显升高而LVEDP明显降低(P<0.05)。结论:在恢复冠脉血流的早期施行缺血后适应可以有效地减少小鼠再灌注心肌梗死面积,降低血清心肌酶的水平,并改善心功能的恶化。

Objective. To evaluate the influence on the myocardial-reperfusion injury of ischemia postconditioning in mice model and provide an experimental evidence of cardiacprotective function after emergency ischemic myocardial events in clinics. Methods.. Sixty male adult KM mice were randomly divided into three different groups, ischemia postconditioning, ischemia-reperfusion and sham operation, 20 mice in each group. Postconditioning group undergone open-chest surgery to induce left coronary artery 45 min oc- clusion and reperfused for 3 h, after LCA occlusion, 3 cycles of 10 s reperfusion followed by 10 s LCA reocclusion were applied during the early minutes of reperfusion. Ischemic size and Infarct size were measured by Evans blue and TTC staining respectively, assessed and evaluate the level of plasma CK, LDH, AST and hemodynamics of different groups. Results. Infarct size was smaller in postconditioning group than in I/R Control （P d0.05）. The level of plasma CK, LDH and AST were decreased and hemodynamic measurement of MAP, LVSP, dp/dtmax dp/dtmin and LVEDP were improved by postconditioning （P〈0. 05）. Conclusions： Ischemia postconditioning at onset of reperfusion can obviously reduce mice myocardial infarct size, decrease the level of plasm myocardial enzyme and improve the level of hemodynamics.