小鼠心肌缺血后适应模型的建立及其相关影响因素

Establishment and Assessment of a Mouse Model of Myocardial Ischemia Postconditioning

目的建立小鼠心肌缺血后适应模型,评价其对缺血再灌注损伤的保护作用以及相关的影响因素。方法120只成年雄性KM小鼠随机接受缺血后适应、缺血再灌注以及假手术3种不同的处理方式。后适应组采用开胸手术结扎左冠状动脉缺血45 min,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。采用Evans blue和TTC染色的方法确定缺血心肌面积以及梗死心肌面积,并测定血清磷酸肌酸激酶(CK)、丙二醛(MDA)及超氧化物歧化酶(SOD)以及血流动力学指标。结果缺血后适应1组、后适应2组以及预适应+后适应组梗死心肌的重量百分比显著小于缺血-再灌注组,P<0.05;后适应2组以及预适应+后适应组与后适应1组比较差异无显著性;延迟后适应组梗死心肌的重量百分比与缺血-再灌注组比较差异无显著性,P>0.05。同时缺血后适应可以明显地降低缺血再灌注血清CK、MDA的浓度,提高SOD的水平以及改善血流动力学的恶化。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损伤。

Objective To establish a mouse model of ischemia postconditioning and assess the cardioprotective function and effective factors of postconditioning to ischemia-reperfusion. Methods 120 male adult KM mice were randomly undergone three different treatment： postconditioning, ischemia reperfusion and sham operation. Postconditioning group undergone open-chest surgery to induce left coronary artery occlusion and reperfused for 3 h, after LCA occlusion, several cycles of 10 s reperfusion followed by 10 s LCA re-occlusion were applied during the early minutes of reperfusion. Ischemic size and infarct size were measured by Evans blue and TTC staining, respectively, to assess the level of plasma CK, MDA, SOD and evaluate hemodynamics in different groups. Result The infarct size was smaller in Postconl, Postcon2 and Precon ＋ Postcon groups than in Control （p 〈 0.05）. There was no further reduction in infarct size with 6 cycles of Post-con and Preconditioning （ p 〉 0.05）. The reduction in infarct size was lost with delayed Post-con. Meanwhile, the levels of plasma CK, MDA and SOD were decreased and hemodynamics was improved by postconditioning. Conclusions Ischemiia postconditioning at onset of reperfusion obviously reduces myocardial injury in the mice model.