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目的观察胰岛素是否能够通过减轻中性粒细胞(PMN)在心肌组织中的浸润、聚集而抑制炎症反应,从而减轻心肌缺血/再灌注(MI/R)损伤。方法建立兔MI/R模型,分为假手术组、GIK组、GK组和对照组,后三组缺血45 min/再灌注6 h,检测各组血浆肌酸激酶同工酶(CK-MB)活性、高敏C反应蛋白(hs-CRP)水平,以及心肌组织中髓过氧化物酶(MPO)活性,利用Evans blue-TTC染色法测定心脏梗死面积。结果与对照组相比,GIK组CK-MB活性下降(P<0.01)、心肌梗死面积减小(P<0.01)、MPO活性降低(P<0.01)、hs-CRP水平下降(P<0.01),GK组上述各指标则无明显变化(P均>0.05)。结论胰岛素能够减轻兔MI/R过程中PMN在心脏组织中的聚集,这可能是胰岛素保护MI/R心脏的重要机制之一。
Objective To observe whether insulin can attenuate myocardial ischemia / reperfusion (MI / R) injury by reducing the infiltration and aggregation of neutrophils (PMNs) in myocardium and inhibiting inflammation. Methods Rabbit MI / R model was established and divided into sham operation group, GIK group, GK group and control group. The last three groups were subjected to ischemia for 45 min / reperfusion for 6 h. Plasma creatine kinase MB ) Activity, hs-CRP level, and myeloperoxidase (MPO) activity in myocardium. The area of infarction was determined by Evans blue-TTC staining. Results Compared with the control group, the CK-MB activity in GIK group decreased (P <0.01), the myocardial infarct size decreased (P <0.01), MPO activity decreased (P <0.01) , GK group had no significant changes in the above indicators (P all> 0.05). Conclusion Insulin can reduce the aggregation of PMN in heart tissue during rabbit MI / R, which may be one of the important mechanisms by which insulin protects MI / R heart.