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目的:观察重组人红细胞生成素(rHuEPO)对心肌梗死大鼠心功能和心肌梗死面积的影响,并探讨其机制.方法:16只Wistar大鼠随机分心肌梗死组和治疗组,结扎左冠前降支制备急性心肌梗死模型,治疗组围手术期连续3d腹腔注射rHuEPO[3000IU/(kg·d)],14d后以相同剂量再连续注射3d;术后2d及3wk二维超声心动图检查心功能;术后3wk处死大鼠,TTC测定心肌梗死面积,免疫组化检测缺血区毛细血管密度、Bcl2和Bax的表达.结果:术后2d两组之间心功能无明显差异,术后3wk对照组左室射血分数(LVEF)和左室收缩末期内径(LVDs)改善程度明显劣于治疗组(P<0.05).与对照组相比,术后3wk治疗组梗死面积明显减少[分别为(26.0±0.9)%,(28.1±1.5)%,P<0.05]、毛细血管密度显著增加[分别为(10.4±1.5)/视野,(6.3±0.7)/视野,P<0.05],Bcl2蛋白表达增加(A值分别为0.116±0.005,0.103±0.007,P<0.05),而Bax表达减弱(A值分别为0.125±0.010,0.147±0.014,P<0.05).结论:rHuEPO能缩小大鼠心肌梗死面积,改善心肌梗死后心功能,其机制可能与减少缺血区心肌细胞凋亡以及促进缺血区毛细血管生成有关.
Objective: To observe the effect of recombinant human erythropoietin (rHuEPO) on cardiac function and myocardial infarction area in myocardial infarction rats and to explore its mechanism.Methods: Sixteen Wistar rats were randomly divided into myocardial infarction group and treatment group, The rats in the treatment group were given intraperitoneal injection of rHuEPO [3000 IU / (kg · d)] continuously for 3 days, and the rabbits in the treatment group were injected with the same dose for three consecutive days. The hearts were examined by two-dimensional echocardiography at 2 and 3 weeks after operation The rats were sacrificed at 3 weeks after operation and the area of myocardial infarction was measured by TTC.The expression of Bcl2 and Bax in the ischemic area were detected by immunohistochemistry.Results There was no significant difference in cardiac function between the two groups at 2 days after operation Compared with the control group, the improvement of LVEF and LVDs in the control group was significantly worse than that in the control group (P <0.05), and the area of infarction in the 3-week post-operation group was significantly decreased (26.0 ± 0.9)%, (28.1 ± 1.5)%, P <0.05] and capillary density increased significantly (10.4 ± 1.5 vs 6.3 ± 0.7 / field, P <0.05) (A values were 0.116 ± 0.005,0.103 ± 0.007, P <0.05), while the expression of Bax was decreased (A values were 0.125 ± 0.010,0.147 ± 0.01 4, P <0.05) .Conclusion: rHuEPO can reduce myocardial infarct size and improve cardiac function after myocardial infarction, and its mechanism may be related to the reduction of myocardial apoptosis and the promotion of angiogenesis in ischemic area.