急性 ST 段抬高型心肌梗死急诊经皮冠状动脉介入治疗术后无复流患者红细胞渗透脆性变化及其机制研究

Objective To analyze the change of erythrocyte osmotic fragility of postoperative no - reflow ASTEMI patients treated by emergency PCI and its mechanism. Methods From January 2014 to October 2015,a total of 150 patients with ASTEMI were selected in the Department of Emergency,Yan′ an University Affiliated Hospital,all of them received emergency PCI. According to the incidence of no - reflow,all of the patients were divided into A group(with no - reflow,n =84)and B group(without no - reflow,n = 66). Difference value of erythrocyte osmotic fragility related index at admission and after PCI〔including red brittleness minimum resistance value difference( ΔOFmin ),red brittleness maximum resistance value difference(ΔOFmax ),hemolytic rate when ΔPBS reached to 5 M,hemolytic rate when ΔPBS reached to 6 M,hemolytic rate when ΔPBS reached to 7 M and mean corpuscular volume difference( ΔMCV)〕,erythrocyte membrane enzymatic activity of Na + - K + - ATP,plasma levels of MDA and SOD were compared between the two groups at admission and after PCI. ResultsΔOFmin ,ΔOFmax ,hemolytic rate when ΔPBS reached to 5 M,hemolytic rate when ΔPBS reached to 6 M,hemolytic rate whenΔPBS reached to 7 M and ΔMCV of B group were statistically significantly smaller than those of A group( P < 0. 05). Nonstatistically significant differences of erythrocyte membrane enzymatic activity of Na + - K + - ATP,plasma level of MDA or SOD was found between the two groups at admission(P ﹥ 0. 05);after PCI,erythrocyte membrane enzymatic activity of Na + - K + -ATP and plasma SOD level of B group were statistically significantly higher than those of A group,while plasma MDA level of B group was statistically significantly lower than that of A group( P < 0. 05). Conclusion The erythrocyte osmotic fragility of postoperative no - reflow ASTEMI patients treated by emergency PCI obviously increases,the mechanism may relate to the decrease of erythrocyte membrane enzymatic activity of Na + - K + - ATP and enhance of oxidative stress reaction.