摘要
目的观察急性ST段抬高性心肌梗死急诊PCI无复流患者红细胞渗透脆性的变化,并探讨可能的机制和临床意义。方法选取急性ST段抬高性心肌梗死行急诊PCI患者120例,其中60例急诊PCI过程中出现冠脉无复流现象,为无复流组;其余60例未出现无复流现象者为对照组。取入院即刻2组外周静脉血5 ml,检测红细胞渗透脆性、红细胞膜Na+-K+-ATP酶活性、血浆脂质过氧化产物MDA及过氧化物歧化酶SOD的变化,并分析导致红细胞渗透脆性变化的原因及其临床意义。结果与对照组比较,无复流组患者红细胞渗透脆性明显降低(P<0.01),红细胞膜Na+-K+-ATP酶活性降低(P<0.05),血浆MDA水平升高(P<0.01),SOD含量减低(P<0.01)。结论急性ST段抬高性心肌梗死急诊PCI冠脉无复流患者红细胞渗透脆性降低会造成红细胞变形性下降,心肌微血管灌注不足,可能是造成预后不良的因素之一。造成无复流组患者红细胞渗透脆性降低的原因可能与红细胞膜Na+-K+-ATP酶活性降低、血浆脂质过氧化增强有关。
Objective To investigate the change of erythrocyte osmotic fragility in acute myocardial infarction（ AMI）patients with ST-segment elevation and no reflow after emergency PCI,and to explore possible action mechanism and clinical significance. Methods One hundred and twenty AMI patients with ST segment elevation admitted in our hospital were enrolled in the study,in which 60 patients underwent no reflow during emergency PCI（ no reflow group）,the other 60 patients who did not undergo no reflow were enrolled as control group. The peripheral vein blood 5ml was taken out immediately after hospitalization,then erythrocyte osmotic fragility,activity of Na＋-K＋-ATP enzyme on RBC membrane and plasma MDA and SOD levels were detected,and the action mechanism and clinical significance were analyzed. Results As compared with those in control group,the erythrocyte osmotic fragility was significantly decreased in no flow group（ P〈0. 01）; activity of Na＋-K＋-ATP enzyme on RBC membrane was obviously reduced（ P〈0. 05）; the plasma levels of MDA significantly increased（ P〈0. 05）,however,the contents of SOD were obviously decreased（ P〈0. 01）. Conclusion The decrease of erythrocyte osmotic fragility in AMI patients with ST segment elevation and no reflow after emergency PCI can reduce red blood cell deformability,and myocardial microvascular hypoperfusion may be one of the reasons that result in poor prognosis. The reason of erythrocyte osmotic fragility reduction in patients with no reflow may be related with to the decrease of Na＋-K＋-ATP enzymes activity on red cell membrane and the enhancement of plasma lipid peroxidation.
出处
《河北医药》
CAS
2014年第15期2250-2252,共3页
Hebei Medical Journal
