氯沙坦对冠心病外周血内皮祖细胞的动员作用及影响内皮功能的机制

Mobilizing effect of losartan on EPCs and its mechanism on improving endothelial dysfunction

目的观察氯沙坦对冠心病患者外周血内皮祖细胞(EPCs)数量及血流介导的内皮舒张功能的影响,并探讨其改善内皮功能的机制。方法选取经冠脉造影确诊为冠心病65例,随机分为标准治疗组32例和ARB治疗组33例,同时选取非冠心病31例作为健康对照组。标准治疗组给予常规药物,ARB治疗组给予常规物药+氯沙坦治疗,随访8周,治疗前后分别用流式细胞术检测EPCs水平、超声测定流量介导血管扩张(FMD)情况。结果基线水平,冠心病内皮功能较健康对照组明显低下、EPCs数量明显减少(P<0.05);FMD与EPCs数量呈正相关(r=0.57,P<0.01)。治疗8周后,标准治疗组和ARB治疗组冠心病患者FMD均有不同程度的改善,循环血EPCs数量均有不同程度的增加,但是ARB治疗组变化更明显(P<0.05);ARB治疗组EPCs的增加与内皮功能的改善呈正相关(r=0.52,P<0.01)。结论氯沙坦对EPCs具有一定的动员作用,ARB类药物氯沙坦可能通过增加外周血EPCs数量,进而改善内皮功能。

Objective To investigate the effect of losartan on endothelial progenitor cells （EPCs） in coronary heart disease （CHD） patients and endothelial function, and probe the mechanism that losartan improves endothelial dysfunction. Methods A total of 65 patients with confirmed CHD by coronary angiography were recruited randomly and divided into two groups randomly, 33 patients were treated with routine drugs and losartan as the ARB treatment group, 32 patients were treated with routine drugs as the standard treatment group. Totally 31 patients without CHD were choosed as health control group. After following, the levels of EPCs were detected by flow cytometry, and humeral flow-mediated-dilation （FMD） were measured with high resolution uhrasonography for each patient. Results At baseline, endothelial function of CHD patients was lower, the number of EPCs decreased compared to control group. There was a significant positive relationship between endothelial function and the number of circulating EPCs, endothelial function improved with the increase in the number of EPCs （ r = O. 57, P 〈 O. O1 ）. After 8 weeks, the FMD of two groups of CHD patients were improved in varying degrees, and circulating EPCs were also increased in varying degrees, especially ARB treatment group （ P 〈 0.05 ） ; there was a significant positive relationship between endothelial function improvement and the increasing number of circulating EPCs （ r = 0.52, P 〈 0.01 ）. Conclusion Losartan has a certain mobilized effect on EPCs, and may remove the endothe- lial dysfunction by increasing the level of circulating EPCs.