Long-term, regular remote ischemic preconditioning improves endothelial function in patients with coronary heart disease

被引:23
|
作者
Liang, Y. [1 ]
Li, Y. P. [1 ]
He, F. [1 ]
Liu, X. Q. [1 ]
Zhang, J. Y. [1 ]
机构
[1] Zhengzhou Univ, Affiliated Hosp 1, Dept Cardiol, Zhengzhou 450052, Peoples R China
关键词
Remote ischemic preconditioning; endothelial function; coronary heart disease; STAT-3; PROGENITOR CELLS; BONE-MARROW; REPERFUSION INJURY; CLINICAL-APPLICATION; FAILURE; NEOVASCULARIZATION; ATHEROSCLEROSIS; MOBILIZATION; MECHANISMS; EXHAUSTION;
D O I
10.1590/1414-431X20144452
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Remote ischemic preconditioning (RIPre) can prevent myocardial injury. The purpose of this study was to assess the beneficial effects of long-term regular RIPre on human arteries. Forty patients scheduled for coronary artery bypass graft (CABG) surgery were assigned randomly to a RIPre group (n=20) or coronary heart disease (CHD) group (n=20). Twenty patients scheduled for mastectomy were enrolled as a control group. RIPre was achieved by occluding arterial blood flow 5 min with a mercury sphygmomanometer followed by a 5-min reperfusion period, and this was repeated 4 times. The RIPre procedure was repeated 3 times a day for 20 days. In all patients, arterial fragments discarded during surgery were collected to evaluate endothelial function by flow-mediated dilation (FMD), CD34(+) monocyte count, and endothelial nitric oxide synthase (eNOS expression). Phosphorylation levels of STAT-3 and Akt were also assayed to explore the underlying mechanisms. Compared with the CHD group, long-term regular RIPre significantly improved FMD after 20 days (8.5 +/- 2.4 vs 4.9 +/- 4.2%, P<0.05) and significantly reduced troponin after CABG surgery (0.72 +/- 0.31 and 1.64 +/- 0.19, P<0.05). RIPre activated STAT-3 and increased CD34(+) endothelial progenitor cell counts found in arteries. Long-term, regular RIPre improved endothelial function in patients with CHD, possibly due to STAT-3 activation, and this may have led to an increase in endothelial progenitor cells.
引用
收藏
页码:568 / 576
页数:9
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