Isometric exercise promotes arteriogenesis in rats after myocardial infarction

被引:5
作者
Zhang, Xintong [1 ]
Zheng, Yu [1 ]
Geng, Canru [2 ]
Guan, Juntao [2 ]
Wang, Lu [1 ]
Zhang, Xiu [1 ]
Cheng, Yihui [1 ]
Li, Jian'an [1 ]
Lu, Xiao [1 ]
机构
[1] Nanjing Med Univ, Dept Rehabil Med, Affiliated Hosp 1, 300 Guangzhou Rd, Nanjing 210029, Jiangsu, Peoples R China
[2] Nanjing Med Univ, Dept Rehabil Med, Affiliated Suzhou Hosp, Suzhou 215000, Jiangsu, Peoples R China
来源
JOURNAL OF BIOMEDICAL RESEARCH | 2021年 / 35卷 / 06期
基金
中国国家自然科学基金;
关键词
isometric exercise training; arteriogenesis; acute myocardial infarction; monocyte chemoattractant protein-1; fibroblast growth factor-2; ENDOTHELIAL GROWTH-FACTOR; SKELETAL-MUSCLE; MONOCYTE RECRUITMENT; ANGIOGENESIS; EXPRESSION; PROLIFERATION; OCCLUSION; IMPACT; CELLS;
D O I
10.7555/JBR.35.20210062
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Isometric exercise (IE) is a promising intervention of noninvasive revascularization in patients with acute myocardial infarction (AMI). This study aimed to investigate the impact and mechanisms of IE training on arteriogenesis in AMI. Male Sprague-Dawley rats were randomly assigned into the sham-operation group (SO), myocardial infarction (MI) group, and 13 IE subgroups treated according to training intensity, frequency, duration, or monocyte chemoattractant protein-1 (MCP-1), or/and fibroblast growth factor-2 (FGF-2) inhibitors for eight weeks. Our results demonstrated that the IE group achieved superior improvement compared with the MI group in terms of left ventricular ejection fraction (LVEF), myocardial infarction size (MIS), arterial density (AD), monocytes (MNCs), smooth muscle cells (SMCs), endothelial cells (ECs), relative collateral blood flow (RCBF), MCP-1, and FGF-2 at the endpoint. Positive correlations between MCP-1 and MNCs, MNCs and FGF-2, FGF-2 and SMCs, SMCs and AD, as well as AD and RCBF were observed. This study demonstrated that with MI of 100% load 20 times daily for eight weeks, the arteriogenesis was improved, which may be attributed to the recruitment of MNCs and SMCs in remote ischemic myocardium caused by increases in MCP-1 and FGF-2 expression.
引用
收藏
页码:436 / 447
页数:13
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