Endothelial function in subjects with isolated low HDL cholesterol: role of nitric oxide and circulating progenitor cells
Endothelial function in subjects with isolated low HDL cholesterol: role of nitric oxide and circulating progenitor cells
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DOI：
10.1152/ajpendo.00394.2009
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发表时间：
2010-02-01
影响因子：
5.1
通讯作者：
Imaizumi, Tsutomu
中科院分区：
文献类型：
--
作者：
Higashi, Yukihito;Matsuoka, Hidehiro;Imaizumi, Tsutomu
Higashi Y，Matsuoka H，Umei H，Sugano R，Fujii Y，Soga J，Kihara Y，Chayama K，Imaizumi T.孤立低高密度脂蛋白胆固醇受试者的内皮功能：一氧化氮和循环祖细胞的作用。Am J Physiol Endocrinol Metab 298：e202-e209,2010。2009年11月10日首次出版；DOI：10.1152/ajpendo.00394.2009。-流行病学研究表明，低水平的高密度脂蛋白胆固醇是心血管疾病的风险因素。这项研究的目的是确定分离的低高密度脂蛋白胆固醇对内皮功能的贡献。从我们人群中的5417名参与者中挑选了39名没有其他心血管危险因素的低高密度脂蛋白胆固醇的受试者。我们评估了39名单独的低高密度脂蛋白胆固醇患者中29名患者在使用HMG-CoA还原酶抑制剂普伐他汀治疗4wk前后的血流介导的血管扩张(FMD)。低高密度脂蛋白胆固醇组(n=29)的FMD低于对照组(n=29)，而NTG诱导的血管扩张作用在两组中相似。普伐他汀增加了15名低高密度脂蛋白受试者的高密度脂蛋白胆固醇、尿亚硝酸盐/硝酸盐排泄量、祖细胞循环水平以及细胞对血管内皮生长因子的迁移反应，但在14名安慰剂对照组受试者中没有。普伐他汀治疗组FMD升高，而对照组无明显变化。两组治疗前和治疗4wk后NTG的血管扩张作用相似。多元回归分析显示，高密度脂蛋白胆固醇的改变、祖细胞数量和祖细胞的迁移是普伐他汀增加FMD的独立预测因素。这些发现表明，低高密度脂蛋白胆固醇是内皮功能障碍的独立危险因素，普伐他汀改善孤立低高密度脂蛋白患者的内皮功能，至少部分是通过增加循环祖细胞来实现的。
Higashi Y, Matsuoka H, Umei H, Sugano R, Fujii Y, Soga J, Kihara Y, Chayama K, Imaizumi T. Endothelial function in subjects with isolated low HDL cholesterol: role of nitric oxide and circulating progenitor cells. Am J Physiol Endocrinol Metab 298: E202-E209, 2010. First published November 10, 2009; doi:10.1152/ajpendo.00394.2009.-Epidemiologic studies have shown that a low level of high-density lipoprotein (HDL) cholesterol is a risk factor for cardiovascular diseases. The purpose of this study was to determine the contribution of isolated low HDL cholesterol to endothelial function. Thirty-nine subjects with low HDL cholesterol who had no other cardiovascular risk factors were selected from the 5,417 participants from our population. We evaluated flow-mediated vasodilation (FMD) before and after 4 wk of treatment with the HMG-CoA reductase inhibitor pravastatin in 29 of the 39 subjects with isolated low HDL cholesterol. FMD was lower in the low-HDL-cholesterol group (n = 29) than in the control group (n = 29), whereas NTG-induced vasodilation was similar in the two groups. Pravastatin increased HDL cholesterol, urinary excretion of nitrite/nitrate, circulating levels of progenitor cells, and cell migration response to vascular endothelial growth factor in 15 subjects with low HDL cholesterol but not in 14 placebo control subjects. FMD increased in the pravastatin treatment group but not in the control group. NTG-induced vasodilation was similar before and after 4 wk of treatment in the two groups. Multiple regression analysis revealed that changes in HDL cholesterol, the number of progenitor cells, and migration of progenitor cells were independent predictors of augmentation of FMD with pravastatin. These findings suggest that low HDL cholesterol is an independent risk factor for endothelial dysfunction and that pravastatin improves endothelial function in individuals with isolated low HDL cholesterol through, at least in part, an increase in circulating progenitor cells.