Intra-arterial vitamin C prevents endothelial dysfunction caused by ischemia-reperfusion
Intra-arterial vitamin C prevents endothelial dysfunction caused by ischemia-reperfusion
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DOI：
10.1016/j.atherosclerosis.2007.06.011
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发表时间：
2008-03-01
期刊：
影响因子：
5.3
通讯作者：
Wolzt, Michael
中科院分区：
文献类型：
--
作者：
Pleiner, Johannes;Schaller, Georg;Wolzt, Michael
目的：缺血再灌注（IR）损伤导致组织损伤和内皮功能障碍。有证据表明，氧化应激起着重要的作用。方法：我们测试，如果IR诱导的内皮功能障碍，可以预防抗氧化剂维生素C的管理。本随机安慰剂对照研究入组了26例健康男性受试者和8例外周动脉疾病（PAD）男性患者。前臂血流量（FBF）测量响应血管扩张剂乙酰胆碱（ACh;内皮依赖性激动剂）或硝酸甘油（NTG;内皮非依赖性）进行前臂缺血前和后20分钟。FBF反应进行了重新评估，在再灌注期间与动脉内共管理24毫克/分钟的维生素C或安慰剂。在6名志愿者中，在缺血前和缺血后（含和不含维生素C）对NO合酶抑制剂N-单甲基-L-精氨酸（L-NMMA）的反应也进行了评估。
Objective: Ischemia-reperfusion (IR) injury causes tissue injury and endothelial dysfunction. There is evidence that oxidative stress plays an important role.Methods: We tested if IR-induced endothelial dysfunction could be prevented by administration of the antioxidant vitamin C. Twenty-six healthy male subjects and eight male patients with peripheral arterial disease (PAD) were enrolled in this randomised placebo-controlled study. Forearm blood flow (FBF) measurements in response to the vasodilators acetylcholine (ACh; endothelium-dependent agonist) or nitroglycerin (NTG; endothelium-independent) were performed before and after forearm ischemia for 20 min. FBF responses were reassessed during reperfusion with intra-arterial co-administration of 24 mg/min vitamin C or placebo. In six volunteers responses to the NO-synthase inhibitor N-monomethyl-L-arginine (L-NMMA) were also assessed before and after ischemia with and without vitamin C.Results: ACh-induced vasodilation was blunted in subjects receiving placebo after reperfusion (p