Vitamin C and coronary microcirculation.
Vitamin C and coronary microcirculation.
复制标题
维生素 C 和冠状动脉微循环。
DOI：
10.1161/01.cir.103.23.e117
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发表时间：
2001
期刊：
影响因子：
37.8
通讯作者：
Levine,M
中科院分区：
文献类型：
--
作者：
Padayatty,SJ;Levine,M
在维生素C对冠状动脉微循环的短期影响的研究中，Kaufmann等人1使用腺苷增加心肌血流量，并通过正电子发射断层扫描进行评估。与对照组相比，吸烟者表现出减弱的反应，通过静脉注射3 g维生素C超过10分钟进行纠正。作者得出结论，香烟烟雾导致氧化损伤，维生素C可以逆转这种损伤。不幸的是，研究条件不是生理性的，这是S形维生素C剂量-浓度关系的结果。当维生素C口服时，它被完全吸收，直到剂量超过200毫克。2在典型的地中海饮食中，每天摄入200 mg维生素C，导致血浆浓度为70 μmol/L。许多细胞，如中性粒细胞，积极运输维生素C，并在血浆之前饱和。70 μmol/L的细胞饱和度对应于主要组织维生素C转运蛋白（钠依赖性维生素C转运蛋白2）的最大速度。3，4较高的维生素C剂量不会增加长期血浆维生素C浓度，因为吸收减少和肾脏排泄增加，当血浆浓度超过60至70 μmol/L时，这开始。口服剂量为1.25 g时，不到一半的剂量被吸收，所有吸收的都被排泄。2相反，当静脉注射维生素C时，限制吸收的机制被绕过，并达到更高的血浆浓度。因此，当在5分钟内静脉给予1.25 g维生素C时，血浆峰浓度达到700 μmol/L，2小时后福尔斯降至200 μmol/L。2几乎全部剂量在12小时内通过尿液排出。我们估计，静脉注射3 g维生素C（如Kaufmann等人的研究1）将导致血浆浓度为1500 μmol/L，在研究过程中可能会下降几百μmol/L。这些维生素C浓度是口服摄入量的10至20倍，显然是不符合生理的。组织对这种药理学浓度的反应5可能与更适度的生理浓度下的维生素C作用关系不大。虽然这项研究证明了使用高剂量静脉注射维生素C在实验情况下产生抗氧化作用的实用性，但它并没有表明维生素C在生理浓度下具有这种作用，不幸的是，它不能形成使用维生素C在冠心病的初级或二级预防中的基础。一个健康的饮食，每天至少包含5份不同的水果和蔬菜，将提供我们所需的所有维生素C。
In their study on the short-term effects of vitamin C on coronary microcirculation, Kaufmann et al1 used adenosine to increase myocardial blood flow, which was assessed by positron emission tomography. When compared with controls, smokers showed an attenuated response that was corrected by 3 g of vitamin C given intravenously over 10 minutes. The authors conclude that cigarette smoke causes oxidant damage that is reversed by vitamin C. Unfortunately, the study conditions are not physiological, which is a consequence of the sigmoidal vitamin C dose-concentration relationship. When vitamin C is given orally, it is completely absorbed until the dose exceeds 200 mg. 2 Consumption of 200 mg of vitamin C daily, which occurs in a typical Mediterranean diet, results in a plasma concentration of 70 μmol/L. Many cells, such as neutrophils, actively transport vitamin C and saturate before plasma. Saturation of cells by 70 μmol/L corresponds to the maximal velocity of the main tissue vitamin C transporter, sodium-dependent vitamin C transporter 2. 3, 4 Higher vitamin C doses do not increase long-term plasma vitamin C concentrations because of decreased absorption and increased renal excretion, which begin when plasma concentrations exceed 60 to 70 μmol/L. With an oral dose of 1.25 g, less than half the dose is absorbed, and all that is absorbed is excreted. 2 In contrast, when vitamin C is given intravenously, the limiting absorptive mechanisms are bypassed, and much higher plasma concentrations are achieved. Thus, when 1.25 g of vitamin C is given intravenously over 5 minutes, a peak plasma concentration of 700 μmol/L is attained, which falls to 200 μmol/L in 2 hours. 2 Almost the entire dose is excreted in the urine in 12 hours. We estimate that 3 g of vitamin C given intravenously, as was done in Kaufmann et al’s1 study, will result in a plasma concentration of 1500 μmol/L, which will fall by perhaps a few hundred micromoles per liter during the course of the study. These vitamin C concentrations, which are 10 to 20 times those that can be obtained by oral intake, are clearly unphysiological. The response of the tissues to such pharmacological concentrations5 may have little bearing on vitamin C actions at the more modest physiological concentrations. Although this study demonstrates the utility of using high-dose intravenous vitamin C to produce antioxidant effects in experimental situations, it does not show that vitamin C has such actions at physiological concentrations and, unfortunately, it cannot form the basis for using vitamin C in primary or secondary prevention of coronary heart disease. A healthy diet containing at least 5 servings of varied fruits and vegetables a day will supply all the vitamin C we need.