Schuschke D A
Center for Applied Microcirculatory Research, University of Louisville, Louisville, KY 40292, USA.
J Nutr. 1997 Dec;127(12):2274-81. doi: 10.1093/jn/127.12.2274.
Dietary copper has long been known to be essential for cardiovascular homeostasis. However, the role of copper and cuproenzymes in the normal control of vascular physiology is not well understood. Most studies in the cardiovascular system have focused on copper deficiency-induced defects in the heart or large vessels. Recently, attention has also focused on the effects of copper deficiency in the microcirculation or the small blood vessels that control blood flow, nutrient and waste exchange, and peripheral vascular resistance. Studies in the microcirculation demonstrate that copper is important in mechanisms of macromolecular leakage, platelet-endothelial interactions and vascular smooth muscle reactivity. There is a significantly greater leakage of proteins from postcapillary venules in copper-deficient rats in response to mast cell-released histamine. This response appears to be the result of increased numbers of mast cells and thereby increased available histamine. Copper deficiency also causes an inhibition of in vivo thrombogenesis, which appears to be related to an inhibition of platelet adhesion. Subsequent studies have demonstrated that this is probably caused by a diminished concentration of the adhesion molecule von Willebrand factor. Nitric oxide (NO)-mediated arteriole vasodilation is also compromised in copper-deficient rats. This functional deficit to NO can be reversed by the addition of Cu, Zn-superoxide dismutase (SOD), suggesting that degradation of NO by superoxide anion occurs during copper deprivation. These observations demonstrate that dietary copper is necessary for several microvascular control mechanisms affecting inflammation, microhemostasis and regulation of peripheral blood flow.
长期以来，人们都知道膳食铜对心血管稳态至关重要。然而，铜和铜酶在血管生理正常调控中的作用尚未得到充分理解。心血管系统的大多数研究都集中在铜缺乏引起的心脏或大血管缺陷上。最近，人们也开始关注铜缺乏在微循环或控制血流、营养物质和废物交换以及外周血管阻力的小血管中的影响。微循环研究表明，铜在大分子渗漏、血小板 - 内皮细胞相互作用和血管平滑肌反应性机制中起着重要作用。在铜缺乏的大鼠中，毛细血管后微静脉对肥大细胞释放的组胺反应时，蛋白质渗漏明显更多。这种反应似乎是肥大细胞数量增加从而组胺可用性增加的结果。铜缺乏还会导致体内血栓形成受到抑制，这似乎与血小板黏附受到抑制有关。随后的研究表明，这可能是由于黏附分子血管性血友病因子浓度降低所致。在铜缺乏的大鼠中，一氧化氮（NO）介导的小动脉血管舒张也受到损害。添加铜锌超氧化物歧化酶（SOD）可以逆转这种对NO的功能缺陷，这表明在铜缺乏期间超氧阴离子会降解NO。这些观察结果表明，膳食铜对于影响炎症、微止血和外周血流调节的几种微血管控制机制是必需的。
