Taddei S, Ghiadoni L, Virdis A, Versari D, Salvetti A
Department of Internal Medicine, University of Pisa, Italy.
Curr Pharm Des. 2003;9(29):2385-402. doi: 10.2174/1381612033453866.
Endothelium-derived NO is not only a potent vasodilator but also inhibits platelet aggregation, vascular smooth muscle cell migration and proliferation, monocyte adhesion and adhesion molecule expression, thus protecting the vessel wall against the development of atherosclerosis. Cardiovascular risk factors are associated with an imbalance of the redox equilibrium towards oxidative stress and, therefore, impair the integrity of the endothelium, leading to endothelial activation which involves blunted endothelium-dependent vasodilation (vasodilator dysfunction) as well as inflammatory processes extending to the milieu within the whole vasculature, making plaques prone to rupture. In prospective studies endothelial dysfunction is associated with increased incidence of cardiovascular events. Thus, the prevention of endothelial dysfunction can determine a strong advantage in the clinical outcome of patients with cardiovascular risk factors. Several non-pharmacological interventions can prevent endothelial dysfunction or improve impaired endothelium-dependent vasodilation. Probably the most effective non-pharmacological measure is represented by aerobic physical activity, which can reduce production of oxidative stress associated to increasing age. Moreover, physical activity can improve endothelial dysfunction even in patients with cardiovascular risk factors such as essential hypertension. In addition several other approaches, including vitamin and fish oil supplementation, or tea and red wine consumption, can lead to an improvement of endothelium-dependent vasodilation, possibly by a restoration of NO availability. It is worth noting that most of non-pharmacological measures act by preventing or reducing oxidative stress.
内皮衍生的一氧化氮不仅是一种强大的血管舒张剂，还能抑制血小板聚集、血管平滑肌细胞迁移和增殖、单核细胞黏附以及黏附分子表达，从而保护血管壁免受动脉粥样硬化发展的影响。心血管危险因素与氧化还原平衡向氧化应激的失衡相关，因此会损害内皮的完整性，导致内皮激活，这涉及内皮依赖性血管舒张减弱（血管舒张功能障碍）以及炎症过程扩展至整个脉管系统内的环境，使斑块易于破裂。在前瞻性研究中，内皮功能障碍与心血管事件发生率增加相关。因此，预防内皮功能障碍可在有心血管危险因素的患者临床结局中带来显著优势。几种非药物干预措施可预防内皮功能障碍或改善受损的内皮依赖性血管舒张。可能最有效的非药物措施是有氧运动，它可减少与年龄增长相关的氧化应激产生。此外，体育活动即使在有心血管危险因素（如原发性高血压）的患者中也可改善内皮功能障碍。此外，其他几种方法，包括补充维生素和鱼油，或饮用茶和红酒，可能通过恢复一氧化氮的可用性来改善内皮依赖性血管舒张。值得注意的是，大多数非药物措施通过预防或减少氧化应激起作用。
