Department of Internal Medicine and Public Health, University of L'Aquila, Viale S. Salvatore, Delta 6 Medicina, 67100 Coppito (AQ), Italy.
Curr Pharm Des. 2010;16(23):2539-50. doi: 10.2174/138161210792062867.
Smoking is a significant independent risk factor for cardiovascular disease and is a leading cause of structural and functional alterations of the cardiovascular system. Increasing evidence supports the hypothesis that oxidative stress and endothelial dysfunction are the fundamental pathophysiological mechanisms linking cigarette smoking to cardiovascular disease. The cardiovascular system is a rich source of NADPH oxidase-derived reactive oxygen species, which under pathological conditions play a fundamental role in vascular damage. Endothelium-derived nitric oxide (NO) plays a major role in the regulation of vascular tone, structure, and function, and endothelial dysfunction could be considered the first step in the pathogenesis of atherosclerosis and cardiovascular disease. Indeed, the bioavailability of NO is modulated by reactive oxygen species that degrade NO, uncouple NO synthase, and inhibit synthesis. Reduced bioavailability of NO and consequent endothelial dysfunction are involved in the initiation, progression and complications of atherosclerosis and also are predictive of future cardiovascular events. Thus, although data from clinical trials exploring the role of antioxidants on cardiovascular risk and disease are equivocal as yet, the role of oxidative stress in cardiovascular disease is an important area of research, which is likely to continue to be fruitful. This review focuses on possible interactions between oxidative stress, endothelial dysfunction and cigarette smoking--favouring the atherosclerotic process and cardiovascular disease--also focusing on the potential role for antioxidants in the prevention of adverse cardiovascular outcomes.
吸烟是心血管疾病的一个重要独立危险因素，也是导致心血管系统结构和功能改变的主要原因。越来越多的证据支持这样一种假设，即氧化应激和内皮功能障碍是将吸烟与心血管疾病联系起来的基本病理生理机制。心血管系统是 NADPH 氧化酶衍生的活性氧的丰富来源，在病理条件下，这些活性氧在血管损伤中起着至关重要的作用。内皮衍生的一氧化氮（NO）在调节血管张力、结构和功能方面发挥着重要作用，内皮功能障碍可以被认为是动脉粥样硬化和心血管疾病发病机制的第一步。事实上，NO 的生物利用度受到活性氧的调节，这些活性氧会降解 NO、使一氧化氮合酶解偶联以及抑制其合成。NO 生物利用度降低和随之而来的内皮功能障碍与动脉粥样硬化的发生、进展和并发症有关，并且可以预测未来的心血管事件。因此，尽管目前关于抗氧化剂对心血管风险和疾病的作用的临床试验数据尚无定论，但氧化应激在心血管疾病中的作用是一个重要的研究领域，可能会继续取得丰硕成果。这篇综述重点关注氧化应激、内皮功能障碍和吸烟之间的可能相互作用——促进动脉粥样硬化过程和心血管疾病——并关注抗氧化剂在预防不良心血管结局方面的潜在作用。
