Korantzopoulos Panagiotis, Galaris Dimitrios, Papaioannides Dimitrios, Siogas Konstantinos
Laboratory of Biological Chemistry, University of Ioannina, Medical School, Ioannina, Greece.
Med Sci Monit. 2003 Jun;9(6):RA120-5.
Heart failure (HF) is a major health problem, causing significant morbidity and mortality. Its complex pathophysiology has not yet been fully elucidated. There is growing evidence that oxidative stress is implicated in the cardiac dysfunction leading to HF. In addition, several components of neurohormonal activation, such as catecholamines, angiotensin, aldosterone, tumor necrosis factor-a, endothelin, and cytokines, have been demonstrated to enhance oxidative stress. On the other hand, various pathophysiological parameters of HF, such as cardiomyocyte apoptosis, ventricular remodeling, mechanoelectric uncoupling, and endothelial dysfunction have been shown to be induced by oxidative stress. Despite substantial experimental evidence, the correlation of oxidative stress with the clinical parameters of HF is unclear. The potential association between oxidative stress and HF has led to the study of antioxidant interventions that may attenuate the oxidative damage. Promising results have been obtained mainly from studies using water-soluble antioxidants (such as vitamin C) and factors that inhibit free radical formation (such as allopurinol). The amelioration of oxidative stress in conjunction with pathophysiological abnormalities has been clearly shown in humans, but studies with clinical end-points are scarce. Furthermore, carvedilol and several other cardiovascular drugs, besides their favorable effects on neurohormonal activation in HF, may have additional intrinsic antioxidant properties. Even though the experimental evidence is promising, many more human clinical trials are needed in order to clarify the exact role of oxidative stress in HF and the potential benefits of antioxidant intervention.
心力衰竭（HF）是一个主要的健康问题，会导致严重的发病率和死亡率。其复杂的病理生理学尚未完全阐明。越来越多的证据表明，氧化应激与导致HF的心脏功能障碍有关。此外，神经激素激活的几个组成部分，如儿茶酚胺、血管紧张素、醛固酮、肿瘤坏死因子-α、内皮素和细胞因子，已被证明会增强氧化应激。另一方面，HF的各种病理生理参数，如心肌细胞凋亡、心室重塑、机械电解偶联和内皮功能障碍，已被证明是由氧化应激诱导的。尽管有大量实验证据，但氧化应激与HF临床参数之间的相关性尚不清楚。氧化应激与HF之间的潜在关联导致了对抗氧化干预措施的研究，这些措施可能会减轻氧化损伤。主要从使用水溶性抗氧化剂（如维生素C）和抑制自由基形成的因子（如别嘌醇）的研究中获得了有希望的结果。氧化应激的改善与病理生理异常的改善在人类中已得到明确证明，但以临床终点为指标的研究很少。此外，卡维地洛和其他几种心血管药物，除了对HF中的神经激素激活有有利影响外，可能还具有额外的内在抗氧化特性。尽管实验证据很有希望，但仍需要更多的人体临床试验来阐明氧化应激在HF中的确切作用以及抗氧化干预的潜在益处。
