Molavi Behzad, Mehta Jawahar L
Department of Internal Medicine, Division of Cardiovascular Medicine, University of Arkansas for Medical Sciences and the Central Arkansas Veterans Healthcare System, Little Rock, Arkansas 72205-7199, USA.
Curr Opin Cardiol. 2004 Sep;19(5):488-93. doi: 10.1097/01.hco.0000133657.77024.bd.
The adoption of immediate reperfusion strategies to treat acutely occluded coronary arteries and the emergence of high-resolution molecular biology techniques have drawn attention to oxidative stress and reactive oxygen species generation in the cardiovascular system. Recent evidence suggests that oxidative stress is a common denominator in many aspects of cardiovascular pathogenesis. This review outlines the current understanding of reactive oxygen species generation and their role in cardiovascular pathophysiology, including atherogenesis, acute myocardial infarction, and congestive heart failure.
Recent studies highlighting endothelial dysfunction as a response to oxidative stress are of particular interest, as are the findings linking myocardial lipid accumulation (cardiac lipotoxicity) and peroxidation to congestive heart failure. Finally, newer methods to detect reactive oxygen species, including urine assays for measurement of 8,12 iPGF2alpha VI along with nuclear magnetic resonance, can help quantitate the reactive oxygen species burden noninvasively.
The body of current evidence from in vitro studies indicates that oxidative stress plays a major role in cardiovascular disease but the details of molecular events in vivo and in particular in humans remains to be determined. This could partly explain the failure of antioxidant therapy in preventing cardiovascular morbidity and mortality in major clinical trials. The emerging technologies, including MRI, can help delineate the events leading to reactive oxygen species generation and dissipation in humans, and potentially provide a more precisely targeted therapy for the population at risk.
采用即刻再灌注策略治疗急性闭塞冠状动脉以及高分辨率分子生物学技术的出现，使人们关注心血管系统中的氧化应激和活性氧生成。最近的证据表明，氧化应激是心血管发病机制诸多方面的共同特征。本综述概述了目前对活性氧生成及其在心血管病理生理学中的作用的理解，包括动脉粥样硬化、急性心肌梗死和充血性心力衰竭。
最近强调内皮功能障碍是对氧化应激反应的研究特别令人关注，将心肌脂质蓄积（心脏脂毒性）和过氧化与充血性心力衰竭联系起来的研究结果同样如此。最后，检测活性氧的新方法，包括用于测量8,12 - iPGF2α VI的尿液检测以及核磁共振，有助于无创地定量活性氧负荷。
目前来自体外研究的证据表明，氧化应激在心血管疾病中起主要作用，但体内尤其是人类分子事件的细节仍有待确定。这可能部分解释了抗氧化治疗在主要临床试验中未能预防心血管发病率和死亡率的原因。包括磁共振成像在内的新兴技术可以帮助描绘导致人类活性氧生成和消散的事件，并有可能为高危人群提供更精准的靶向治疗。
