Singal P K, Khaper N, Farahmand F, Belló-Klein A
Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre and Department of Physiology, Faculty of Medicine, University of Manitoba, 351 Tache Avenue, R3022, Winnipeg MB R2H 2A6, Canada.
Curr Cardiol Rep. 2000 May;2(3):206-11. doi: 10.1007/s11886-000-0070-x.
Heart failure is considered to be a complex clinical syndrome, with alterations in the multiple neurohumoral systems and subcellular cardiac sites that correlate with abnormal cardiac function. Strong evidence for the role of oxidative stress in the pathogenesis of heart failure has been provided by studies on experimental animals as well as humans. This concept is gaining more acceptance due to the fact that during heart failure, changes in different neurohormones, cytokines, nitric oxide, and activated inflammatory cells are closely linked to oxidative stress at the cellular and molecular levels. The present article provides a simple description of oxygen free radicals as well as the antioxidant defense system. Evidence for the role of oxidative stress in the pathogenesis of heart failure is reviewed in a concise manner.
心力衰竭被认为是一种复杂的临床综合征，其多种神经体液系统和心脏亚细胞部位发生改变，这些改变与心脏功能异常相关。对实验动物和人类的研究均提供了强有力的证据，证明氧化应激在心力衰竭发病机制中发挥作用。由于在心力衰竭期间，不同神经激素、细胞因子、一氧化氮和活化的炎症细胞的变化在细胞和分子水平上与氧化应激密切相关，这一概念正得到越来越多的认可。本文简要介绍了氧自由基以及抗氧化防御系统。本文还简要综述了氧化应激在心力衰竭发病机制中作用的证据。
