Seta Y, Shan K, Bozkurt B, Oral H, Mann D L
Department of Medicine, Veterans Administration Medical Center, Houston, Texas 77030, USA.
J Card Fail. 1996 Sep;2(3):243-9. doi: 10.1016/s1071-9164(96)80047-9.
Although the development and progression of heart failure have traditionally been viewed as hemodynamic disorders, there is now an increasing awareness that the syndrome of heart failure cannot be simply and/or precisely defined solely in hemodynamic terms. The inability of the so-called hemodynamic hypothesis to explain the progression of heart failure has given rise to the notion that heart failure may progress as a result of the overexpression of an ensemble of biologically active molecules referred to generically as neurohormones. More recently, it has become apparent that in addition to neurohormones, another portfolio of biologically active molecules, termed cytokines, are also expressed in the setting of heart failure. This article reviews recent clinical and experimental material that suggests that the cytokines, much like the neurohormones, may represent another class of biologically active molecules that are responsible for the development and progression of heart failure.
尽管传统上一直将心力衰竭的发生和进展视为血流动力学紊乱,但现在人们越来越意识到,心力衰竭综合征不能仅用血流动力学术语简单和/或精确地定义。所谓的血流动力学假说无法解释心力衰竭的进展,这引发了一种观点,即心力衰竭可能是由于一组通常被称为神经激素的生物活性分子过度表达所致。最近,很明显,除了神经激素外,另一组被称为细胞因子的生物活性分子也在心力衰竭的情况下表达。本文回顾了最近的临床和实验资料,这些资料表明,细胞因子与神经激素非常相似,可能代表另一类导致心力衰竭发生和进展的生物活性分子。