Kapadia S R
Department of Cardiology, The Cleveland Clinic Foundation, Ohio 44195, USA.
Cardiol Rev. 1999 Jul-Aug;7(4):196-206. doi: 10.1097/00045415-199907000-00011.
The current interest in understanding the role of stress-induced cytokines in heart failure relates to the observation that many of the untoward pathophysiologic responses of the failing circulation might be explained by these compounds. These small molecules appear to cause left ventricular dysfunction, precipitate pulmonary edema, cause cardiomyopathy, reduce peripheral organ perfusion, induce ventricular remodeling, activate the fetal gene program in animal models, and cause anorexia and cachexia. Thus, the elaboration of cytokines, similar to the upregulation of neurohormones, may represent a biochemical mechanism that is responsible for producing symptoms and remodeling in heart failure patients. To better understand how cytokines play a role in heart failure, it is important to delineate the concept of cytokine bioactivity in this setting.
目前对于了解应激诱导的细胞因子在心力衰竭中作用的关注，源于这样一种观察结果：衰竭循环系统的许多不良病理生理反应可能可用这些化合物来解释。这些小分子似乎会导致左心室功能障碍、引发肺水肿、导致心肌病、减少外周器官灌注、诱导心室重塑、在动物模型中激活胎儿基因程序，并导致厌食和恶病质。因此，细胞因子的释放，类似于神经激素的上调，可能代表了一种导致心力衰竭患者出现症状和重塑的生化机制。为了更好地理解细胞因子在心力衰竭中如何发挥作用，明确这种情况下细胞因子生物活性的概念很重要。
