Division of Cardiology, Department of Medicine, University of California San Diego, School of Medicine, La Jolla, CA 92093-0613, USA.
Trends Cardiovasc Med. 1997 Jul;7(5):161-7. doi: 10.1016/S1050-1738(97)00029-7.
Heart failure is a complex syndrome characterized by inability of the heart to supply sufficient cardiac output to meet the metabolic needs of the body. Over the past few decades, a number of animal models of heart failure have been developed to study questions that cannot be readily studied in the clinical setting. Because the syndrome of heart failure in humans has many underlying causes, ranging from primary myocardial disease (often of unknown etiology) to myocardial failure consequent to ventricular overload with secondary cardiac hypertrophy (as in hypertension, valvular heart disease, or myocardial infarction), no single animal model can successfully mimic the pathophysiology of these clinical settings. Regardless of the original cardiac abnormality, however, the end-stage heart failure syndrome generally presents a picture of cardiac dilation and circulatory congestion associated with maladaptive neurohumoral responses affecting the heart and peripheral circulation, which provide prime targets for new treatment strategies. An ideal animal model of heart failure should mimic the clinical setting as closely as possible, be accessible and reproducible, relatively stable under chronic conditions, and sufficiently economical to permit experiments in a large number of animals. In this review, we discuss the advantages and disadvantages of naturally occurring models of heart failure and models in which heart failure is induced in normal animals, focusing in particular on models that are useful for exploring disease mechanisms and interventions to prevent or treat heart failure. Much is being learned from large animals such as the dog and pig, although small animal models (rat and hamster) have many favorable features, and as genetic methods and miniaturized physiologic techniques mature, the mouse is beginning to provide gene-based models of cardiac failure aimed at better understanding of molecular mechanisms. (Trends Cardiovasc Med 1997;7:161-167). © 1997, Elsevier Science Inc.
心力衰竭是一种复杂的综合征，其特征是心脏无法提供足够的心输出量以满足身体的代谢需求。在过去的几十年中，已经开发出许多心力衰竭的动物模型，以研究在临床环境中不易研究的问题。由于心力衰竭在人类中的综合征有许多潜在的原因，从原发性心肌疾病（通常病因不明）到继发于心室负荷过重的心肌衰竭和继发性心肌肥厚（如高血压、瓣膜性心脏病或心肌梗死）不等，没有单一的动物模型可以成功模拟这些临床环境的病理生理学。然而，无论最初的心脏异常如何，终末期心力衰竭综合征通常表现为心脏扩张和循环充血的特征，同时伴有影响心脏和外周循环的适应性神经激素反应，这些反应为新的治疗策略提供了主要靶点。心力衰竭的理想动物模型应尽可能紧密地模拟临床环境，易于获得且可重现，在慢性条件下相对稳定，并且经济上足够允许在大量动物中进行实验。在这篇综述中，我们讨论了自然发生的心力衰竭模型和在正常动物中诱导心力衰竭的模型的优缺点，特别关注对探索疾病机制和预防或治疗心力衰竭的干预措施有用的模型。从狗和猪等大型动物中学到了很多东西，尽管小型动物模型（大鼠和仓鼠）具有许多优点，并且随着遗传方法和小型化生理技术的成熟，小鼠开始提供针对心力衰竭的基因模型，旨在更好地理解分子机制。（趋势心血管医学 1997; 7:161-167）。©1997，Elsevier Science Inc.
