Zelis R, Sinoway L I, Leuenberger U, Clemson B S, Davis D
Division of Cardiology, Milton S. Hershey Medical Centre, Pennsylvania State University, College of Medicine, Hershey 17033.
Eur Heart J. 1991 Aug;12 Suppl C:2-7. doi: 10.1093/eurheartj/12.suppl_c.2.
The circulatory compensatory mechanisms designed to cope quickly with physiological stress (e.g. sympathetic nervous system and the Frank-Starling mechanism) are less effective when there is chronic pathological stress, such as congestive heart failure (CHF). Other mechanisms come into play that operate over a longer time (e.g. activation of the renin-angiotensin-aldosterone system, myocardial hypertrophy and physiological deconditioning). Changes in blood vessels and skeletal muscle metabolism that result from inadequate delivery of oxygenated blood to working muscles belong to the group of mechanisms that develop slowly. When CHF therapy is successful, the abnormalities produced by this latter group of mechanisms will improve, but slowly. The concept that compensatory mechanisms have either short or long time constants for activation and reversal may explain why exercise tolerance improves much later than haemodynamics, which can be reversed acutely with vasodilator therapy.
旨在快速应对生理应激的循环代偿机制(如交感神经系统和Frank-Starling机制)在存在慢性病理应激(如充血性心力衰竭,CHF)时效果较差。其他机制开始发挥作用,这些机制作用时间更长(如肾素-血管紧张素-醛固酮系统激活、心肌肥大和生理失健)。因向工作肌肉输送含氧血液不足而导致的血管和骨骼肌代谢变化属于缓慢发展的机制组。当CHF治疗成功时,后一组机制产生的异常情况会改善,但改善过程缓慢。代偿机制激活和逆转的时间常数有长有短这一概念,可能解释了为什么运动耐力的改善比血流动力学的改善晚得多,而血流动力学可通过血管扩张剂治疗急性逆转。