Svanegaard J, Johansen J B, Thayssen P, Haghfelt T
Kardiologisk afdeling B, Odense Sygehus.
Ugeskr Laeger. 1993 Jun 7;155(23):1784-8.
The maintenance of cardiac pumping ability in the presence of a primary disturbance of myocardial contractility and/or an excessive haemodynamic strain on the heart is dependent on several compensatory mechanisms. Particular attention has formerly been paid to the importance of the Frank-Starling mechanism and cardiac hypertrophy and dilatation in maintaining a blood supply sufficient to cover the metabolic needs of various tissues in heart failure. In recent years, however, it has been found that certain neurohormonal systems (the sympathetic nervous system, the renin-angiotensin-aldosterone system, atrial natriuretic peptide and several locally acting vaso-active substances) undergo considerable changes according to the degree of heart failure. These compensatory mechanisms support the circulation wholly or partially in acute heart failure, however sustained neurohormonal activation may be harmful in chronic heart failure, where several neurohormonal factors may be activated to ill-effect. The most significant neurohormonal systems and their importance in heart failure are reviewed on the basis of the available literature.
在存在心肌收缩力原发性紊乱和/或心脏过度血流动力学负荷的情况下,心脏泵血能力的维持依赖于多种代偿机制。以往特别关注弗兰克 - 斯塔林机制以及心脏肥大和扩张在维持足以满足心力衰竭时各种组织代谢需求的血液供应方面的重要性。然而,近年来发现某些神经激素系统(交感神经系统、肾素 - 血管紧张素 - 醛固酮系统、心房利钠肽以及几种局部作用的血管活性物质)会根据心力衰竭的程度发生显著变化。这些代偿机制在急性心力衰竭中全部或部分支持循环,然而在慢性心力衰竭中持续的神经激素激活可能是有害的,因为在慢性心力衰竭中几种神经激素因素可能被激活并产生不良影响。根据现有文献对最重要的神经激素系统及其在心力衰竭中的重要性进行综述。