Dietz R, Osterziel K J
Abteilung für Kardiologie, Medizinischen Universitätsklinik Heidelberg.
Z Kardiol. 1991;80 Suppl 8:31-6.
An increased activity of the sympathetic nervous system has been regarded as a sensible compensatory mechanism in heart failure. Further stimulation of this system by therapeutic interventions has proven useful in the situation of acute heart failure; however, the contractile reserve elicited by beta-stimulation is markedly reduced. By long-term stimulation of the sympathetic nervous system in the treatment of chronic heart failure mostly unfavorable effects are evoked, i.e.: 1) An increase in impedance for the failing heart by stimulation of peripheral alpha 1-adrenoreceptors. 2) An increase in myocardial oxygen consumption which causes further deterioration of the energy balance in the failing heart. 3) A fall in serum potassium concentration by stimulation of beta 2-receptors combined with a reduction of the fibrillation threshold favor the genesis of malignant arrhythmias. 4) Stimulation of myocardial alpha 1-adrenoreceptors may lead to a de-differentiation with a preferential synthesis of fetal myosins. Because of a reduced rate of calcium removal during diastole, increases in heart rate lead to an elevated myocardial stiffness. An increased sympathetic activity in patients with heart failure represents an independent marker of a reduced life expectancy. Interventions that either cause a reduction in sympathetic activity or which protect the heart from high catecholamine concentrations in heart failure are associated with an improvement of survival and quality of life.
交感神经系统活性增加被认为是心力衰竭时一种合理的代偿机制。在急性心力衰竭情况下，通过治疗干预进一步刺激该系统已被证明是有用的；然而，β刺激引起的收缩储备明显降低。在慢性心力衰竭治疗中，长期刺激交感神经系统大多会引发不利影响，即：1）刺激外周α1肾上腺素能受体增加衰竭心脏的阻抗。2）心肌耗氧量增加，导致衰竭心脏能量平衡进一步恶化。3）刺激β2受体导致血清钾浓度降低，同时颤动阈值降低，有利于恶性心律失常的发生。4）刺激心肌α1肾上腺素能受体可能导致去分化，优先合成胎儿肌球蛋白。由于舒张期钙清除率降低，心率增加会导致心肌僵硬度升高。心力衰竭患者交感神经活性增加是预期寿命缩短的独立标志。降低交感神经活性或保护心脏免受心力衰竭时高儿茶酚胺浓度影响的干预措施与生存率和生活质量的改善相关。
