Schnabel P, Böhm M
Klinik III für Innere Medizin der Universität zu Köln, Joseph-Stelzmann-Str. 9, D-50924 Köln, Germany, Germany.
Z Kardiol. 1999 Oct;88(Suppl 3):S005-11. doi: 10.1007/s003920050575.
In heart failure, decreased cardiac output leads to a number of adaptive mechanisms. Among these, neuroendocrine activation including activation of the renin-angiotensin-aldosterone system, augmentation of vasopressin and endothelin release, and activation of the sympathetic nervous system occur. The increase of adrenergic drive is characterized by decreased baroreceptor sensitivity, increased plasma norepinephrine levels and cardiac norepinephrine spillover, and desensitization of postsynaptic β-adrenergic signal transduction. While increased sympathetic drive initially helps to maintain contractile performance of the damaged heart, the above changes chronically result in catecholamine refractoriness and are associated with a poor prognosis.Besides diuretics, the current therapy of heart failure includes ACE inhibitors, digitalis, and β-blockers. In addition, there is evidence that AT1 receptor antagonists might be useful, and, in the presence of arrrhythmia, amiodarone is widely used. The current review briefly summarizes how these drugs interfere with the sympathetic nervous system and speculates that antiadrenergic properties might contribute to the beneficial effects of some of these agents with respect to exercise tolerance and survival of patients with heart failure.
在心力衰竭中，心输出量降低会引发多种适应性机制。其中包括神经内分泌激活，这其中有肾素 - 血管紧张素 - 醛固酮系统的激活、血管加压素和内皮素释放增加以及交感神经系统激活。肾上腺素能驱动增加的特征是压力感受器敏感性降低、血浆去甲肾上腺素水平升高和心脏去甲肾上腺素溢出增加，以及突触后β - 肾上腺素能信号转导脱敏。虽然交感神经驱动增加最初有助于维持受损心脏的收缩功能，但上述变化长期会导致儿茶酚胺不应性，并与不良预后相关。除利尿剂外，目前心力衰竭的治疗包括血管紧张素转换酶抑制剂、洋地黄和β受体阻滞剂。此外，有证据表明血管紧张素Ⅱ1型受体拮抗剂可能有用，并且在存在心律失常时，胺碘酮被广泛使用。本综述简要总结了这些药物如何干扰交感神经系统，并推测抗肾上腺素能特性可能有助于其中一些药物对心力衰竭患者运动耐量和生存率产生有益影响。
