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慢性心力衰竭的药物治疗:正性肌力药、血管扩张剂还是血管扩张性正性肌力药?

Medical management of chronic heart failure: inotropic, vasodilator, or inodilator drugs?

作者信息

Lang R

机构信息

Frankenklinik, Bad Kissingen, West Germany.

出版信息

Am Heart J. 1990 Dec;120(6 Pt 2):1558-64. doi: 10.1016/0002-8703(90)90059-7.

Abstract

On the basis of pathophysiologic mechanisms, the medical therapy of today for chronic heart failure is reviewed. The advantages and disadvantages of the vasodilator drugs and the inotropic drugs are presented. Finally, the therapeutic value of the inodilator drugs, which combine the central myocardial effects of positive inotropic agents with those of peripheral vasodilators, is discussed. In particular, the orally available dopaminergic agents, such as ibopamine, which interact with beta-receptors in the heart (mediating a positive inotropic effect) as well as with dopaminergic receptors in the peripheral vessels (mediating a systemic vasodilator effect) and in the kidneys (potentiating the natriuretic effect of diuresis), seem to be an advancement in the modern medical therapy of chronic heart failure. Data are shown during long-term treatment with ibopamine, in which the sustained clinical benefit in heart failure was not diminished, despite a decrease of the adrenergic receptors in blood cells. Dopamine plasma concentration was permanently normalized during long-term treatment. The discrepancy between clinical improvement and the measured adrenergic downregulation may be due to the interference of the inodilator with neurohormonal systems at multiple sites and is probably independent of receptor activation. It is suggested that the biosynthesis of noradrenaline is improved by increasing intracellular dopamine transport.

摘要

基于病理生理机制,对当今慢性心力衰竭的药物治疗进行了综述。介绍了血管扩张剂和正性肌力药物的优缺点。最后,讨论了兼具正性肌力药物的中心性心肌效应和外周血管扩张剂效应的血管扩张性正性肌力药物的治疗价值。特别是口服可用的多巴胺能药物,如异波帕胺,它与心脏中的β受体相互作用(介导正性肌力作用),以及与外周血管中的多巴胺能受体相互作用(介导全身血管扩张作用)和在肾脏中(增强利尿的利钠作用),似乎是慢性心力衰竭现代药物治疗的一项进展。展示了异波帕胺长期治疗期间的数据,其中尽管血细胞中的肾上腺素能受体减少,但心力衰竭的持续临床益处并未减弱。长期治疗期间多巴胺血浆浓度永久恢复正常。临床改善与所测肾上腺素能下调之间的差异可能是由于血管扩张性正性肌力药物在多个部位对神经激素系统的干扰,并且可能与受体激活无关。有人提出,通过增加细胞内多巴胺转运可改善去甲肾上腺素的生物合成。

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