Weber S, Cabanes L, Guérin F
Service des maladies cardiovasculaires, hôpital Cochin, Paris.
Arch Mal Coeur Vaiss. 1990 Nov;83(13):1957-61.
Noradrenergic sympathetic tone is always increased in chronic left ventricular failure of which it is one of the main compensatory mechanisms. Beta-1-adrenergic stimulation increases the heart rate and left ventricular contractility. However, the efficacy of this "compensatory" mechanism is limited on the one hand by the energetic cost of inotropic stimulation and, on the other hand, by the phenomenon of desensitisation and down-regulation of myocardial beta-1-receptors during intense and prolonged noradrenergic stimulation as observed in chronic cardiac failure. These physiopathological concepts raise the question of the indications of drugs affecting betareceptors in cardiac failure. Positive inotropic beta-mimetics can only be used during short periods of acute decompensation: low dose betablocker therapy protects the betareceptors from the phenomenon of desensitisation and seem to exert a beneficial action in this way in some cases of cardiac failure; these preliminary results require confirmation by large scale controlled therapeutic trials. Finally, a new pharmacological class of drugs, the beta-1 adrenergic partial agonists, seems to be useful in the management of moderate degrees of cardiac failure due to ischemic heart disease.
在慢性左心室衰竭中，去甲肾上腺素能交感神经张力总是增加的，它是主要的代偿机制之一。β1肾上腺素能刺激可增加心率和左心室收缩力。然而，这种“代偿”机制的效能一方面受到变力性刺激的能量消耗限制，另一方面受到慢性心力衰竭中强烈且持久的去甲肾上腺素能刺激期间心肌β1受体脱敏和下调现象的限制。这些生理病理概念引发了关于影响心力衰竭中β受体的药物适应证的问题。正性肌力β激动剂仅可在急性失代偿的短时间内使用：低剂量β受体阻滞剂疗法可保护β受体免受脱敏现象影响，并且在某些心力衰竭病例中似乎以此方式发挥有益作用；这些初步结果需要大规模对照治疗试验予以证实。最后，一类新的药物，即β1肾上腺素能部分激动剂，似乎对缺血性心脏病所致中度心力衰竭的管理有用。
