Mann D L
Department of Medicine, Veterans Administration Medical Center, and Baylor College of Medicine, Houston, TX 77030, USA.
Prog Cardiovasc Dis. 1998 Jul-Aug;41(1 Suppl 1):1-8. doi: 10.1016/s0033-0620(98)80025-x.
This review examines experimental evidence that suggests that excessive adrenergic stimulation of the heart may actually contribute to the untoward natural history of congestive heart failure. The basic mechanisms for catecholamine-mediated cardiac toxicity are discussed, as well as relatively new evidence that catecholamine-mediated toxicity is the result of beta-adrenoceptor-mediated cyclic adenosine monophosphate-dependent calcium overload of the cardiac myocyte. The studies reviewed herein provide a plausible biological rationale for the use of beta-adrenergic blocking agents in patients with heart failure.
本综述探讨了实验证据，这些证据表明心脏过度的肾上腺素能刺激实际上可能促使充血性心力衰竭的不良自然病程发展。文中讨论了儿茶酚胺介导的心脏毒性的基本机制，以及儿茶酚胺介导的毒性是由β-肾上腺素能受体介导的心肌细胞环磷酸腺苷依赖性钙超载导致的这一相对较新的证据。本文所综述的研究为心力衰竭患者使用β-肾上腺素能阻滞剂提供了合理的生物学依据。
