Takahashi M, Yamada T, Kinoshita M
First Department of Internal Medicine, Shiga University of Medical Science.
Nihon Rinsho. 1993 May;51(5):1268-75.
Catecholamines bind to cardiac beta-adrenoceptor to introduce positive inotropic, chronotropic, dromotropic and lucinotropic effects of the heart. Therapeutic catecholamines causes less effects to failing myocardium in comparison to normal myocardium. Down-regulation of cardiac beta-adrenoceptor (decrease in receptor number) and uncoupling of beta-adrenoceptor to G protein (increase in Gi alpha) have been demonstrated in failing human myocardium. Rapid improvement can be obtained in cardiac function by intravenous catecholamines, usually with dopamine and/or dobutamine in patients with acute heart failure. But, tachyphylaxis occurs in 72 hours which limits usefulness of the drugs. Dopamine has DA1-receptor activity which increases renal blood flow and natriuresis. Dobutamine is superior to dopamine in positive lucinotropic effects in reducing PCWP in patients with heart failure. Mechanisms of beta blocker therapy with special reference to molecular mechanisms are discussed.
儿茶酚胺与心脏β-肾上腺素能受体结合，产生心脏正性肌力、正性变时、正性传导和正性舒张效应。与正常心肌相比，治疗用儿茶酚胺对衰竭心肌的作用较小。在衰竭的人类心肌中已证实存在心脏β-肾上腺素能受体下调（受体数量减少）以及β-肾上腺素能受体与G蛋白解偶联（Giα增加）。对于急性心力衰竭患者，静脉注射儿茶酚胺（通常为多巴胺和/或多巴酚丁胺）可使心功能迅速改善。但是，72小时内会出现快速耐受性，这限制了这些药物的效用。多巴胺具有DA1受体活性，可增加肾血流量和利钠作用。在心力衰竭患者中，多巴酚丁胺在降低肺毛细血管楔压（PCWP）的正性舒张效应方面优于多巴胺。讨论了β受体阻滞剂治疗的机制，特别提及分子机制。
