Braunwald E
J Am Coll Cardiol. 1985 May;5(5 Suppl A):51A-59A. doi: 10.1016/s0735-1097(85)80463-0.
Although it has been known for more than a century that digitalis glycosides exert a powerful beneficial effect on patients with heart failure, atrial fibrillation and a rapid ventricular rate, it was believed for many years that the drug exerts this clinical effect primarily by slowing the heart rate. It was also thought that the extra-cardiac vascular actions of digitalis might be responsible for its therapeutic effect. It has now been established that cardiac glycosides cause arteriolar and venous constriction in a variety of mammalian species including human beings, and that this vasoconstriction involves the coronary vascular bed as well, but it is believed that these actions are not responsible for any beneficial clinical effect. A variety of investigations on cardiac muscle in vitro, anesthetized and conscious dogs and anesthetized and conscious human subjects have shown that cardiac glycosides improve the contractility of failing mammalian myocardium. It has become clear that digitalis also stimulates the contractility of the nonfailing heart. The degree of augmentation of contractility induced by cardiac glycosides is related inversely to the baseline contractile state. Myocardial oxygen consumption, which is increased in the normal heart by the positive inotropic action of glycosides, is actually reduced or remains constant in the failing heart. Cardiac glycosides increase the contractility of the globally ischemic heart, but their actions in chronic ischemic heart disease with regional impairment of function are complex. Deterioration of segmental performance occurs in ischemic and necrotic segments, while improvement of contractility occurs in adjacent normal segments.(ABSTRACT TRUNCATED AT 250 WORDS)
尽管一个多世纪以来人们都知道洋地黄糖苷对心力衰竭、心房颤动且心室率快的患者有强大的有益作用,但多年来人们一直认为该药物主要通过减慢心率发挥这种临床作用。人们还认为洋地黄的心脏外血管作用可能是其治疗效果的原因。现在已经确定,强心苷在包括人类在内的多种哺乳动物中会引起小动脉和静脉收缩,这种血管收缩也涉及冠状动脉床,但人们认为这些作用并非任何有益临床效果的原因。对体外心肌、麻醉和清醒犬以及麻醉和清醒人类受试者进行的各种研究表明,强心苷可改善衰竭哺乳动物心肌的收缩力。很明显,洋地黄也能刺激非衰竭心脏的收缩力。强心苷引起的收缩力增强程度与基线收缩状态呈反比。在正常心脏中,糖苷的正性肌力作用会增加心肌耗氧量,但在衰竭心脏中实际上会降低或保持不变。强心苷可增加全心缺血心脏的收缩力,但其在伴有局部功能障碍的慢性缺血性心脏病中的作用较为复杂。在缺血和坏死节段,节段性能会恶化,而在相邻正常节段,收缩力会改善。(摘要截选至250字)