Smith T W
Therapie. 1989 Nov-Dec;44(6):431-5.
Evidence from several sources, including electrophysiologic studies and cation flux and content measurements, now allows a reasonably cohesive synthesis of the molecular and cellular events that lead from inhibition of the Na pump by digitalis to the enhancement of the generation of contractile force by cardiac muscle. It is generally agreed that Na pump inhibition, with consequent elevation in [Na+]i and [Ca2+]i, underlies both the therapeutic (positive inotropic) and toxic (arrhythmic) responses of the heart, and accounts for the well-known difficulty in separating therapeutic and toxic clinical effects of digitalis glycosides. In the intact patient or experimental animal, cardiac glycosides also exert effects that are mediated through neural pathways, and these can exert important influences on the integrated response to digitalis administration.
包括电生理研究以及阳离子通量和含量测量在内的多个来源的证据，现在使得对从洋地黄抑制钠泵到心肌收缩力生成增强这一过程中的分子和细胞事件进行合理连贯的综合成为可能。人们普遍认为，钠泵抑制以及随之而来的细胞内钠离子（[Na+]i）和钙离子（[Ca2+]i）浓度升高，是心脏治疗性（正性肌力）和毒性（心律失常）反应的基础，并且解释了洋地黄苷治疗和毒性临床效应难以区分的这一众所周知的难题。在完整的患者或实验动物中，强心苷还通过神经通路发挥作用，并且这些作用会对洋地黄给药的综合反应产生重要影响。
