Comparative effects of strophanthidin in tilapia and human heart tissues

It is well documented that the cardiotonic steroid strophanthidin increases myocardial contractile force through an inhibition of the sarcolemmal Na(+)-K+ pump in mammalian heart cells. The aim of the present study was to determine the effect of this digitalis substance on action potential and contraction in cardiac tissues obtained from a cultured freshwater fish tilapia (Oreochromis sp.) and compare with those observed in human heart tissues obtained at cardiac surgery. In tilapia atria superfused at 25 degrees C 1-2 microM strophanthidin shortened the spontaneous cycle length while increased progressively the twitch force. In tilapia ventricular tissues, strophanthidin also increased the force but shortened the APD50. When temperature of the superfusate was elevated from 25 to 37 degrees C, strophanthidin induced a smaller positive or even negative inotropic effect but increased significantly the diastolic tension through an inhibition of the relaxation process. High temperature also facilitated the occurrence of delayed afterdepolarizations, repetitive slow response action potentials and episodes of contracture. The same concentration of stroph induced rather sustained positive inotropic effects without deteriorating actions in human ventricular trabeculae driven at 37 degrees C. In human atrial trabeculae, however, 2 microM strophanthidin readily induced abnormal automatic and triggered rhythms along with the positive inotropy. The present findings provide the functional evidence for the presence of sarcolemmal Na+, K(+)-pump in fish myocardial fibers. The major differences in the electro-mechanical actions of strophanthidin in tilapia versus human heart tissues are the smaller positive inotropy and the proneness to contracture in tilapia heart at 37 degrees C.