Inotropic and electrophysiologic effects of amrinone in untreated and digitalized ventricular tissues.

The purposes of this study were to determine whether amrinone induces oscillatory afterpotentials (OAP) or aftercontractions (AC) in Purkinje tissue or myocardium, to determine whether a relationship exists between the production of OAP or AC and the inotropic effects of amrinone and to determine possible effects of amrinone on the oscillations and the positive inotropic effect produced by digitalis. Isolated canine papillary and trabecullar muscles, as well as false tendons, were exposed to 5.3 X 10(-4) M amrinone. Some of the preparations had been pretreated with acetylstrophanthidin (AS) in a dose just sufficient to induce OAP or AC. Standard electrophysiologic techniques were used to record transmembrane action potentials. Developed tension also was recorded. Amrinone by itself did not induce OAP or AC in myocardium or false tendons. This was true even when the resting membrane potential of the false tendons was reduced by means of focal current application. Amrinone increased the amplitude of AS-induced oscillations in both myocardium and false tendons. Amrinone increased strength of contraction of untreated myocardium at all basic cycle lengths and of AS-treated myocardium, especially at shorter basic cycle lengths. Amrinone decreased strength of contraction both of untreated and AS-treated false tendons at all basic cycle lengths. The results suggest that there may be important differences in the mechanisms of action of amrinone and digitalis.