Endogenous Digitalis in Acute Myocardial Ischemia

Abstract

The evidence that endogenous digitalis-like factor (EDLF) may act as an endogenous inotrope includes presence of digitalis-like immunoreactive material in the hearts of mammals (14), high-affinity binding of this material to digitalis receptor sites in ventricular myocardium (15), and digitalis-like positive inotropic effects of EDLF demonstrated in different isolated heart preparations (17, 12). Acute myocardial ischaemia/infarction (AMI) is known to sensitize myocardium to the arrhythmogenic effect of digitalis (13). AMI is associated with both inhibition of Na+/K+-ATPase in the myocardium (6, 10) and with loss of myocardial digitalis receptors (11). Analyzing these observations one can speculate that these effects observed in AMI at least in part may be explained by the action of one or more circulating Na+/K+-pump inhibitors, and that EDLF may participate in the genesis of arrhythmias in AMI. Based on this hypothesis we have shown that pretreatment of coronary ligated cats with antidigoxin antiserum leads to a significant increase of the electric threshold of ventricular fibrillation (1). In coronary ligated rats AMI was assocciated with a 2.5 fold increase in plasma level of EDLF, antidigoxin antibody along with the antifibrillatory effect prevented the inhibition of Na+/K+-ATPase in erythrocytes and myocardium, which were otherwise observed in acute myocardial ischaemia (2, 3). Clinical observations have shown significant inhibition of Na+/K+-ATPase in erythrocytes in patients during the initial period after first transmural AMI (4). This inhibition was associated with the increase in plasma Na+/K+-ATPase inhibitory activity and digoxin-like immunoreactivity (4, 5).