Effect of Experimental Congestive Heart Failure and Acetyl Strophanthidin on Myocardial Electrolyte and Water Content

Abstract

The syndrome of chronic congestive heart failure was produced in female dogs by progressive pulmonary artery constriction. A factorial experimental design, containing seven experiments of four dogs each, was employed. Each experiment was completed in one day and consisted of two groups of two dogs each, one group containing dogs with heart failure and the other, normal dogs. One animal from each group received intravenous acetyl strophanthidin, 0.015 mg/kg ascites-free weight, while the other was given an injection of inert material. The heart was quickly removed from the chest nine minutes after the injection and the right ventricle was taken for analysis. Previous work indicated that this dose of the drug produced and inotropic effect both in normal animals and in dogs with heart failure without producing digitalis toxicity. The myocardium from animals with congestive heart failure contained significantly less potassium but more sodium, chloride, and water per kilogram of dry fat-free blood-free myocardium than the myocardium from normal dogs. The concentration of sodium plus potassium in tissue water was subnormal in failing hearts. The sodium and chloride composition of the fluid gained by failing hearts differed significantly from that of interstitial fluid. Acetyl strophanthidin increased myocardial chloride and water. Although potassium in the myocardium was unchanged in treated control dogs, it increased significantly after acetyl strophanthidin in animals with heart failure. The findings are consistent with myocardial cellular swelling in congestive heart failure. The quantity of blood in each kilogram of failing myocardial tissue was severely reduced, probably because of muscle fiber hypertrophy. The possibility is considered that this alteration, together with the increased tissue water, may lead to lowered oxygen tension in failing heart muscle. It is suggested that digitalis exerts two opposing effects on ion transport through the myocardial cell membrane and that neither of these is fundamental to its inotropic action.