High Energy Phosphate Compounds in the Myocardium during Experimental Congestive Heart Failure. Purine and Pyrimidine Nucleotides, Creatine, and Creatine Phosphate in Normal and in Failing Hearts*

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Abstract
Congestive heart failure produced in dogs by progressive stenosis of the main pulmonary artery was more severe than the circulatory congestion produced by a combination of tricuspid insufficiency and mild pulmonary arterial stenosis. Purine and pyrimidine nucleotides, creatine, creatine phosphate, inorganic phosphate, and total acid-soluble phosphate were measured in the right and left ventricles of normal, hypertrophied and failing hearts extirpated and frozen within 10 seconds. Among normal hearts, the right and left ventricles contained equal amounts of nucleotides, but the right ventricles contained 30% more creatine phosphate. Induction of cardiac arrest before extirpation of the hearts improved recovery of creatine phosphate. Hearts with right ventricular hypertrophy unassociated with failure showed no changes in content of creatine or creatine phosphate. With chronic heart failure due to pulmonary arterial stenosis, right ventricles showed decreases in adenosine triphosphate of -12%, in creatine phosphate of -33 and -43% by 2 methods, and in total creatine of -37%. The decreases in these compounds were much less pronounced in the paired left ventricles. Nucleoside triphosphates other than adenosine triphosphate were not changed significantly. Hearts from animals with circulatory congestion produced by ligation of the thoracic inferior vena cava, and skeletal muscle samples from animals in heart failure did not show decreases from the normal levels of creatine or creatine phosphate. The chemical changes found may or may not have had a relationship to the mechanical performance of the failing heart, but might reflect an altered metabolic steady state within the myocardial cells.

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