The concept of a defect in the conversion of chemical energy to work as the cause of low output heart failure has been based on the finding of normal myocardial extraction of substrate and oxygen in this clinical state (1, 2). However, the alternative view, that there is failure in transformation of the energy of substrate oxidations to a biologically useful form, cannot be excluded (3). Of particular interest, as regards the former theory, is the problem of evaluating those physical-chemical factors which initiate or contribute to the alteration of myocardial protein in heart failure.A consideration of the role of changes in intracellular ionic content in the regulation of cardiac performance has been stimulated by finding an intimate relation between these parameters in the staircase phenomenon (4). Other isolated muscle work has shown that changes in electrolyte concentration at the superficial level of the cell can affect contractile strength of muscle before the ion penetrates the interior of the muscle (5, 6).Although there is at present no adequate methodology for precise study of these phenomena in the human heart in vivo, it was considered of im-.portance to seek information concerning the myo- (1954)(1955)(1956).:Public Health Trainee of the National Heart Institute (1955)(1956). § Research Fellow, R. C. Mahon Foundation (1956)(1957).
Public Health Research Fellow of the National HeartInstitute (1953)(1954)(1955).of drug-induced recovery from cardiac failure. In a prior report (7), data were presented which indicated the facility with which acetyl strophanthidin mobilized electrolytes in the myocardium of the intact dog, its abrupt course of action enabling detection of these changes.
METHODSThe design of this study was such as to rely on the assumption that the coronary arteriovenous differences of electrolytes and metabolites could be validly accepted as a measure of their net uptake by, or release from, the myocardium. Although the transcapillary exchange rates of an ion, such as potassium, are blood flow dependent (8), an estimation of the effects of altered blood flow per se upon measured arteriovenous differences appeared in order. In the intact human, two procedures which usually increase coronary blood flow, exercise (9) and hypoxia (10), were chosen to study coronary arteriovenous differences of potassium. Five minutes of exercise produced no significant change in six patients. The mean of the planimetered A-V difference areas for potassium was + 0.01 + 0.08 square inches in the control and + 0.06+ 0.20 in the experimental period. Similar results were obtained with hypoxia, induced by 10 per cent oxygen inhalation for 25 minutes in five patients.The mean control value was + 0.06 + 0.25 square inch and the hypoxia value, + 0.27 ± 0.23. These findings are in agreement with those of Driscol and Berne (11), in which coronary blood in the dog was increased up to 100 per cent by varied procedures without significant change in the potassium arteriovenous differences.The effects of digitalis preparat...