Mechanochemistry of Cardiac Muscle

Abstract
This investigation was designed to determine whether a defect in energy utilization exists in heart failure. Accordingly, the direct conversion of chemical energy to mechanical work was studied in right ventricular papillary muscles from normal cats and cats with experimental right ventricular failure secondary to pulmonary artery constriction. Energy production was inhibited by iodoacetic acid and N2. After resting or performing variable amounts of internal contractile element work under isometric conditions, muscles were instantly frozen, and the total amount of chemical energy (∼ P = creatine phosphate + ATP) used was correlated with work performed and the number of contractions. The contractile properties of papillary muscles from cats with heart failure were severely depressed. There was a significant depression in initial ∼P stores in muscles from cats with heart failure, but there was no significant change in the resting rate of ∼P utilization. Although the muscles from cats with heart failure performed, on the average, 13% as much work and were activated 64% as many times, the average amount of energy used was only 7% of that used by normal muscles. It is concluded that in this form of experimentally produced heart failure the utilization of ∼P is reduced but only in relation to the reduction in contractile element work and that the direct conversion of chemical energy to mechanical work is not an inefficient process in this state.