To determine if the high energy phosphate stores are preserved during inotropic stimulation in heart failure (HF), myocardial biopsies were obtained in 10 normal dogs (N) and in 10 with HF (caused by a chronic volume overload). During inotropic stimulation in N, ADP (-25%) and AMP (-30%)-declined with both drugs without ATP or creatinephosphate (CP) changes; (ATP/ADP) rose by 28%* and adenylate charge by 5%. In HF, the effects of both drugs were similar. These results suggest an impaired adaptability of the failing myocardium to inotropic stimuli, which appears independent of the drug used and could be related to an adenine loss with a secondary accumulation of CP.
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Pouleur, H., Maréchal, G., Rousseau, M. F., & Charlier, A. A. (1983). Abnormal changes in high energy phosphate stores during inotropic stimulation of the failing myocardium. Journal of Molecular Cell Biology, 15(1), 154. https://hdl.handle.net/2078.5/214415 (Original work published 1983)