ISSN:
1573-7322
Keywords:
ATP
;
phosphocreatine
;
heart failure
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract There is now compelling evidence that the [ATP] in both failed human myocardium and animal models of severe heart failure is as much as 25% lower than in normal myocardium. We also know that the tissue contents of phosphocreatine and creatine and the capacity of the creatine kinase reaction (Vmax) are also lower in the dysfunctional/failing heart. These observations increase our understanding of two important aspects of cardiac energetics: the kinetics of ATP synthesis and the thermodynamics of ATP utilization, i.e., the chemical driving force for the ATP-consuming reactions, ΔG∼P. In this chapter, we will first review the fundamentals of the chemistry of ATP synthesis in the heart and then summarize what is known about the energetics of the failing heart from the viewpoints of the kinetics of ATP synthesis and the thermodynamics of ATP utilization. We present a new model of the energetics of the failing heart and suggest that the loss of creatine from the failing heart protects the heart from an even greater loss of ATP.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1023/A:1009857906567
