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Glycolysis in heart failure: a31P-NMR and surface fluorometry study

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Summary

Glycolysis is slow in the heart, especially in the cardiomyopathic heart. Glycolysis is partially rate-limited by phosphofructokinase (PFK), an enzymc which is inhibited by calcium (Ca2+)i and hydrogen ions (H+)i and activated by cAMP. (H+)i and (Ca2+)i are augmented in cardiomyopathy. With glucose as the only substrate (NADH)/(NAD) the phosphorylation potential and developed pressure were significantly lower, and concentrations of phosphomonoester sugars and hydrogen ions (H+)i were significantly higher in isolated cardiomyopathic hearts as compared to healthy hamster hearts. Pyruvate lowered diastolic (Ca2+)i in cardiomyopathic hamster hearts. With pyruvate as the substrate (NADH)/(NAD), the phosphorylation potential and developed pressure incrcased significantly and concentrations of phosphomonoester sugars (PME), (H+)i and diastolic (Ca2+)i decreased significantly in myopathic hamster hearts. The results suggest that late heart failure in the myopathic hamster is associated with calcium and/or hydrogen ion-induced inhibition of glycolysis.

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Supported in part by the George D. Smith Foundation and NIH Grant AA 07413-01. W. Auffermann supported by # AU 70/2-2 from Deutsche Forschungsgemeinschaft, Bonn, FRG

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Auffermann, W., Wu, S.T., Parmley, W.W. et al. Glycolysis in heart failure: a31P-NMR and surface fluorometry study. Basic Res Cardiol 85, 342–357 (1990). https://doi.org/10.1007/BF01907127

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