GLYCOLYSIS IN HEART-FAILURE - A P-31-NMR AND SURFACE FLUOROMETRY STUDY

被引:18
作者
AUFFERMANN, W
WU, ST
PARMLEY, WW
WIKMANCOFFELT, J
机构
[1] UNIV CALIF SAN FRANCISCO, DEPT MED, ROOM M-1186, 505 PARNASSUS AVE, SAN FRANCISCO, CA 94143 USA
[2] UNIV CALIF SAN FRANCISCO, CARDIOVASC RES INST, SAN FRANCISCO, CA 94143 USA
关键词
D O I
10.1007/BF01907127
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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. © 1990 Dr. Dietrich Steinkopff Verlag.
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页码:342 / 357
页数:16
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