PMID- 1497576
OWN - NLM
STAT- MEDLINE
DCOM- 19920904
LR  - 20190902
IS  - 0300-8428 (Print)
IS  - 0300-8428 (Linking)
VI  - 87 Suppl 1
DP  - 1992
TI  - Adenine nucleotide metabolism and contractile dysfunction in heart 
      failure--biochemical aspects, animal experiments, and human studies.
PG  - 321-9
AB  - In myocardial hypertrophy and heart failure a series of adaptational changes 
      occur some multiplying contractile units, others slowing shortening velocity and 
      increasing economy of contraction. The demonstration of energy-saving mechanisms 
      in heart failure has prompted further investigations of energy providing and 
      utilizing metabolic pathways. The use of myocardial ATP as a substrate occurs 
      mainly at the myosin-ATPase and at the Ca-ATPase of the sarcoplasmic reticulum. 
      As the Michaelis constant of both enzymes for ATP is in the micromolar (microM) 
      range, whereas cellular ATP content is about 5000 microM, these enzymes are not 
      controlled by the availability of ATP as a substrate. In experimental heart 
      failure in large animals, normal or reduced creatine phosphate levels (in most 
      cases together with normal adenine nucleotides) have been described. Reduced 
      creatine phosphate is found in models with increased oxygen consumption, and 
      creatine phosphate may buffer the ATP pool in these models. In human heart 
      failure due to dilated cardiomyopathy, where resting oxygen consumption per unit 
      mass and lactate extraction are normal in most patients, normal adenine 
      nucleotides, creatine phosphate, and mitochondrial function have been described 
      in the initial studies. These results have been challenged by one study showing 
      decreased ATP levels in dilated cardiomyopathy, correlating with the decrease in 
      ejection fraction. However, only ATP has been measured in this study, whereas 
      total adenine nucleotides may be a more suitable parameter. Recently published 
      results have again demonstrated normal ATP and total adenine nucleotides in human 
      heart failure. In the same patients, significantly decreased myocardial 
      norepinephrine was measured, indicating that metabolic changes had occurred in 
      these hearts, but were independent of adenine nucleotides.(ABSTRACT TRUNCATED AT 
      250 WORDS)
FAU - Regitz, V
AU  - Regitz V
AD  - Department of Internal Medicine and Cardiology, German Heart Institute Berlin.
FAU - Fleck, E
AU  - Fleck E
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - Basic Res Cardiol
JT  - Basic research in cardiology
JID - 0360342
RN  - 0 (Adenine Nucleotides)
RN  - X4W3ENH1CV (Norepinephrine)
SB  - IM
MH  - Adaptation, Physiological
MH  - Adenine Nucleotides/analysis/*metabolism
MH  - Animals
MH  - Heart Failure/*physiopathology
MH  - Humans
MH  - Myocardial Contraction
MH  - Myocardium/chemistry/*metabolism
MH  - Norepinephrine/analysis
EDAT- 1992/01/01 00:00
MHDA- 1992/01/01 00:01
CRDT- 1992/01/01 00:00
PHST- 1992/01/01 00:00 [pubmed]
PHST- 1992/01/01 00:01 [medline]
PHST- 1992/01/01 00:00 [entrez]
AID - 10.1007/978-3-642-72474-9_28 [doi]
PST - ppublish
SO  - Basic Res Cardiol. 1992;87 Suppl 1:321-9. doi: 10.1007/978-3-642-72474-9_28.