PMID- 17174234
OWN - NLM
STAT- MEDLINE
DCOM- 20070126
LR  - 20131121
IS  - 1532-8414 (Electronic)
IS  - 1071-9164 (Linking)
VI  - 12
IP  - 9
DP  - 2006 Dec
TI  - Catabolism of adenine nucleotides favors adenosine production following exercise 
      in patients with chronic heart failure.
PG  - 720-5
AB  - BACKGROUND: Adenosine 5'-triphosphate is catabolized to adenosine 
      5'-monophosphate (AMP), which is further degraded by 2 pathways: deamination to 
      inosine 5'-monophosphate and ammonia by AMP deaminase, or dephosphorylation to 
      adenosine and inorganic phosphate by 5'-nucleotidase. Because adenosine is 
      believed to be cardioprotective and we have reported that ammonia production 
      decreased after exercise in patients with chronic heart failure (CHF), we 
      determined if plasma adenosine levels after exercise increases in patients with 
      CHF. METHODS AND RESULTS: Maximal ergometer exercise tests with expired gas 
      analysis were performed in 51 patients with CHF (age = 61 +/- 2 years, New York 
      Heart Association [NYHA] class I/II/III = 19/18/14) and 20 age-matched normal 
      controls. Serial changes in both plasma ammonia and adenosine levels were 
      determined. The ratio for delta ammonia to peak work rate became smaller 
      (control, NYHA I/II/III: 0.59 +/- 0.13/0.41 +/- 0.06/0.37 +/- 0.10/0.22 +/- 0.11 
      microg/dL x watts, respectively) and the ratio for delta adenosine to peak work 
      rate was significantly higher in class III CHF (control, NYHA I/II/III: 0.93 +/- 
      0.21/0.86 +/- 0.14/1.11 +/- 0.27/2.92 +/- 0.67 nmol/L x watts, respectively). 
      CONCLUSION: In patients with CHF after exercise, the plasma levels of adenosine 
      increased along with the decrease in the plasma levels of ammonia. Considering 
      the physiologic cardioprotective actions of adenosine, the enhanced adenosine 
      production after exercise may be an important adaptive response in patients with 
      CHF.
FAU - Kinugawa, Toru
AU  - Kinugawa T
AD  - Department of Cardiovascular Medicine, Faculty of Medicine, Graduate School of 
      Medicine, Tottori University, Yonago, Japan.
FAU - Fujita, Masashi
AU  - Fujita M
FAU - Ogino, Kazuhide
AU  - Ogino K
FAU - Kato, Masahiko
AU  - Kato M
FAU - Osaki, Shuichi
AU  - Osaki S
FAU - Igawa, Osamu
AU  - Igawa O
FAU - Shigemasa, Chiaki
AU  - Shigemasa C
FAU - Hisatome, Ichiro
AU  - Hisatome I
FAU - Kitakaze, Masafumi
AU  - Kitakaze M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Card Fail
JT  - Journal of cardiac failure
JID - 9442138
RN  - 0 (Adenine Nucleotides)
RN  - 0 (Cardiotonic Agents)
RN  - 2TN51YD919 (Hypoxanthine)
RN  - 7664-41-7 (Ammonia)
RN  - K72T3FS567 (Adenosine)
SB  - IM
MH  - Adenine Nucleotides/*metabolism
MH  - Adenosine/*biosynthesis/blood
MH  - Aged
MH  - Ammonia/blood
MH  - Blood Pressure
MH  - Cardiac Output, Low/blood/metabolism/*physiopathology
MH  - Cardiotonic Agents/blood/*metabolism
MH  - Chronic Disease
MH  - *Exercise
MH  - Female
MH  - Heart/physiopathology
MH  - Heart Rate
MH  - Humans
MH  - Hypoxanthine/blood
MH  - Lung/physiopathology
MH  - Male
MH  - Middle Aged
MH  - Oxygen Consumption
EDAT- 2006/12/19 09:00
MHDA- 2007/01/27 09:00
CRDT- 2006/12/19 09:00
PHST- 2006/02/22 00:00 [received]
PHST- 2006/08/15 00:00 [revised]
PHST- 2006/08/29 00:00 [accepted]
PHST- 2006/12/19 09:00 [pubmed]
PHST- 2007/01/27 09:00 [medline]
PHST- 2006/12/19 09:00 [entrez]
AID - S1071-9164(06)01113-4 [pii]
AID - 10.1016/j.cardfail.2006.08.215 [doi]
PST - ppublish
SO  - J Card Fail. 2006 Dec;12(9):720-5. doi: 10.1016/j.cardfail.2006.08.215.