Skip to main content
British Heart Journal logoLink to British Heart Journal
. 1990 Dec;64(6):359–361. doi: 10.1136/hrt.64.6.359

Excess purine degradation caused by an imbalance in the supply of adenosine triphosphate in patients with congestive heart failure.

I Hisatome 1, R Ishiko 1, H Miyakoda 1, M Saito 1, H Kitamura 1, T Kinugawa 1, M Kobayashi 1, H Kotake 1, H Mashiba 1, R Sato 1
PMCID: PMC1224810  PMID: 2271341

Abstract

To evaluate purine degradation in patients with congestive heart failure concentrations of serum hypoxanthine, lactate, and noradrenaline were measured before and after submaximal treadmill exercise in 12 patients with chronic congestive heart failure and nine healthy volunteers. In four patients the concentration of hypoxanthine was significantly higher than in the controls or in the remaining eight patients with congestive heart failure. Venous lactate and noradrenaline in the four patients with high concentrations of hypoxanthine were also significantly higher than those in the eight patients with normal concentrations of hypoxanthine. Patients who responded normally were also more likely to have been treated with vasodilators and angiotensin converting enzyme inhibitors. Exercise induced arrhythmias were more common in the patients with high concentrations of hypoxanthine. These results suggest that the excess purine degradation in patients with congestive heart failure might be the result of a "relative" disturbance in the supply of adenosine triphosphate caused by the shift of cellular metabolism from aerobic glycolysis to anaerobic glycolysis during submaximal exercise and that hypoxanthine (a substrate for xanthine oxidase and a source of free radicals) was increased after submaximal exercise in some patients with congestive heart failure.

Full text

PDF
359

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Fox I. H., Palella T. D., Kelley W. N. Hyperuricemia: a marker for cell energy crisis. N Engl J Med. 1987 Jul 9;317(2):111–112. doi: 10.1056/NEJM198707093170209. [DOI] [PubMed] [Google Scholar]
  2. Grum C. M., Simon R. H., Dantzker D. R., Fox I. H. Evidence for adenosine triphosphate degradation in critically-ill patients. Chest. 1985 Nov;88(5):763–767. doi: 10.1378/chest.88.5.763. [DOI] [PubMed] [Google Scholar]
  3. Hansen J. F., Christensen N. J., Hesse B. Determinants of coronary sinus noradrenaline in patients with ischaemic heart disease: coronary sinus catecholamine concentration in relation to arterial catecholamine concentration, pulmonary artery oxygen saturation and left ventricular end-diastolic pressure. Cardiovasc Res. 1978 Jul;12(7):415–421. doi: 10.1093/cvr/12.7.415. [DOI] [PubMed] [Google Scholar]
  4. Hisatome I., Ishiko R., Takeuchi T., Kobayashi M., Fujimoto Y., Hasegawa J., Kotake H., Mashiba H. Excess purine degradation in skeletal muscle with hyperthyroidism. Muscle Nerve. 1990 Jun;13(6):558–559. doi: 10.1002/mus.880130615. [DOI] [PubMed] [Google Scholar]
  5. Ketai L. H., Simon R. H., Kreit J. W., Grum C. M. Plasma hypoxanthine and exercise. Am Rev Respir Dis. 1987 Jul;136(1):98–101. doi: 10.1164/ajrccm/136.1.98. [DOI] [PubMed] [Google Scholar]
  6. Mineo I., Kono N., Hara N., Shimizu T., Yamada Y., Kawachi M., Kiyokawa H., Wang Y. L., Tarui S. Myogenic hyperuricemia. A common pathophysiologic feature of glycogenosis types III, V, and VII. N Engl J Med. 1987 Jul 9;317(2):75–80. doi: 10.1056/NEJM198707093170203. [DOI] [PubMed] [Google Scholar]
  7. Sutton J. R., Toews C. J., Ward G. R., Fox I. H. Purine metabolism during strenuous muscular exercise in man. Metabolism. 1980 Mar;29(3):254–260. doi: 10.1016/0026-0495(80)90067-0. [DOI] [PubMed] [Google Scholar]

Articles from British Heart Journal are provided here courtesy of BMJ Publishing Group

RESOURCES