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Volume 17 (2003), Issue 2-3, Pages 503-510

Clinical motivation for 31P MRS studies on the myocardial energy metabolism of brain dead cats

G. J. Brandon Bravo Bruinsma1,2,4 and C. J. A. Van Echteld3

1Department of Cardiothoracic Surgery, Isala Clinics, Zwolle, The Netherlands
2Heart Lung Center, Utrecht, The Netherlands
3CardioNMR Laboratory, University Medical Center, Utrecht, The Netherlands
4Department of Cardiothoracic Surgery, Isala Klinieken, Locatie Weezenlanden, Groot Wezenland 20, 8011 JW Zwolle, The Netherlands

Copyright © 2003 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Hemodynamic instability of the brain dead potential heart donor is an exclusion criterion for heart donation for transplantation. Based on the results of myocardial biopsies it has been reported that brain death-related catecholamine induced damage of the heart causes depletion of high-energy phosphates which could explain contractile dysfunction. Our group has shown in a series of 31P MRS experiments in cats that neither the onset of brain death, nor the hemodynamic deterioration which follows, nor its treatment with high dosages of dopamine affect the heart energetically as expressed by PCr/ATP ratios. However, after cardioplegic arrest and explantation, an initial and prolonged lower ATP content and an anomalous higher PCr/ATP ratio in the brain death group was found when compared with controls during long-term unperfused cold storage of the hearts. During subsequent reperfusion of the hearts, ATP and PCr levels in the brain death group were lower than in controls but equal partial recovery of PCr/ATP ratios was observed in both groups. It was concluded that PCr/ATP ratios need to be interpreted with great caution. Secondly, brain death-related hemodynamic instability is not related to significant changes of myocardial energy metabolism. Thirdly, brain death does affect the myocardial energy metabolism but the impact became apparent only during hypothermic storage and subsequent reperfusion of the donor heart.