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J Thorac Cardiovasc Surg 2004;128:323-324
© 2004 The American Association for Thoracic Surgery
Letter to the editor |
a Institute I for Anatomy, University of Cologne, Cologne, Germany
b Department of Cardiothoracic Surgery, University of Cologne, Cologne, Germany
| The first 20% of the full text of this article appears below. |
To the Editor:
We read with great interest the article by Szabo and associates1 in which they reported the use of state-of-the-art animal instrumentation and molecular biologic techniques to demonstrate that polyadenosine diphosphateribose polymerase (PARP) inhibition protects against myocardial and endothelial reperfusion injury after crystalloid cardioplegic arrest. In the discussion, they attributed this primarily to energy-saving effects, because activation and (more importantly) activity of the enzyme PARP require energy.1 However, they did not address the physiologic functions
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