J Thorac Cardiovasc Surg 2007;133:926
© 2007 The American Association for Thoracic Surgery
Cardiopulmonary Support and Physiology |
Discussion
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Dr Frank L. Hanley
(Stanford, Calif). Dr Ananiadou, you and your colleagues have designed and executed an excellent study that convincingly shows in this particular porcine model that increased levels of hypothermia from 18°C down to 10°C during 75 minutes of HCA results in less DNA fragmentation and greater expression of the anti-apoptotic protein Bcl-2 in the vulnerable neocortex and hippocampus.
The results of this nicely designed study stand on their own. They are very clear and I would have no argument with what you have shown. However, when it comes to the suggested mechanism and causality that you have implied, there is a little less clarity. That is where I would like to focus just one comment and question and see what you think about it.
You have stated . . . [Full Text of this Article]
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Effect of profound hypothermia during circulatory arrest on neurologic injury and apoptotic repressor protein Bcl-2 expression in an acute porcine model
- Olga G. Ananiadou, Katherine Bibou, George E. Drossos, Antonia Charchanti, Mary Bai, Saleem Haj-Yahia, Constantine E. Anagnostopoulos, and Elizabeth O. Johnson
J. Thorac. Cardiovasc. Surg. 2007 133: 919-926.
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Copyright © 2007 by The American Association for Thoracic Surgery.