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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Philippe Menasché Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Menasché, P. Search for Related Content PubMed Articles by Menasché, P. Related Collections Cardiac - physiology Coronary disease Related Article

Ann Thorac Surg 2001;71:1303-1304
© 2001 The Society of Thoracic Surgeons

Invited commentary

^a Department of Cardiovascular Surgery, Hôpital Bichat, 46, rue Henri-Huchard, 75018 Paris, France

e-mail: ccv-bloc.sec3{at}bch.ap-hop-paris.fr

In this elegant, carefully designed and well executed study, Li and coworkers have used a transgenic strain of mice developing severe atherosclerosis to assess the effects of preconditioning. The basic message conveyed in their article is that postischemic function is depressed to a greater extent in these hearts compared with nonatherosclerotic controls but that the protective effects of ischemic preconditioning are still manifested in this setting, thereby resulting in an improved recovery and a concomitant reduction in infarct size.

This study highlights three important points:

1. Until now, most of the studies of preconditioning have used normal hearts. It is obviously important to document that this adaptive phenomenon still occurs in diseased hearts because if an appropriate, clinically acceptable preconditioning protocol could be developed, it would then be relevant to patients eligible for coronary artery bypass surgery.
   
2. Likewise, very few studies have looked at the effects of preconditioning in mice. The observation that endogenous cardioprotective mechanisms are also operative in these animals is important because this species is (almost) the only one which is amenable to genetic manipulations which are useful to better understand the pathophysiology of preconditioning. An example of how these manipulations can provide some insight into the mechanisms whereby preconditioning elicits cardioprotection is given by experiments in which transfection of K_ATP-deficient cells with genes encoding cardiac K_ATP channel subunits was shown to confer cytoprotective properties.
   
3. An interesting finding of this study is that the protective effects of ischemic preconditioning could be duplicated by exposure of the hearts to hyperoxia. Such a condition is expected to generate oxygen-derived free radicals and although, at first glance, the protective effect of these reactive species may look paradoxical, the authors’ findings support the hypothesis that free radicals could indeed be involved in preconditioning by oxidatively activating a kinase cascade leading to a cytoprotective end-effector, possibly the heat shock protein 27. Indirectly, these data also support a role for K_ATP channels as important mediators of the preconditioning pathway since their opening could also cause a generation of free radicals through uncoupling of the mitochondrial electron transport chain and, consequently, set the stage for the production of a more distal end-effector.
   

Thus, this excellent piece of work provides information relevant to both basic research and clinical applications pertaining to preconditioning. As such, it represents an important contribution to our knowledge in this area and might contribute to better define the place of this phenomenon in our armamentarium of intraoperative myocardial preservation techniques.

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Preconditioning protects the severely atherosclerotic mouse heart

Guohu Li, Shinichi Tokuno, Peeter Tähepôld, Jarle Vaage, Christian Löwbeer, and Guro Valen
Ann. Thorac. Surg. 2001 71: 1296-1303. [Abstract] [Full Text] [PDF]

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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Philippe Menasché Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Menasché, P. Search for Related Content PubMed Articles by Menasché, P. Related Collections Cardiac - physiology Coronary disease Related Article