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Copyright of Archives of Cardiovascular Diseases is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Archives of Cardiovascular Diseases is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Archives of Cardiovascular Diseases is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Archives of Cardiovascular Diseases is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Purpose: Apoptosis contributes to myocardial cell death after cardiac ischemia and reperfusion. Using beta-actin Daxx-DN transgenic mice, we have previously shown that Daxx, a Fas-associated protein, is involved in apoptotic cell death in myocardial reperfusion injury. The aim of our study was to better characterize Daxx-DN cardioprotective properties during ischemia/reperfusion (IR) injury. Material and Methods: Daxx-DN (+/-) versus wild-type (WT) mice were subjected to a postconditioning protocol (PostC) in a surgical model of myocardial IR. 9 Daxx-DN and 12 WT mice underwent a PostC protocol comprising, after 40 minutes of left coronary artery occlusion, 3 cycles of 1-minute reperfusion and 1-minute reocclusion before the 60 minutes of reperfusion. Results were compared to those obtained in mice IR Daxx-DN (n=10) and IR WT (n=19) subjected to an IR protocol (ischemia: 40 minutes of - reperfusion: 60 minutes). An additional group of PreC WT mice (n=7) were subjected to the same algorithm than PostC but applied 10 minutes before ischemia. Determination of area at risk and infarct size (Inf/AR) was assessed by dual staining by triphenyltetrazolium chloride and phtalocyanine blue dye. DNA fragmentation as a marker of apoptosis was quantified in ischemic versus non ischemic parts of left ventricles at the end of surgery. Comparisons between groups were assessed by one-way or two-way ANOVA and statistical significance was defined as a value P<0.05. Results: Area at risk was comparable among groups (p=ns). Interestingly, infarct size was significantly reduced both in PostC WT and PostC Daxx-DN mice versus IR WT and IR Daxx-DN, respectively (p<0.0001). The cardioprotective effect offered by PostC was as efficient as PreC (p=ns). DNA fragmentation was decreased in the ischemic part of PostC Daxx-DN and PostC WT when compared to the non ischemic part taken as control. Conclusion: This study shows that Daxx-DN hearts are sensitive to postconditioning in vivo and that the efficiency of cardioprotection upon postconditioning is maximal compared to the Daxx-DN transgene-induced cardioprotection. This suggests either that postconditioning induces a maximal activation of the underlying mechanisms involved in Daxx-DN cardioprotection or that the postconditioning activates additional specific cellular pathways. [Copyright &y& Elsevier]