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Ann Thorac Surg 2008;86:1292. doi:10.1016/j.athoracsur.2008.07.012
© 2008 The Society of Thoracic Surgeons

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Original Articles: Adult Cardiac

Invited Commentary

David J. Chambers, PhD

Cardiac Surgical Research, The Rayne Institute (King's College London), Guy's and St. Thomas' NHS Foundation Trust, St. Thomas' Hospital, London, SE1 7EH United Kingdom

(Email: david.chambers@kcl.ac.uk).

The first 20% of the full text of this article appears below.

Mitochondria have been shown to have an ever increasing importance in determining the outcome of hearts subjected to ischemia-reperfusion. In particular, the role of the mitochondrial permeability transition pore (mPTP) appears fundamental to cardioprotection, with prolonged pore opening during reperfusion, inducing an injury that ultimately leads to cell death (by necrosis or apoptosis). This injury occurs by excessive calcium influx (through reverse Na/Ca exchange) that swamps the ATP-dependent efflux mechanisms. Consequently, agents that will inhibit mPTP opening should reduce ischemia-reperfusion injury and improve cardioprotection. One such agent, cyclosporine A (CsA) has been shown in many studies . . . [Full Text of this Article]


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Cyclosporine Preserves Mitochondrial Morphology After Myocardial Ischemia/Reperfusion Independent of Calcineurin Inhibition
Bradley G. Leshnower, Shinya Kanemoto, Muneaki Matsubara, Hiroaki Sakamoto, Robin Hinmon, Joseph H. Gorman, III, and Robert C. Gorman
Ann. Thorac. Surg. 2008 86: 1286-1292. [Abstract] [Full Text] [PDF]






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