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Ann Thorac Surg 2005;79:1095
© 2005 The Society of Thoracic Surgeons

Correspondence

MCC-135 Diminishes the Egress of CK-MB but Not of Troponin-I From Cardiomyocytes During Reperfusion

Jiri T. Beranek, MD

4101 S Wappel Dr, Columbia, MO 65203, USA

jiriberanek@hotmail.com

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

To the Editor:

Apoptosis eliminates injured cells without inflammation. It is in the interest of the organism that injured cardiomyocytes die by apoptosis and not oncosis or that they do not die at all. High intracellular levels of Ca2+ promote oncosis, and lower levels promote apoptosis [1]. Yarbrough and associates [2] used a calcium modulator, MCC-135, which limits calcium overload, to mitigate reperfusion injury. They observed . . . [Full Text of this Article]


Related Article

MCC-135 Diminishes the Egress of CK-MB but Not of Troponin-I From Cardiomyocytes During Reperfusion: Reply
William M. Yarbrough and Francis G. Spinale
Ann. Thorac. Surg. 2005 79: 1095. [Extract] [Full Text] [PDF]





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