Copyright © 2006, European Society of Cardiology
The sarcoplasmic reticulum as the primary target of reperfusion protection
Institute of Physiology, Justus Liebig University, D-35392 Giessen, Germany
* Corresponding author. Physiologisches Institut, Justus-Liebig-Universität, Aulweg 129, D-35392 Giessen, Germany. Tel.: +49 6419947240; fax: +49 6419947219. Email address: Michael.Piper@physiologie.med.uni-giessen.de
Received 10 March 2006; accepted 14 March 2006
| The first 150 words of the full text of this article appear below. |
Prolonged myocardial ischemia leads to the loss of viable tissue in the heart, even if the ischemic episode is eventually ended by reperfusion. As we now know today, the extent of infarct is only partially due to the ischemic injury. Another part of tissue loss is due to death signals generated at the time of and by the specific circumstances of reperfusion, a phenomenon termed "reperfusion injury" [1,2]. The existence of reperfusion injury has been revealed by successful attempts to interfere with such causes at the time of reperfusion and limit, thereby, the extent of final tissue loss. Reperfusion injury is initiated within the first minutes of reperfusion. This is why these minutes represent a valuable "window of opportunity" for myocardial protection. One of the most recent strategies to interfere within that time window is postconditioning, i.e. the repetitive application of brief bouts of ischemia within the first minutes
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