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Ann Thorac Surg 2003;75:S644-S648
© 2003 The Society of Thoracic Surgeons


I: Pathophysiology of ischemic-reperfusion injury

Cellular mechanisms of ischemia-reperfusion injury

H. Michael Piper, MD, PhDa*, Karsten Meuter, MDa, Claudia Schäfer, PhDa

a Physiologisches Institut, Justus-Liebig-Universität, Giessen, Germany

* Address reprint requests to Dr Piper, Physiologisches Institut, Justus-Liebig-Universität, Aulweg 129, D-35392 Giessen, Germany.
e-mail: michael.piper{at}physiologie.med.uni-giessen.de

Presented at the 3rd International Symposium on Myocardial Protection From Surgical Ischemic-Reperfusion Injury, Asheville, NC, June 2–6, 2002.

Abstract

As of yet, only a few strategies to prevent myocardial reperfusion injury have been tested clinically. In the first minutes of reperfusion, the myocardium can be damaged by contracture development, causing mechanical stiffness, tissue necrosis, and the "stone heart" phenomenon. Reperfusion-induced contracture can have two different causes, namely, Ca2+overload–induced contracture or rigor-type contracture. Ca2+ contracture results from rapid re-energization of contractile cells with a persistent Ca2+ overload. Strategies to prevent this type of injury are directed at cytosolic Ca2+ control or myofibrillar Ca2+ sensitivity. Rigor-contracture occurs when re-energization proceeds very slowly. It does not depend on Ca2+ overload. It may be prevented by strategies improving early mitochondrial reactivation




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