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Ann Thorac Surg 1999;68:1913-1919
© 1999 The Society of Thoracic Surgeons
a Physiologisches Institut, Klinikum der Justus-Liebig-Universität, Giessen, Germany
b Servicio de Cardiología, Hospital General Vall d’Hebron, Barcelona, Spain
Address reprint requests to Dr Piper, Physiologisches Institut, Klinikum der Justus-Liebig-Universität, Aulweg 129, D-35392 Giessen, Germany
e-mail: michael.piper{at}physiologic.med.uni-giessen.de
Presented at the International Symposium on Myocardial Protection From Surgical Ischemic-Reperfusion Injury, Asheville, NC, Sep 21–24, 1997.
Abstract
In ischemic-reperfused myocardium, necrosis of cardiomyocytes may develop not only due to the ischemic conditions but also the specific circumstances of reperfusion. The existence of reperfusion injury becomes apparent when modifications of the conditions of reperfusion can prevent cell death otherwise occurring. Three prime causes of rapidly developing reperfusion injury are here discussed, ie, reenergization of cells at increased cytosolic Ca2+ contents, rapid normalization of tissue pH, and rapid normalization of tissue osmolality. All three causes lead to severe mechanical stress of cardiomyocytes which can cause their rapid deterioration. Propagation of cell injury among adjacent cells can cause a spreading of necrosis throughout myocardial tissue. The understanding of these initial causes of rapidly developing lethal reperfusion injury leads to new concepts for specific protection of reperfused myocardium.
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