Cellular mechanisms of ischemia-reperfusion injury

• Published in: The Annals of thoracic surgery Vol. 75; no. 2; pp. S644 - S648
• Main Authors: Piper, H.Michael, Meuter, Karsten, Schäfer, Claudia
• Format: Journal Article Conference Proceeding
• Language: English
• Published: New York, NY Elsevier Inc 01.02.2003; Elsevier Science
• Subjects: Adenosine Triphosphate - analysis; Biological and medical sciences; Cardiology. Vascular system; Coronary heart disease; Cytosol - physiology; Endothelium, Vascular - physiopathology; Heart; Heart - physiopathology; Humans; Medical sciences; Mitochondria, Heart - physiology; Myocardial Contraction - physiology; Myocardial Reperfusion Injury - pathology; Myocardial Reperfusion Injury - physiopathology; Myocardium - chemistry; Myocardium - cytology; Myocardium - pathology; Sarcolemma - physiology; Sodium-Calcium Exchanger - physiology; 30; Pathophysiology; Pathogenesis; Contractility; Cardiovascular disease; Coronary heart disease; Myocardial disease; Contracture; Myocyte; Vascular disease; Stunning; Calcium ion; Reperfusion; Ischemia; Myocardium; Complication
• ISSN: 0003-4975; 1552-6259
• DOI: 10.1016/S0003-4975(02)04686-6

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, Ca 2+overload–induced contracture or rigor-type contracture. Ca 2+ contracture results from rapid re-energization of contractile cells with a persistent Ca 2+ overload. Strategies to prevent this type of injury are directed at cytosolic Ca 2+ control or myofibrillar Ca 2+ sensitivity. Rigor-contracture occurs when re-energization proceeds very slowly. It does not depend on Ca 2+ overload. It may be prevented by strategies improving early mitochondrial reactivation