• Bernhard Dorweiler, Diethard Pruefer, Terezia B Andrasi, Sasa M Maksan, Walther Schmiedt, Achim Neufang, and Christian F Vahl.
• Department of Cardiothoracic and Vascular Surgery, University Hospital, Johannes-Gutenberg Medical School, Langenbeckstrasse 1, 55131, Mainz, Germany. dorweiler@htg.klinik.uni-mainz.de.
• Eur J Trauma Emerg S. 2007 Dec 1;33(6):600-12.

AbstractThe term ischemia-reperfusion injury describes the experimentally and clinically prevalent finding that tissue ischemia with inadequate oxygen supply followed by successful reperfusion initiates a wide and complex array of inflammatory responses that may both aggravate local injury as well as induce impairment of remote organ function. Conditions under which ischemia-reperfusion injury is encountered include the different forms of acute vascular occlusions (stroke, myocardial infarction, limb ischemia) with the respective reperfusion strategies (thrombolytic therapy, angioplasty, operative revascularization) but also routine surgical procedures (organ transplantation, free-tissue-transfer, cardiopulmonary bypass, vascular surgery) and major trauma/shock. Since the first recognition of ischemia-reperfusion injury during the 1970s, significant knowledge has accumulated and the purpose of this review is to present an overview over the current literature on the molecular and cellular basis of ischemia-reperfusion injury, to outline the clinical manifestations and to compile contemporary treatment and prevention strategies. Although the concept of reperfusion injury is still a matter of debate, it is corroborated by recent and ongoing clinical trials that demonstrated ischemic preconditioning, inhibition of sodium-hydrogen-exchange and administration of adenosine to be effective in attenuating ischemia-reperfusion injury.

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