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Ann Thorac Surg 2003;75:S691-S699
© 2003 The Society of Thoracic Surgeons
a The Cardiothoracic Research Laboratory, Department of Surgery, Division of Cardiothoracic Surgery, Emory University School of Medicine, Atlanta, Georgia, USA
* Address reprint requests to Dr Vinten-Johansen, The Cardiothoracic Research Laboratory, Carlyle Fraser Heart Center, 550 Peachtree St NE, Atlanta, GA 30308-2225, USA
e-mail: jvinten{at}emory.edu
Presented at the 3rd International Symposium on Myocardial Protection From Surgical Ischemic-Reperfusion Injury, Asheville, NC, June 26, 2002.
Abstract
Adenosine is most well known for its potent vasodilation of the vasculature. However, it also promotes glycolysis, and activates potassium-sensitive adenosine triphosphate (KATP) channels. Adenosine also strongly inhibits neutrophil function such as superoxide anion production, protease release, and adherence to coronary endothelial cells. Hence adenosine attenuates ischemic injury as well as neutrophil-mediated reperfusion injury. Adenosine has also been implicated in the cardioprotective phenomenon of ischemic preconditioning. Accordingly experimental evidence shows that adenosine reduces postischemic injury when administered before ischemia and at the onset of reperfusion. Clinical studies in cardiology and cardiac surgery show cardioprotective trends with adenosine treatment but the effects are not as dramatic as those reported by experimental studies.
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