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Ann Thorac Surg 2003;75:S700-S708
© 2003 The Society of Thoracic Surgeons
a Department of Surgery, University of Kentucky, Lexington, Kentucky, USA
b Aventis Inc, Bridgewater, New Jersey, USA
c Department of Pharmacology and Toxicology, University of Western Ontario, London, Ontario, Canada
* Address reprint requests to Dr Mentzer, Professor and Chairman, Department of Surgery, University of Kentucky, MV 264 UKMC, 800 Rose St, Lexington, KY 40536, USA
e-mail: mentzer{at}pop.uky.edu
Presented at the 3rd International Symposium on Myocardial Protection From Surgical Ischemic-Reperfusion Injury, Asheville, NC, June 2–6, 2002.
Abstract
Although the mechanisms underlying ischemia/reperfusion injury remain elusive, evidence supports the etiologic role of intracellular calcium overload and oxidative stress induced by reactive oxygen species. Activation of the sodium hydrogen exchanger (NHE) is associated with intracellular calcium accumulation. Inhibition of the NHE-1 isoform may attenuate the consequences of this injury. Although there is strong preclinical and early clinical evidence that NHE inhibitors may be cardioprotective, definitive proof of this concept in humans awaits the results of ongoing clinical trials.
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