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Ann Thorac Surg 2000;70:356-357
© 2000 The Society of Thoracic Surgeons
a Department of Surgery, University of Kentucky, Lexington, Kentucky, USA
Address reprint requests to Dr Mentzer, Department of Surgery, University of Kentucky, 800 Rose St, MN264, Lexington, KY 40536-0298
e-mail: mentzer@pop.uky.edu
It is well established experimentally that a brief interval of ischemic stress prior to a period of prolonged ischemia enhances the tolerance of the heart to the insult. This phenomenon, known by the term ischemic preconditioning (IPC), is not confined to the heart and is currently under intense investigation in other organs as well, eg, the brain, skeletal muscle, and the liver. In the heart, this increased tolerance is manifested as a reduction in ventricular arrhythmias and infarct size. Metabolically, it is associated with reduced rates of myocardial adenosine triphosphate (ATP) depletion and interstitial adenosine accumulation.
Despite the fact that classic IPC is one of the most potent methods for lessening infarct size, several aspects of the phenomenon limit direct clinical applicability. The timing of the conditioning event appears to be important, ie, the stimulus must be applied at least 3 minutes prior to the prolonged occlusion. Repeated episodes at short intervals do not enhance the degree of protection; the protection is short-lived and usually disappears within 2 to 3 hours. Ischemic preconditioning can be renewed, but tolerance develops within a short time. Finally, although a decrease in postoperative ventricular arrhythmias and a reduction in infarct size is desirable, a much more
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