Abstract

During periods of ischemia and hypoxia, intracellular adenosine triphosphate stores are rapidly depleted. Its metabolism results in release of purine nucleosides into the systemic circulation. While the potential of purine nucleosides as a biomarker of ischemia has long been recognized, this has been limited by their complex physiological role and inherent instability leading to problematic sampling and prolonged, complex analysis procedures.Purine release has been demonstrated from cerebral tissue in patients undergoing carotid endarterectomy and patients presenting to hospital with stroke and transient ischemic attack. Rises in purine nucleosides have also been demonstrated in patients with angina and myocardial infarction, during systemic hypoxia, exercise, in patients with peripheral arterial disease and during surgery.This article reviews purine nucleoside production in ischemia, the development of purine analysis technology and details results of the studies investigating purine nucleosides as a biomarker of ischemia with suggestions for areas of future research.

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