Reperfusion syndrome: cellular mechanisms of microvascular dysfunction and potential therapeutic strategies

Abstract

Reperfusion injury is the paradoxical and complex phenomenon of exacerbation of cellular dysfunction and increase in cell death after the restoration of blood flow to previously ischemic tissues. It involves biochemical and cellular changes causing oxidant production and complement activation, which culminates in an inflammatory response, mediated by neutrophil and platelet cell interactions with the endothelium and among the cells themselves. The mounted inflammatory response has both local and systemic manifestations. Despite improvements in imaging, interventional techniques, and pharmacological agents, morbidity from reperfusion remains high. Extensive research has furthered the understanding of the various pathophysiological mechanisms involved and the development of potential therapeutic strategies. Preconditioning has emerged as a powerful method of ameliorating ischemia reperfusion injury to the myocardium and in transplant surgery. More recently, postconditioning has been shown to provide a therapeutic counter to vasoocclusive emergencies. More research and well-designed trials are needed to bridge the gap between experimental evidence and clinical implementation.