Abstract

Ischemia and reperfusion (I/R) – induced injury has been described as one of the main factors that contribute to the observed morbidity and mortality in a variety of clinical entities, including myocardial infarction, ischemic stroke, cardiac arrest and trauma. An imbalance between oxygen demand and supply, within the organ beds during ischemia, results in profound tissue hypoxia. The subsequent abrupt oxygen re-entry upon reperfusion, may lead to a burst of oxidative aggression through production of reactive oxygen species by the primed cells. The predominant role of oxidative stress in the pathophysiology of I/R mediated injury, has been well established. A number of strategies that target the attenuation of the oxidative burst have been tested both in the experimental and the clinical setting. Despite these advances, I/R injury continues to be a major problem in everyday medical practice. The aim of this paper is to review the existing literature regarding an alternative approach, termed hypoxemic reperfusion, that has exhibited promising results in the attenuation of I/R injury, both in the experimental and the clinical setting. Further research to clarify its underlying mechanisms and to assess its efficacy in the clinical setting is warranted.

Highlights

  • Tissue hypoxia due to ischemia is the common denominator in a variety of clinical emergencies of either regional distribution such as myocardial infarction and mesenteric embolism, or of systemic involvement such as cardiac arrest and hemorrhagic shock, both of which represent the equivalent of whole body ischemia

  • The aim of this review is to summarize the existing literature regarding the underlying mechanisms and potential applications of hypoxemic reperfusion in a variety of clinical scenarios of regional and systemic ischemia – reperfusion (I/R) injury

  • Medical research has focused on the elucidation of the underlying pathophysiologic mechanisms in an attempt to develop strategies to attenuate this I/R injury

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Summary

Introduction

The aforementioned conditions are sometimes fatal because of the injury that lurks to appear, the so called ischemia – reperfusion (I/R) injury. This represents somehow, the cost of optimal reperfusion or effective resuscitation from longstanding insults of ischemia. Reperfusion injury does not occur during the preceding ischemic period; rather, this injury refers to a causal event associated with reperfusion. Oxidative stress generated during reperfusion, may mediate injury to the insulted tissues This phenomenon is part of the term «oxygen paradox», in which reoxygenation of an ischemic tissue produces a degree of injury that greatly exceeds the injury induced by ischemia alone [2].

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