Hypoxemic reperfusion of ischemic states: an alternative approach for the attenuation of oxidative stress mediated reperfusion injury

Marios-Konstantinos Tasoulis, Emmanuel E Douzinas, Marios-Konstantinos Tasoulis, Emmanuel E Douzinas

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.

Figures

Fig. 1
Fig. 1
Representation of biochemical events that lead to the production of reactive oxygen species (ROS) and subsequent tissue damage during ischemia and reperfusion (Panel a). Panel b represents the hypothesis of restoration of cellular energy resources achieved by reperfusion of the previously ischemic tissues under lower PaO2 (hypoxemic reperfusion) with gradual return to normoxemia

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