Though it is axiomatic that the most effective treatment for an ischemic organ or limb is early restoration of blood flow, it is also evident that ischemic tissue is not well adapted to the rapid return of oxygenated blood. Not all ischemic tissue is salvaged by reperfusion; cell death can increase or cell function deteriorates further in ischemic tissue during reperfusion. The adaptive mechanisms that are activated in response to ischemia have evolved, of course, when humans did not benefit from technologies that can immediately reestablish blood flow to tissue deprived of oxygen. For example, the compensatory mechanisms of hemorrhagic shock (in essence, whole-body or systemic ischemia) limit blood flow to many organs for hours, if not days. Arguably, physiologic mechanisms have evolved over eons only to protect humans during a gradual restoration of perfusion. Rapid restoration of blood flow, that is, reperfusion, is itself a relatively new environmental stress encountered by humans, for which no inherent physiologic responses have evolved. In contrast, modern treatments of infectious challenges with, for example, antibiotics and surgical debridement of infected tissue or drainage of abscesses are achieved in concert with highly evolved innate and adaptive immune responses in humans. Furthermore, reperfusion of ischemic tissue can induce dysfunction in non-ischemic organs remote from the site of ischemia. Thus the term reperfusion injury encompasses several pathologic states, which include local injury to ischemic tissue induced by reperfusion and systemic injury to non-ischemic tissue induced by reperfusion of ischemic tissue.
KeywordsReperfusion Injury Hemorrhagic Shock Ischemic Precondition Ischemic Tissue Mononuclear Phagocyte
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