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8 - Inflammatory and Immunologic responses to ischemia and reperfusion
- from Part II - Basic science
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- By Jason S. Haukoos, Department of Emergency Medicine, Denver Health Medical Center, Department of Preventive Medicine and Biometrics, University of Colorado Health Sciences Center, Denver, CO, USA, Ronald J. Korthuis, Department of Medical Pharmacology & Physiology and, The Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, USA, James T. Niemann, Department of Emergency Medicine, Harbor-UCLA Medical Center, Torrance, CA, USA, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA
- Edited by Norman A. Paradis, University of Colorado, Denver, Henry R. Halperin, The Johns Hopkins University School of Medicine, Karl B. Kern, University of Arizona, Volker Wenzel, Douglas A. Chamberlain, Cardiff University
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- Book:
- Cardiac Arrest
- Published online:
- 06 January 2010
- Print publication:
- 18 October 2007, pp 163-178
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- Chapter
- Export citation
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Summary
Introduction
Despite advances in the treatment of cardiac arrest, the development of organ dysfunction following return of spontaneous circulation causes considerable morbidity and mortality. The complex pathophysiologic mechanisms underlying this postresuscitation syndrome likely result from global ischemia, reperfusion, and the triggering of a profound systemic inflammatory response syndrome. To understand such mechanisms and to improve therapy for victims of cardiac arrest, it is essential to identify the principal mediators that contribute to this disease process, and to identify their roles in the development of organ dysfunction. By understanding the roles of key inflammatory and immunologic mediators during the resuscitation and postresuscitation periods, it may be possible to improve understanding of the whole-body response to ischemia and reperfusion, and to develop effective therapeutic strategies for patients who suffer cardiac arrest and for those who achieve return of spontaneous circulation.
Systemic inflammatory response
The pathophysiology of cardiac arrest is complex and, like sepsis, induces a profound systemic inflammatory response syndrome. Unlike sepsis, however, the systemic inflammatory response syndrome following cardiac arrest results from whole-body ischemia (i.e., low or noflow) and reperfusion (i.e., restoration of flow following ischemia). The development of a systemic inflammatory response syndrome has been divided into three stages. The first stage occurs in response to an insult, resulting in a local cytokine response primarily intended to evoke an inflammatory response to promote local cellular repair by recruiting cells from the reticuloendothelial and immune systems. The second stage involves release of small quantities of cytokines into the systemic circulation in order to enhance, or magnify, this local response. This acute-phase response is usually tightly controlled by endogenous proinflammatory antagonists, and cytokines and immunologic mediators are kept in check by specific downregulation and antagonism.
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