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Remote ischemic perconditioning—a simple, low-risk method to decrease ischemic reperfusion injury: Models, protocols and mechanistic background. A review
Abstract Interruption of blood flow can cause ischemic reperfusion injury, which sometimes has a fatal outcome. Recognition of the phenomenon known as reperfusion injury has led to initial interventional approaches to lessen the degree of damage. A number of efficient pharmacologic agents and surgic...
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Published in: | The Journal of surgical research 2012-12, Vol.178 (2), p.797-806 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Abstract Interruption of blood flow can cause ischemic reperfusion injury, which sometimes has a fatal outcome. Recognition of the phenomenon known as reperfusion injury has led to initial interventional approaches to lessen the degree of damage. A number of efficient pharmacologic agents and surgical techniques (e.g., local ischemic preconditioning and postconditioning) are available. A novel, alternative approach to target organ protection is remote ischemic conditioning triggered by brief repetitive ischemia and reperfusion periods in distant organs. Among the different surgical techniques is so-called remote ischemic perconditioning, a method that applies short periods of ischemic reperfusion to a distant organ delivered during target organ ischemia. Although ischemic reperfusion injury is reduced by this technique, the explanation for this phenomenon is still unclear, and approximately only a dozen reports on the topic have appeared in the literature. In our study, therefore, we investigated the connective mechanisms, signal transduction, and effector mechanisms behind remote perconditioning, with a review on molecular background and favorable effects. In addition, we summarize the various treatment protocols and models to promote future experimental and clinical research. |
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ISSN: | 0022-4804 1095-8673 |
DOI: | 10.1016/j.jss.2012.06.067 |