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Authordc.contributor.authorRomanque U, Pamela 
Authordc.contributor.authorUribe M, Mario 
Authordc.contributor.authorVidela Cabrera, Luis 
Cita de ítemdc.identifier.citationRevista Medica de Chile, Volumen 133, Issue 4, 2018, Pages 469-476
Abstractdc.description.abstractIschemia-reperfusion (IR) liver injury is associated with temporary clamping of hepatoduodenal ligament during liver surgery, hypoperfusion shock and graft failure after liver transplantation. Mechanisms of IR liver injury include: i) loss of calcium homeostasis, ii) reactive oxygen and nitrogen species generation, iii) changes in microcirculation, iv) Kupffer cell activation, and (v) complement activation. Pre-exposure of the liver to transient ischemia increases the tolerance to IR injury, a phenomenon known as hepatic ischemic preconditioning (IP). IP involves: i) recovery of the energy supply and calcium, sodium and pH homeostasis, ii) enhancement in the antioxidant potential, and iii) expression of multiple stress-response proteins, including acute phase proteins, heat shock proteins, and heme oxygenase. These observations and preliminary studies in humans give a rationale for the assessment of IP in minimizing or preventing IR injury during surgery and non surgical conditions of
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
Link to Licensedc.rights.uri
Sourcedc.sourceRevista Medica de Chile
Keywordsdc.subjectIschemia-reperfusion injury
Keywordsdc.subjectLiver transplantation
Keywordsdc.subjectShock, surgical
Títulodc.titleMolecular mechanisms in liver ischemic-reperfusion injury and ischemic preconditioning Mecanismos moleculares en el daño por isquemia-reperfusión hepática y en el preacondicionamiento isquémico
Document typedc.typeArtículo de revista
Indexationuchile.indexArtículo de publicación SCOPUS

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Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Chile