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dc.creatorRomanque U,Pamela
dc.creatorUribe M,Mario
dc.creatorVidela,Luis A
dc.date2005-04-01
dc.date.accessioned2020-02-17T15:35:56Z
dc.date.available2020-02-17T15:35:56Z
dc.identifierhttps://scielo.conicyt.cl/scielo.php?script=sci_arttext&pid=S0034-98872005000400012
dc.identifier.urihttps://revistaschilenas.uchile.cl/handle/2250/132152
dc.descriptionIschemia-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 tissue hypoperfusion
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dc.languagees
dc.publisherSociedad Médica de Santiago
dc.relation10.4067/S0034-98872005000400012
dc.rightsinfo:eu-repo/semantics/openAccess
dc.sourceRevista médica de Chile v.133 n.4 2005
dc.subjectIschemia-reperfusion injury
dc.subjectLiver transplantation
dc.subjectShock, surgical
dc.titleMecanismos moleculares en el daño por isquemia-reperfusión hepática y en el preacondicionamiento isquémico


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