Mecanismos moleculares en el daño por isquemia-reperfusión hepática y en el preacondicionamiento isquémico
Autor: | Pamela Romanque U, Mario Uribe M, Luis A. Videla |
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Rok vydání: | 2005 |
Předmět: |
Liver injury
Pathology medicine.medical_specialty Liver transplantation business.industry medicine.medical_treatment Kupffer cell Ischemia-reperfusion injury General Medicine Pharmacology medicine.disease medicine.disease_cause Shock surgical Heme oxygenase medicine.anatomical_structure Shock (circulatory) Heat shock protein Medicine Ischemic preconditioning medicine.symptom business Oxidative stress |
Zdroj: | Revista médica de Chile v.133 n.4 2005 SciELO Chile CONICYT Chile instacron:CONICYT |
ISSN: | 0034-9887 |
Popis: | Ischemia-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. |
Databáze: | OpenAIRE |
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