[Molecular mechanisms in liver ischemic-reperfusion injury and ischemic preconditioning].
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.
Romanque U
Pamela
P
Unidad de Cirugía e Investigación Experimental, Hospital del Salvador, Chile. promanque@med.chile.cl
Uribe M
Mario
M
Videla
Luis A
LA
D015870:Gene Expression; D006801:Humans; D019194:Ischemic Preconditioning / Q000379:methods*; D008099:Liver / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology; D016031:Liver Transplantation; D008833:Microcirculation; D017942:Nitric Acid / Q000378:metabolism; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015427:Reperfusion Injury / Q000235:genetics / Q000378:metabolism / Q000473:pathology*
D017382:Reactive Oxygen Species; D017942:Nitric Acid