Ischemic Preconditioning Preserves Liver Energy Charge and Function on Hepatic Ischemia/Reperfusion Injury in Rats
Autor: | Selene Paulina López-De la Torre, Sergio Rodríguez-Reynoso, Eliseo Portilla-de Buen, Caridad Leal-Cortés |
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Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Male Lipid Peroxides Adenosine Ischemia Pharmacology Nitric Oxide Nitric oxide Rats Sprague-Dawley 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine Animals Bile Endothelial dysfunction Energy charge Ischemic Preconditioning biology Chemistry Tumor Necrosis Factor-alpha Alanine Transaminase General Medicine Hypoxia (medical) medicine.disease Glutathione Rats Nitric oxide synthase 030104 developmental biology Liver Reperfusion Injury biology.protein Ischemic preconditioning Cytokines 030211 gastroenterology & hepatology medicine.symptom Reactive Oxygen Species Reperfusion injury Interleukin-1 |
Zdroj: | Archives of medical research. 49(6) |
ISSN: | 1873-5487 |
Popis: | Background Cell energy during ischemia/reperfusion depends on mechanisms including adenosine diphosphate degradation, oxygen species and cytokine liberation, neutrophil infiltration, and endothelial dysfunction. Preconditioning—a brief ischemic episode that confers a state of protection against subsequent ischemia-reperfusion injury—involves NO and adenosine production, reduction in oxygen species liberation, and preservation of microcirculation. During hypoxia, constitutive NO production assures adequate oxygen delivery and reduced energy loss. The aim was to determine the role of ischemic preconditioning in the stimulation of constitutive endothelial nitric oxide (NO) production and its effect on energy charge, radical oxygen species generation, cytokine liberation, and neutrophil infiltration during reperfusion. Materials and Methods Rats were assigned to one of four groups depending on the preconditioning protocol: hepatic ischemia/reperfusion, or hepatic ischemia/reperfusion and ischemic preconditioning, for 5, 10, or 20 min. A portosystemic shunt was established between the portal and left jugular veins during ischemia. Results Preconditioning produced rises in plasma nitrites, but no rise in inducible nitric oxide synthase gene expression. A 5 or 10 min preconditioning period allowed for higher energy charge, bile production, and glutathione levels, with less lipoperoxide, alanine aminotransferase, tumor necrosis factor-α, and interleukin-1 production and neutrophil infiltration, compared with 20 min or control. Survival was 80% in the G10 group, 70 in G5, 10 in GC, and 0% in the G20 group. Conclusions Ten-min liver preconditioning improves survival and prevents energy loss during hepatic ischemia/reperfusion by stimulating constitutive NO production, maintaining glutathione concentrations and reducing oxygen species and proinflammatory cytokine generation as well as neutrophil infiltration. |
Databáze: | OpenAIRE |
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