ABSTRACT
OBJECTIVES: Ischemic preconditioning (IP) affords resistance to liver ischemia-reperfusion (IR) injury, providing an early phase of protection. Development of delayed IP against IR injury was assessed using partial IR in rat liver. METHODS: The IP manuver (10 minutes of ischemia and up to 72 hours of reperfusion) was induced before 1 hour of ischemia and 20 hours of reperfusion. At the end of the reperfusion period, blood and liver samples were analyzed for serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), haptoglobin and tumor necrosis factor-alpha (TNF-alpha) levels, hepatic histology, protein carbonyl and glutathione (GSH) contents as well as nuclear factor-kappaB (NF-kappaB), and activating protein-1 (AP-1) DNA binding. RESULTS: The IP manuver significantly increased protein carbonyl/GSH ratios (275%), serum ALT (42%), and AST (58%); these changes normalized after 12 hours. Serum AST, ALT, and LDH levels were significantly increased by IR (4-, 5.6-, and 7.0-fold, respectively), with significant changes in liver histology, protein carbonyl/GSH ratio (481% enhancement), and serum TNF-alpha (6.1-fold increase). Delayed IP in IR animals reduced serum AST (66%), ALT (57%), and LDH (90%) and liver GSH depletion (89%), with normalization of protein carbonyl content, serum TNF-alpha levels, and liver histology. Enhanced AP-1/NF-kappaB DNA binding ratios and diminished haptoglobin expression induced by IR were normalized by IP. CONCLUSION: These data support that delayed IP suppresses IR-induced liver injury, oxidative stress, and TNF-alpha response, which coincide with recovery of IR-altered signaling functions represented by normal AP-1/NF-kappaB DNA binding ratios and acute phase responses.
Subject(s)
Ischemic Preconditioning/methods , Liver/pathology , Reperfusion Injury/prevention & control , Alanine Transaminase/blood , Alanine Transaminase/metabolism , Animals , Aspartate Aminotransferases/blood , Aspartate Aminotransferases/metabolism , Glutathione/metabolism , Haptoglobins/metabolism , Inflammation/prevention & control , L-Lactate Dehydrogenase/blood , L-Lactate Dehydrogenase/metabolism , Liver/metabolism , Liver/physiopathology , Male , NF-kappa B/genetics , NF-kappa B/metabolism , Oxidative Stress/physiology , Rats , Rats, Sprague-Dawley , Transcription Factor AP-1/metabolismABSTRACT
BACKGROUND: BICAP tumor probe is a device that consists in an energy source and olives that deliver bipolar electricity. It can be used for the fulguration of esophageal tumors after endoscopic dilatation. AIM: To report the experience in the treatment of malignant esophageal stenoses using the BICAP tumor probe. PATIENTS AND METHODS: Patients with advanced esophageal tumors in aphagia, that were not candidates for palliative surgery were included in this study. After endoscopic dilatation, the tumor was fulgurated with the BICAP tumor probe. RESULTS: Twenty one patients (nine male, aged 43 to 91 years old) were treated with the device. A mean of 1.3 sessions with BICAP were necessary to obtain tumor permeabilization, which was obtained in all patients. One patient died of pneumonia 15 days after the procedure. All other patients were ingesting liquid or semisolid diets after two months of follow up. Mean survival after the procedure was 3.8 months. CONCLUSIONS: Electrical fulguration of esophageal tumors is a valid therapeutic alternative in aphagic patients.
