Aim: Description of an anesthetic recovery model with endotracheal intubation in rabbits which provides metabolic stability for the study of the late phase of liver ischemia/reperfusion (I/R) injury. Materials and Methods: Two groups of New Zealand rabbits, n=7 in each, were used: Ischemia/reperfusion (I/R) group (45 min of partial liver ischemia/reperfusion) and no intervention (sham) group. Blood alanine aminotransferase, lactate, pH values, mean arterial pressure and pCO 2 were calculated at baseline, and at 2 and 24 h post reperfusion. Tissue samples from left (ischemic) and right (non-ischemic) liver lobes were examined at 2 and 24 h after reperfusion. Results: The I/R group presented significantly higher levels of alanine aminotransferase (p=0.001) at 2 and 24 h, and of lactate (p=0.016) at 2 h post reperfusion. No differences were documented for pH, mean arterial pressure and pCO 2 .
Histological exanimation revealed significant injury at 24 h post reperfusion for the I/R group. Conclusion: This anesthetic recovery model permitted avoidance of hypoxia and respiratory acidosis, allowing the study of the late phase of I/R injury.The amelioration of liver ischemia-reperfusion (I/R) injury is very important in different clinical settings such as in liver resections for hepatic neoplasms, liver transplantation, hemorrhagic shock, and low-flow cardiothoracic surgery. Liver I/R injury has two phases: early (<4 h) and late (4-48 h). The early phase is characterized by the production of reactive oxygen species (ROS), which have direct hepatotoxic effects, and by activation of endothelial cells, which release inflammatory mediators. The late phase is characterized by a cellular phase involving the migration and activation of neutrophils, CD4 + T-lymphocytes, and platelets into the liver (1).Τhe importance of the study of the late phase of liver I/R lies in the significance of the reactions that take place and their consequences. Indeed, although ROS which are produced during the initial phase provoke hepatocellular injury, ROS produced by activated neutrophils in the late phase are mainly responsible for the most direct injury to hepatocytes (2). Indeed, the damage produced to the liver during the late phase is more severe compared to the early stage. Recruited neutrophils and hepatocytes, which are attracted by chemokines released from sinusoidal endothelial cells, produce ROS and proteases. The diffusion of ROS into the cytoplasm of liver cells causes dysfunction of the mitochondrial membranes and cellular apoptosis, whereas proteases destroy the basement membrane and extracellular matrix (3).In order to study the late phase of liver I/R injury, a longterm experiment (>8 h) under general anesthesia, or a recovery experiment is required. In the field of hepatic I/R injury, albeit animals such as mice and rats can be easily handled for experimental research purposes, rabbits have several advantages (4). The main advantage over the use of rats is that they allow blood withdrawal at different time points, with mainten...