Establishment and evaluation of rat trauma hemorrhagic liver injury model.

Trauma hemorrhagic shock is a common and critical disease, which induces multiple organ failure, especially of the liver, when combined with fracture. However, no effective trauma hemorrhagic liver injury model that mimics the real-life condition has been developed so far. This study aims to develop an effective trauma hemorrhagic liver injury model based on a fracture and hemorrhage approach. The levels of the following proteins were determined by the enzyme-linked immunosorbent assay (ELISA) in our fracture and hemorrhage-based model system: serum alanine transaminase (ALT), aspartate aminotransferase (AST), inflammatory cytokines such as interleukin-1β, interleukin-6, and tumor necrosis factor-α, chemokines such as C-C motif ligand 2, C-C motif ligand 5, C-C motif ligand 13, and C-X-C motif ligand 2. Pathological changes in the liver and the numbers of CD45+ cells and polymorphic nuclear neutrophils (PMNs) in the liver parenchyma were analyzed by hematoxylin-eosin staining, periodic acid-Schiff staining, and flow cytometry, respectively. As expected, the serum levels of ALT and AST increased significantly with trauma time and peaked at 16 hrs post-trauma. Similarly, the levels of the inflammatory cytokines also increased significantly with trauma time, and peaked after 8 hrs or 16 hrs of trauma. Analysis of hepatic morphology at the time-point when the trauma was inflicted and at later time-points post-trauma, revealed invasion of inflammatory cells, formation of hyperchromatic nuclei, and presence of loose and irregular acinus and vacuolus; the phenotype was most severe at 16 hrs post-trauma. The number of CD45+ cells and PMNs increased significantly with trauma time and peaked after 16 hrs of trauma. These observations indicated that the trauma hemorrhagic liver injury model was successfully established and that it could provide an effective system to study the mechanisms of trauma hemorrhagic liver injury.