Systemic Inflammatory Response and Multiple Organ Dysfunctions Following Crush Injury: a New Experimental Model in Rabbits.

Abstract

In this study, we aim to develop a new, reproducible crush injury (CI) model in rabbits. Anesthetized rabbits were compressed on both hind limbs using a special instrument for 6h followed by 3h of reperfusion. Blood samples and injured muscles were collected for biochemical analysis and morphological evaluation. Survival observation lasted for 72h. Bilateral compressions with 10kg/kg body weight (BW), but not with 5kg/kg BW, reduced serious systemic impairment. Bilateral compressions with 10kg/kg BW resulted in severe lactic acidosis; increased serum K+, creatine phosphokinase, aspartate transaminase, alanine transaminase, blood urea nitrogen, and creatinine levels; and a sharply decreased mean arterial blood pressure after compression release. Serious tissue edema and inflammation were observed in the damaged muscles. The mortality rates in compression groups were 20% (5kg/kg BW) and 60% (10kg/kg BW). There was a significant increase in plasma concentrations of TNF-α and IL-1β after compression. Plasma IL-1β levels returned to control levels at 6h after compression release, whereas TNF-α peaked at 12h following reperfusion. Furthermore, antiinflammatory cytokines, including IL-4 and IL-10, were also increased after compression, and these two cytokines peaked at 12h after compression release. Our data suggested that bilateral compression with 10kg/kg BW on rabbits' hind limbs is a reproducible CI model, and we also reported the CI-induced systemic inflammatory responses and changes of cytokines over time.