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

• Published in: Inflammation 2018-02, Vol.41 (1), p.240-248
• Main Authors: Xu, Peng, Wang, Fei, Zhou, Xian-Long, Li, Lei, Xiong, Dan, Yong, Yong-Quan, Zhao, Yan, Jiang, Wang-Xiang
• Format: Article
• Language: English
• Subjects: Acidosis; Alanine; Alanine transaminase; Animals; Aspartate transaminase; Biochemical analysis; Biomarkers - blood; Biomedical and Life Sciences; Biomedicine; Blood pressure; Body Temperature Regulation; Body Weight; Carbon Dioxide - blood; Compression; Creatine; Creatine kinase; Creatinine; Crush Injuries - blood; Crush Injuries - complications; Crush Injuries - immunology; Crush Injuries - physiopathology; Cytokines; Cytokines - blood; Disease Models, Animal; Edema; Hemodynamics; Hindlimb; Immunology; Inflammation; Inflammation - blood; Inflammation - etiology; Inflammation - immunology; Inflammation - physiopathology; Inflammation Mediators - blood; Interleukin 10; Interleukin 4; Interleukin-10 - blood; Interleukin-1beta - blood; Interleukin-4 - blood; Internal Medicine; Lactic Acid - blood; Lactic acidosis; Limbs; Male; Multiple Organ Failure - blood; Multiple Organ Failure - etiology; Multiple Organ Failure - immunology; Multiple Organ Failure - physiopathology; Muscles; Original Article; Oxygen - blood; Pathology; Pharmacology/Toxicology; Potassium - blood; Rabbits; Reperfusion; Rheumatology; Time Factors; Transaminase; Tumor Necrosis Factor-alpha - blood; Tumor necrosis factor-α; Urea; Weaning
• ISSN: 0360-3997; 1573-2576
• DOI: 10.1007/s10753-017-0683-5

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 6 h followed by 3 h of reperfusion. Blood samples and injured muscles were collected for biochemical analysis and morphological evaluation. Survival observation lasted for 72 h. Bilateral compressions with 10 kg/kg body weight (BW), but not with 5 kg/kg BW, reduced serious systemic impairment. Bilateral compressions with 10 kg/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% (5 kg/kg BW) and 60% (10 kg/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 6 h after compression release, whereas TNF-α peaked at 12 h following reperfusion. Furthermore, antiinflammatory cytokines, including IL-4 and IL-10, were also increased after compression, and these two cytokines peaked at 12 h after compression release. Our data suggested that bilateral compression with 10 kg/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.