Systemic Inflammatory Response and Multiple Organ Dysfunctions Following Crush Injury: a New Experimental Model in Rabbi
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ORIGINAL ARTICLE
Systemic Inflammatory Response and Multiple Organ Dysfunctions Following Crush Injury: a New Experimental Model in Rabbits Peng Xu,1,2 Fei Wang,3 Xian-Long Zhou,1 Lei Li,1 Dan Xiong,1 Yong-Quan Yong,3,4 Yan Zhao,1,4 and Wang-Xiang Jiang3
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. Abstract—
KEY WORDS: crush injury; experimental model; rabbit; inflammatory response.
INTRODUCTION Peng Xu and Fei Wang contributed equally to this work. 1
Emergency Center, Zhongnan Hospital of Wuhan University, 169 Donghu Road, Wuhan, Hubei 430071, China 2 Department of Emergency, Xiangyang Hospital, Hubei University of Medicine, 15 Jiefang Road, Xiangyang, Hubei 441000, China 3 Wuhan Medical Emergency Center, 10 Xinhua Road, Wuhan, Hubei 430000, China 4 To whom correspondence should be addressed to Yong-Quan Yong at Wuhan Medical Emergency Center, 10 Xinhua Road, Wuhan, Hubei 430000, China. E-mail: [email protected]; and Yan Zhao at Emergency Center, Zhongnan Hospital of Wuhan University, 169 D o n g h u R o a d , Wu h a n , H u b e i 4 3 0 0 7 1 , C h i n a . E - m a i l : [email protected]
Crush injury (CI), occurring as a consequence of traumatic events, including accidents and natural disasters, has been investigated from many angles to date. Its systematic manifestation was named as crush syndrome (CS), which is common in earthquakes [1, 2]. CS is the second most frequent cause of mortality after the direct impact of trauma [3, 4], and its typical clinical features are predominantly a result of traumatic rhabdomyolysis and subsequent re
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