Lung injury following lower extremity blast trauma in rats.
BACKGROUND
Lower extremity blast trauma is a common injury during armed conflict and after terrorist attacks with a high mortality, which is likely associated with distant vital organ injury. The current study aimed to investigate the underlying mechanisms of remote lung injury after blast lower extremity trauma.


METHODS
Sprague-Dawley rats were randomly divided into two groups: sham and blast. The blast group underwent blast trauma to the left hind limb using chartaceous electricity detonators, which was then subdivided into the time at which they were sacrificed: 0.5, 1, 3, and 6 hours. The sham group was also subdivided into the baseline control and time course groups. The baseline group was sacrificed 0.5 hours after artery cannulation and the time course at 6 hours after sham blast. The lungs were harvested for histologic analysis and water content measurement. Blood samples were harvested at each end of experiment and analyzed for cytokines, myeloperoxidase, malondialdehyde, and superoxide dismutase and cystathionine γ-lyase activity and hydrogen sulfide.


RESULTS
Blast hind limb trauma induced alveolar injury and cell infiltration, together with an increase in lung water content, in a time-dependent manner. Plasma and lung levels of proinflammatory cytokines, tumor necrosis factor-α and interleukin 6, and malondialdehyde, were found to be significantly increased in conjunction with a rise in myeloperoxidase and a concurrent fall in superoxide dismutase, cystathionine γ-lyase, and hydrogen sulfide.


CONCLUSIONS
Our data demonstrated that blast limb trauma causes remote lung injury, which is likely associated with remarkable inflammatory response, oxidative stress, and depletion of protective mechanisms.
Department of Anesthesiology, Southwest Hospital, Third Military Medical University, Chongqing, China.
Jiao-Lin
JL
Ning
Li-Wen
LW
Mo
Kai-Zhi
KZ
Lu
Xi-Nan
XN
Lai
Zheng-Guo
ZG
Wang
Daqing
D
Ma
D000818:Animals; D001753:Blast Injuries / Q000150:complications*; D016207:Cytokines / Q000032:analysis / Q000097:blood; D015850:Interleukin-6 / Q000032:analysis / Q000097:blood; D007869:Leg Injuries / Q000150:complications*; D008168:Lung / Q000737:chemistry / Q000473:pathology; D055370:Lung Injury / Q000209:etiology* / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000032:analysis / Q000097:blood; D018384:Oxidative Stress; D009195:Peroxidase / Q000032:analysis / Q000097:blood; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000032:analysis / Q000097:blood; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000097:blood
D016207:Cytokines; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D009195:Peroxidase; D013482:Superoxide Dismutase