A novel model of burn-blast combined injury and its phasic changes of blood coagulation in rats.
Burn-blast combined injury has a complex pathological process that may cause adverse complications and difficulties in treatment. This study aims to establish a standard animal model of severe burn-blast combined injury in rats and also to investigate early phasic changes of blood coagulation. By using 54 Wistar rats, distance from explosion source (Hexogen) and size of burned body surface area were determined to induce severe burn-blast combined injury. Thereafter, 256 rats were randomly divided into four groups (n = 64): blast injury group, burn injury group, burn-blast combined injury group, and sham injury group. Gross anatomy and pathological changes in lungs were investigated at 3, 24, 72, and 168 h, respectively. Blood was also collected for analyzing coagulation parameters as prothrombin time, activated partial thromboplastin time, and plasma levels of fibrinogen, D-dimer, antithrombin III, and α2-antiplasmin from 0 to 168 h after injury. Severe burn-blast combined injury was induced by inflicting rats with a moderate blast injury when placing rats 75 cm away from explosion source and a full-thickness burn injury of 25% total body surface area. The rats with burn-blast combined injury had more severe lung injuries when compared with the other three groups. Pathological examination in the BBL group showed diffused alveolar hemorrhage, fluid filling, alveolar atelectasis, rupture and hyperplasia of partial alveolar septum, emphysema-like change, reduced capillary bed, and infiltration of extensive polymorphonuclear cells after injury. The blood of combined injured rats was in a hypercoagulable state within 24 h, shortly restored from 24 to 48 h, and rehypercoagulated from 48 to 72 h after injury. A secondary excessively fibrinolytic function was also found thereafter. The rat model of burn-blast combined injury was successfully established by simulating real explosion characteristics. Rats with burn-blast combined injuries suffered from more severe lung injuries and abnormal coagulation and fibrinolytic function than those induced by a burn injury or a blast injury component. Hence, a time-dependent treatment strategy on coagulation function should be emphasized in clinical therapy of burn-blast combined injury.
*Department of Burn and Plastic Surgery, the First Affiliated Hospital of PLA General Hospital; and †Department of Clinical Laboratory, PLA General Hospital, Beijing, People's Republic of China.
Jia-ke
JK
Chai
Wei
W
Liu
Hu-ping
HP
Deng
Jian-hua
JH
Cai
Qing-gang
QG
Hu
Xiao-fang
XF
Zou
Chuan-an
CA
Shen
Hui-nan
HN
Yin
Yan-fu
YF
Han
Xi-bo
XB
Zhang
Yun-fei
YF
Chi
Li
L
Ma
Tian-jun
TJ
Sun
Rui
R
Feng
Ya-ting
YT
Lan
D000818:Animals; D001753:Blast Injuries / Q000097:blood* / Q000150:complications* / Q000473:pathology; D001777:Blood Coagulation; D002056:Burns / Q000097:blood* / Q000150:complications* / Q000473:pathology; D004195:Disease Models, Animal; D005342:Fibrinolysis; D008168:Lung / Q000473:pathology; D055370:Lung Injury / Q000097:blood / Q000473:pathology; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley