Abstract：Objective To create an easy and specific rat model of isolated bilateral pulmonary contusion and determine the maximal sublethal injury energy. Methods Injury energy was produced by free falling weights and passed through a designed precordial shield to rats’ bilateral posterolateral chest wall. The rats were divided into 2.1 J, 2.4 J, 2.7 J and 3.0 J groups, according to the volume of injury energy. Percentage of lung contusion volume in bilateral lung was measured by blood gas analysis and three dimensional CT (3DCT) at four hours postinjury to assess lung injury severity after contusion. Pathological examination of heart and lung tissue was performed to confirm pulmonary contusion and rule out myocardial contusion. Results Death rate in 3.0 J and 2.4 J groups was 33% and 11%, respectively. PaO2 in 2.7 J group was significantly lower than that in 2.4 J group (P<0.01), but pulmonary contusion percentage in 2.7 J group was significantly higher than that in 2.4 J group (P<0.01). All groups showed negative correlation between PaO2 and pulmonary contusion percentage measured by 3DCT (R2=0.762). Hemorrhage, atelectasis and neutrophil infiltration were documented in lung biopsy. No evidence of myofiber break was recorded in heart biopsy. Conclusion This method can duplicate satisfactory models of isolated bilateral pulmonary contusion and 2.7 J can be regarded as the maximal sublethral injury energy.
WANG Shao-hua,WANG Jin,CHEN Xi et al. A method for establishment of rat model with pulmonary contusion[J]. CHINESE JOURNAL OF TRAUMA, 2013, 29(2): 180-184.
［3］Raghavendran K, Davidson BA, Woytash JA, et al. The evolution of isolated, bilateral lung contusion from blunt chest trauma in rats: Cellular and cytokine responses. Shock, 2005, 24（2）:132-138.
［4］Border JR, Hopkinson BR, Schenk WG Jr. Mechanisms of pulmonary trauma: an experimental study. J Trauma, 1968, 8（1）:47-62.
［5］Nichols RT, Pearce HJ, Greenfield LJ. Effects of experimental pulmonary contusion on respiratory exchange and lung mechanics. Arch Surg, 1968, 96（5）:723-730.
［6］Davis KA, Fabian TC, Ragsdale DN, et al. Endogenous adenosine and secondary injury after chest trauma. J Trauma, 2000, 49（5）:892-898.
［7］Knferl MW, Liener UC, Seitz DH, et al. Cardiopulmonary, histological, and inflammatory alterations after lung contusion in a novel mouse model of blunt chest trauma. Shock, 2003, 19（6）:519-525.
［8］Hoth JJ, Hudson WP, Brownlee NA, et al. Toll-like receptor 2 participates in the response to lung injury in a murine model of pulmonary contusion. Shock, 2007, 28（4）:447-452.
［9］Wang ND, Stevens MH, Doty DB, et al. Blunt chest trauma: an experimental model for heart and lung contusion. J Trauma, 2003, 54（4）:744-748.
［11］Tyburski JG, Collinge JD, Wilson RF, et al. Pulmonary contusions: quantifying the lesions on chest X-ray films and the factors affecting prognosis. J Trauma, 1999, 46(5):833-838.
［12］Caironi P, Carlesso E, Gattinoni L. Radiological imaging in acute lung injury and acute respiratory distress syndrome. Semin Respir Crit Care Med, 2006, 27(4):404-415.
［13］Darly M, Miller PR, Carr JJ, et al. Traumatic pulmonary pathology measured with computed tomography and a semiautomated analytic method. Clin Imaging, 2008, 32（5）：346-354.
［14］Wang S, Ruan Z, Zhang J, et al. The Value of pulmonary contusion volume measurement with three-dimensional computed tomography in predicting acute respiratory distress syndrome development. Ann Thorac Surg, 2011, 92(6):1977-1983.
［15］Moomey CB Jr, Fabian TC, Croce MA, et al. Cardiopulmonary function after pulmonary contusion and partial liquid ventilation. J Trauma, 1998, 45（2）:283-290.
