Experimental study on acute respiratory distress syndrome and analysis of relevant factors in rabbits subjected to thoracic blast trauma

Abstract

To reproduce acute respiratory distress syndrome (ARDS) model in rabbit induced by chest blast injury and to analyze the pathogenesis and causes of early death in order to provide the basis for the early diagnosis of lung blast injury and its early warning system to facilitate an early treatment. Sixty healthy New Zealand white rabbits were divided into six groups according to the different explosion distance with the random number table method. The survival rate and its resulting pathological changes were observed and patho physiological indexes and lung fluid content were determined at sequential time points post explosion. Shock wave pressure less than 1 210.5 mm Hg (1 mm Hg=0.133 kPa, group A, B) resulted in limited injury to the lung within grade 2 as assessed with the abbreviated injury scale (AIS). The rabbits in these groups recovered soon and survived without any complication. Shock pressure higher than 2 036.1 mm Hg (group D, E) caused severe injuries to the lung, including deep laceration , disruption of lung hilus and large hematoma in the lung, and the injury severity of lungs was assessed above grade 5 as assessed with AIS. All rabbits died within 1 hour post explosion. The groups described above failed to meet the demand of an ARDS model for the present study. Shock wave pressure at 1 917.3 mm Hg (group C) produced extensive contusion from grade 4 to grade 5 as assessed with AIS. The rabbits survived in poor general condition, and arterial partial pressure of oxygen (PaO(2)) lowered within 6 hours . Pathological examination showed extensive and constant multi focal bleeding involving more than four lobes. The alveolar wall was edematous, with partial rupture and alveolar fusion in lung tissues was observed in the group C. Alveoli were filled with inflammatory cells, and hyaline membrane was formed occasionally . Compared with control group, the wet to dry weight ratio (W/D) in lungs increased obviously (6.46±0.24 vs. 3.98±0.19, P<0.01) in group C within 6 hours postinjury. The contents of tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6) in plasma and bronchoalveolar lavage fluid (BALF) were also increased distinctly compared with the control group [TNF-α (ng/L) in plasma: 328.89±6.26 vs. 62.12±2.98, TNF-α (ng/L) in BALF: 164.87±4.59 vs. 29.51±1.12; IL-6 (ng/L) in plasma: 128.51±4.13 vs. 19.32±1.53, IL-6 (ng/L) in BALF: 94.97±1.14 vs. 22.72±0.19, all P<0.05]. In an airtight environment, rabbit ARDS model can be reproduced successfully by blast injury with 1 917.3 mm Hg explosion pressure; TNF-α and IL-6 are involved in the pathogenesis and development of ARDS in blast injury. Pneumothorax as a result of lung rupture is the chief reason for early death and dysfunction of circulatory system is also an important reason in producing early death.