Background There are few studies on damage after smoke inhalation injury and it is still controversial about lung fibrosis after smoke inhalation injury in the advanced stage. Establishment of an animal model of smoke inhalation and evaluation of the lung fibrosis are of great significance to investigate the injury mechanism caused by smoke inhalation.
Objective To establish lung injured rat model after repeated smoke inhalation and explore the lung injured status.
Methods A total of 120 healthy male SD rats were divided into 4 groups at random, with 30 rats in each group, group A as control group without any intervention, group B was exposed to smoke inhalation for once (15min each time per day for one day), group C was exposed to smoke inhalation for three times (15min each time per day for three days), group D was exposed to smoke inhalation for seven times (15min each time per day for seven days). Rat lung tissues were obtained on the 1st day, the 7th day and the 28th day among each group for inflammation test, arterial blood gas analysis, wet to dry ratio calculation and pathological staining.
Results There was no death in the group A, however, 4, 7, and 10 rats died in groups B, C, and D, respectively. Compared with the group A, wet to dry ratio, IL-6, TNF-α, and COHb increased in the group B on the first day, while the PaO2 of arterial blood decreased. Pathology results showed pulmonary alveoli was destroyed at mass, the alveolar cavity was infiltrated with red and white blood cells, and the alveolar septum got thicker and the infiltration of inflammatory cells was obvious. On the 7th day, the indexes in the group B were partly improved compared with that of the 1st day; On the 28th day, some parameters returned to normal and the Masson staining showed no manifest collagen fiber deposition. Compared with the group B, the wet to dry ratio, inflammation index and COHb in group C and group D had an increasing trend, and the Masson staining on the 28th day showed obvious blue collagen fiber desposition.
Conclusion Repeated smoke inhalation may induce more serious inflammation reaction in lung tissue and aggravate the injury of lung, and more obvious pulmonary fibrosis may occur in the later stage.