| Objective To investigate the indexes of pulmonary fibrosis and their mechanism in neonatal rats with ventilator induced lung injury(VILI).Methods 24 neonatal rats were randomly assigned to three groups(N=8), group I was hyperventilation group which tidal volume of ventilation was 25ml/kg, group II was conventional ventilation group which tidal volume of ventilation was 10ml/kg. The Duration of ventilation in group I and II were 5 hours. GroupIIIwas control group without ventilation. Rats were sacrificed after ventilation with different tidal volume. Lungs were obtained and lung-to-weight ratio were worked out. Morphological change was obversed after hematoxylin and eosin stain and the expression of CTGF by immunohistochemistry was detected with the left lung. The level of IL-6 in lung tissue was detected by ELISIA and expression of procollagenIIImRNA(PcolIIImRNA), cysteinyl leukotriene mRNA (cysltsmRNA) and connective tissue growth factormRNA (ctgfmRNA) were detected by PCR method with the right lung.Results Compared with groupâ…¢, alveolar septum in groupâ…¡was thick, congestive and with inflammatory cell infiltration. In groupâ…¢, the thick, congestive and inflammatory cell infiltration in alveolar septum were more serious, alveolar space became narrow, some of them were disappeared. Inflammatory cells leaking to alveolar space, edema, alveolar ectasia and pneumonorrhagia could be seen occasionally. The level of IL-6 in lung tissue were significant increased with the tidal volume increase. The PcolIIImRNA, CysLTsmRNA in groupâ… ,â…¡andâ…¢were 41.2±18.8,8.4±3.3,2.2±1.2 and 2.14±1.45.0.23±0.09,0.04±0.01 respectively, the difference among groups was significant (P<0.05).The CTGFmRNA in group I was higher than other two groups (P<0.05). The PcolIIImRNA in lungs were positively correlated to the degree of lung injury.Conclusions VILI caused lung fibrosis in neonatal rats, the mechanism may be relate to the increase of CysLTs and the activation of CTGF. |