Expression Of Aquaporin-5 In Rats With Acute Lung Injury Induced By Different Mechanical Ventilation Times

Objective:1.To establish the acute lung injury(ALI)of rat models induced by different mechanical ventilation time and observe lung tissue edema and injury degree.2.To evaluate the expression of aquaporin(AQP5)in the lung tissue of each group and analyze the relationship between the expression of AQP5 and the lung coefficient.To investigate the role of AQP5 in ALI induced by mechanical ventilation in rats.3.To investigate whether the inflammatory factors TNF-a and IL-6 released in ALI affect the expression of AQP5.Methods:30 male SD rats were selected and randomly divided into 5 groups according to different hours of mechanical ventilation(h MV),namely the control group,0.5h MV group,1h MV group,1.5h MV group and 2h MV group,with 6 rats in each group.Observation indicators: Observe lung tissue edema and injury degree by gross specimen of lung tissue,lung coefficient,and HE staining.Immunohistochemistry was used to evaluate the expression of AQP5 in lung tissue of each group by pathological section staining and scoring.The spearman correlation analysis was used to analyze the relationship between the expression of AQP5 and the lung coefficient.Results:With the extension of mechanical ventilation time,the lung tissue edema and injury gradually increased,the expressions of TNF-a m RNA and IL-6 m RNA in lung tissue increased and the comparison between groups was P <0.05,the lung coefficient gradually increased,and the expression level of AQP5 in the lung tissue gradually decreased.Correlation analysis showed that there was a negative correlation between the expression of AQP5 in lung tissues and lung coefficient,and the correlation was significant(r=-0.925,P<0.01;r=-0.951,P<0.01).Conclusion:With the extension of mechanical ventilation time,over-expression of inflammatory factors,the degree of pulmonary edema gradually increased and the expression of AQP5 in lung tissue gradually decreased that indicated AQP5 is involved in the occurrence and development of pulmonary edema induced by mechanical ventilation.