Study of Sustained Inflation and Its Mechanism for Exogenous Acute Lung Injury Animal Models on Lung Protection
- VernacularTitle:控制性肺膨胀对兔外源性肺损伤的疗效及其机制探讨
- Author:
Yang WANG
;
Xiaowei LIU
;
Zhihong XU
;
Yanfei ZHANG
- Publication Type:Journal Article
- Keywords:
acute lung injury;
sustained inflation;
IL-10;
IL-6;
pulmonary surfactant;
apoptosis
- From:
Journal of China Medical University
2015;(6):498-502
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the lung protective effect of sustained inflation(SI)and its mechanism for exogenous acute lung injury(ALI) animal models. Methods Exogenous acute lung injury animal models were replicated using intravenous injection of oleic acid. Immunohistochemis?try and double antibody sandwich ELISA were carried out to detect IL?10 and IL?6 protein levels in lung tissues and serum. Western blot was used to detect the expression level of SP?A in lung tissue and bronchoalveolar lavage fluid(BALF). The expression of ICAM?1 and SP?A mRNA in lung tis?sue was measured by reverse transcription PCR. The apoptosis of lung tissue cells was detected by flow cytometry. Results The maintenance of 20 s lung recruitment method of 35 cmH2O pressure could improve PaO2 and PaO2/FiO2,reduce PaCO2,and improve oxygenation and pulmonary com?pliance. The re?expansion effect of sustained inflation for exogenous acute lung injury was good. The IL?10 and IL?6 levels in lung tissue and serum for SI group were significantly higher than those of the control group(P<0.05). The SP?A expression level of lung tissue and BALF in SI group was significantly reduced compared with the control group(P<0.05). Flow cytometry analysis showed that the apoptosis rate of SI group was significant?ly higher than that of the control group(P<0.05). Conclusion Sustained inflation played an important role in lung protection against exogenous ALI through inhibition of apoptosis,lightening of inflammatory response,reduction of pulmonary edema and SP?A degradation in lung tissue,as well as promotion of SP?A synthesis and secretion in pulmonary alveolus.
