| Objective: To investigate the matter pulmonary surfactant protein A (SP-A) in severeacute pancreatitis-induced (SAP-induced) acute respiratory distress syndrome (ARDS)dynamic expression and clinical diagnosis.Methods: Ninety SD rats were randomly divided into three groups, sham operationgroup (CO group), acute pancreatitis is not associated with acute respiratory distress group(AP group), acute pancreatitis, acute respiratory distress syndrome group (ARDS group).After modeling the success of each group were measured in serum and bronchoalveolarlavage fluid (BALF) of SP-A concentrations in the postoperative6,12,24,36,48Henzyme-linked immunosorbent assay (ELISA); rat lung organizations calculate lungwet/dry weight (W/D) ratio; mRNA and protein in rat lung tissue expression of SP-Ameasurement applications RealTime-PCR method and Western-Blot method;immunohistochemical staining was observed in rat pancreas, lung histopathologymorphological changes.Results: ARDS serum SP-A began to rise from6H,36H reached a peak,48Hremains high expression compared to the same time period CO group, AP group SP-Aexpression was significantly increased, the gap was statistically significant (P <0.05);SP-A expression in BALF ARDS group compared with the same period in the CO group,AP group decreased significantly, the gap was statistically significant (P<0.05); ARDSlung W/D ratio than the CO group, AP group had a significantly elevated, mRNA andprotein expression ARDS lung tissue SP-A significantly reduced, mRNA and proteinexpression and lung injury in ARDS group SP-A showed a significant negative correlation;ROC curve to determine the critical value of SP-A in SAP-induced ARDS. Conclusion: Alveolar type II epithelial cell function caused by ARDS conclusionSAP damage caused by elevated serum SP-A and SP-A in BALF decreased, and the degreeof lung injury related, SP-A clinical diagnosis of ARDS as a result of SAP judgmentindex. |
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