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Objective: To investigate the vascular endothelial growth factor (Vascular endothelial growth factor, VEGF) in acute lung injury (Acute lung injury, ALI) and the dynamic changes of the effect of dexamethasone, for clinical application of glucocorticoid treatment caused different incentives ALI / ARDS provide a theoretical basis. Methods: 112 male SD rats were clean randomly divided into 14 groups, intravenous injection of 1ml saline control group, intravenous injection of lipopolysaccharide (LPS 8mg/kg) 2h, 4h, 6h model group, intratracheal instillation standard strains of E. coli suspension (E.coli 3ml/kg) 12h, 24h, 36h model group, NS Dex group and LPS 2h Dex group, 4h Dex group, 6h Dex group, E.coli12h Dex group, 24h Dex group , 36h Dex intervention group, n = 8. Modeling intervention group immediately after intraperitoneal injection of dexamethasone 2mg/kg. Modeling at different time points after the end of 10% chloral hydrate anesthetized by intraperitoneal injection (3ml/kg), fixed on the operating table. Femoral artery bleeding, blood was collected by centrifugation (3000 rpm, 4 ℃, 10min), the supernatant, packaging, -80 ℃ preservation, used for VEGF determination thoracotomy were sacrificed animals exposed lung tissue, hemostatic clamp off the right main bronchus after complete resection of the right lung, take the right upper lobe of lung tissue for wet / dry weight ratio testing, take right middle lobe of lung tissue in 10% neutral formalin fixed, leaving pathological and immunohistochemical chemical examination. Isolated trachea, endotracheal intubation and left lung bronchoalveolar lavage, bronchoalveolar lavage fluid (BALF), centrifuged (1200 rpm, 4 ℃, 10min), the supernatant aliquots, -80 ℃ preservation, for Determination of protein content and VEGF. Cell pellet was resuspended in 200 microliters saline, leukocyte count, while observing dexamethasone on the impact of these indicators. Results: (1) pathological lung tissue: light microscopy 2 hours after LPS pulmonary vascular congestion, inflammatory cell infiltration, interstitial pulmonary edema, 4 hours the typical manifestations of ALI: hyaline membrane formation, 6 hours and four hours pathological semiquantitative score was no significant difference; intratracheal instillation of E. coli in 12 hours, we found a large number of inflammatory cell infiltration, airway epithelial cell shedding, alveolar edema, alveolar epithelial cells appeared 24 hours vacuoles, necrosis, cell proliferation, a large number of fibrin exudation, hyaline membrane formation, some pulmonary consolidation. 36 hours compared to 24 hours pathological semiquantitative score was no significant difference. Given hormones after the intervention, LPS model in 2 hours, 4 hours, 6 hours seen infiltrating inflammatory cells decreased protein exudation less pathological semiquantitative score corresponding reduction; E.coli model in 24 hours, 36 hours alveolar edema occurs reducing inflammatory cell infiltration and transparent film to reduce pathological semiquantitative score is reduced accordingly. (2) BALF total cells, protein content and lung W / D changes: In the LPS model in BALF cell counts over time, lavage fluid cell count increased significantly, given hormones after lavage in cell count decreased; lavage fluid protein peaked at 4 hours, 6 hours began to decline, representing a corresponding decline in hormone intervention group; wet-dry ratio, two hours in the LPS group was significantly higher than the control group, but as time goes on, does not appear statistically significant further increase in the intervention group representing a corresponding decline in hormone; in E.coli model lavage fluid cell counts in bronchoalveolar lavage fluid protein, wet to dry ratio, with time, not appear statistically significant increase, 12 hours, 24 hours and 36 hours showed no statistical significance, given hormones after 24 hours, 36 hours were significantly decreased. (3) VEGF concentrations in serum and BALF changes: serum VEGF in LPS significantly higher model 2 hours, 6 hours and reached the peak; model in E.coli was significantly higher in 12 hours, with time and increased, but not statistically significant, hormone intervention in two levels of serum VEGF did not show significant differences, BALF in LPS model of VEGF was significantly higher in two hours, gradually increased with time; model in E.coli 12 hours was significantly higher, with time, gradually increasing; hormones after the intervention of two models of VEGF in BALF decreased. (4) VEGF expression in the lung tissue changes: VEGF percentage of positive cells in the LPS model was significantly lower than the control group, two hours, four hours appeared to rise and higher, six hours was significantly higher than four hours, hormonal intervention group each time point were decreased; Model 12 hours in E.coli significantly higher expression increased with time, giving hormone decline; positive IOD target model 2 hours of LPS was significantly lower than the control group, with the extension of time increased, but only up to the control level 6 hours, given hormones decreased significantly, in E.coli model 12 hours significantly higher expression increased with time, giving hormone decline. (5) Linear correlation analysis showed: E.coli positive rate of VEGF and alveolar lavage fluid cell count, positive IOD goal was a significant positive correlation with serum VEGF was negatively correlated; LPS in BALF VEGF and lavage lotion cell count, pathological scores, BALF positive rate of VEGF positive IOD goal was a significant positive correlation with serum VEGF was negatively correlated. Conclusion: Successful copied into the airway due to endogenous E. coli suspension acute lung injury model and intravenous injection of exogenous LPS induced acute lung injury. 2 LS-induced VEGF expression in lung tissue of acute lung injury decreased with time increased expression of VEGF in serum and bronchoalveolar lavage fluid increased expression; E.coli-induced acute lung injury in lung tissue and lavage fluid VEGF expression increased with time. 3 Dexamethasone reduces lung tissue and bronchoalveolar lavage fluid VEGF expression in the early reduce pulmonary edema inhibition in advanced epithelial cells.
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