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Objective: To investigate plateau region at different altitudes in serious burn and delayed the injury and its mechanisms of the on recovery of the Organization of the rat lung. Methods: the male Wistar rats were 240,, respectively, in the the 1517m and 3848m the two height above sea level were randomly divided into delayed fluid resuscitation group (DFR, n = 50), real-time resuscitation group (IFR, n = 60) and the control group (CG, n = 10), the scald model of the the Ⅲ degree of the to establish the total body surface area 30% of the, respectively, in after injury, 1,6,12,24,72 and 168h drawn. The use of organizational pathology, tissue microarray technology, in situ end labeling (TUNEL) Act, immune-based organizations of Chemical dyeing and image analysis technology, In the the on the basis of of dynamic observation of the of pathological changes in of the lung tissues were observed, it was detected that the severe burns of the the at different altitudes in of the plateau region after delayed resuscitation in apoptosis in lung tissue, BCL-2, of HIF-1alpha, of P53, NF-kappa B and TRAIL, but since in the lung tissue in the expression its relationship with apoptosis the relationship between. Results: 1. Sui an altitude of a a high degree of increase in, alveolar wall was significantly thickening, the swelling of the of the capillary endothelial, appears in the the the alveolar cavity edema fluid and there is inflammatory cell infiltration, was statistically significant of the the difference of the DFR group compared with the IFR group, the apoptosis of alveolar epithelial cells The gradually increased, the of each above sea level the height of DFR group than those of changes in the IFR group Large (P <0.05). 2.BCL-2, HIF-1α, P53, NF-κB positive expression are located in the the the nucleus of or cytoplasm of of the alveolar epithelial cells, and its expression strength experimental group higher than control group, along altitude gradient on rise BCL-2, of HIF-1alpha, of P53, NF-kappa B expression enhanced to, the of each above sea level-a high degree of DFR Group BCL-2, HIF-1α, P53, NF-κB expression intensity of higher than that of IFR group (P <0.05). 3.TRAIL The positive expression is located in the the both cytoplastic and membrane of the of alveolar epithelial cells, the higher than control group of the its The expression intensity of experimental group, With the rise of the above sea level gradient expression of TRAIL in enhancement, of each above sea level's the a high degree of DFR group expression of TRAIL in higher than the IFR group provided to us by the strength (P < 0.05), in the the above sea level 3848m DFR group 24h expression was significantly. 4. Of cells cycle block with the apoptosis in BCL-2, of HIF-1alpha and expression of TRAIL in strength. Find and compare changes in in showed a positive correlation (r, respectively 0.872,0.945,0.969, P <0.05). Conclusions: 1. Sui an altitude of a a high degree of increase in, severe burns delayed fluid resuscitation in lungs of rats organization pathological changes obvious aggravate; 2. At different altitudes in of the plateau region severe burns delayed fluid resuscitation apoptosis in lung tissue in rats the number of along altitude gradient on elevated while the increase the; 3.HIF-1α, P53, NF-κB may be involved in the the the damage of the lung tissue in the the plateau region different above sea level a high degree of rats to cause serious burns is after delayed resuscitation in; the 4.BCL-2 and HIF-1alpha on the a high degree of serious of the different above sea level of the plateau region burn and delayed to recover rat apoptosis in lung tissue has a regulatory role; 5.TRAIL apoptosis pathway may involved in the-mediated plateau region at different altitudes in a serious scald the the the apoptosis of of the lung tissue of rats cells in the after delayed resuscitation in.
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