Ultrastructural Changes In Pneumocyte Type Ⅱ Cells, Inflammatory Mediator And SP-A Fllowing Trauma Brain Injury In Rat Lungs

OBJECTIVES:1.Femoral shaft fracture, trauma brain injury, femoral shaft fracture with traumatic brain injury in three different models of rat lung typeⅡcells ultrastructure.2.Femoral shaft fracture, trauma brain injury, femoral shaft fracture with traumatic brain injury in three different models of rat lung SP-A effect.3.Femoral shaft fracture,trauma brain injury, femoral shaft fracture with traumatic brain injury in three different models of local inflammatory mediators in the lung and type II cell ultrastructure and changes of SP-A correlation.METHOD:1.Self-made rat femoral shaft fractures and trauma brain injury blow closed device, with about 300g Sprague-Dawley rats modeling. Were divided into control group, closed femoral fracture group, trauma brain injury, closed femoral shaft fracture with trauma brain injury group, each group at 1,6,12,24 hours in time after sampling. Drawn before the electron microscope perfusion with paraformaldehyde, drawn parts of the right lung lower lobe, cut into 1mm3 small number, placed in special fixative electron microscope (Beijing Neurosurgical Institute) 4℃preservation for transmission electron microscopy. Inspection of inflammatory mediators and SP-A was not perfusion, derived lesions were right lower lung and lung tissue frozen in liquid nitrogen, after marking, the extraction supernatant was later transferred to-80℃refrigerator to save for the SP-A, and TNF-a, IL 16, IL-10 detection2. Transmission electron microscopy of lung tissue ACE-Ⅱultrastructural pathological changes, Wester Blot method using semi-quantitative determination of lung tissue SP-A protein content, using Elisan lung tissue TNF-a, IL 16, IL-10 content. SPSS13.0 statistics with statistical analysis software packageResults:1.ACE-Ⅱmore sensitive to trauma, severe trauma can cause apoptosis2.Post-traumatic cause of lung TNF-a, IL 16, IL-10 and SP-A increased, but with the severity of injury, occurs when there decompensation decline in SP-A. Conclusion:1.ACE-Ⅱmore sensitive to traumatic brain injury can cause ACE-Ⅱof the injury, but may not be specific injury.2.Post-traumatic inflammatory reaction occurs, so that a large number of inflammatory mediators into the lungs, resulting in ACE-Ⅱof the injury, caused by SP-A production was reduced, leading to post-traumatic ALI/ARDS an important factor in the occurrence and development...