Wednesday, June 27, 2012

HBOT after Blast Brain Injury, Study


Hyperbaric Oxygen Treatment after the Blast Injury of Rabbitbrain the Expression of AQP4 and PWI in the Study Phase

Title
Hyperbaric Oxygen Treatment after the Blast Injury of Rabbit brain the Expression of AQP4 and PWI in the Study Phase
Abstract
Objective:To establish explosive brain injury model in rabbits;To investigate the expression of aquaporin 4(AQP4) in model of explosive brain of rabbits injury,and perfusion changes in the expression, to explore the formation of brain edema after blast injury mechanism, and early hyperbaric oxygen treatment of traumatic brain edema formation and development of the role of early treatment for clinical hyperbaric oxygen provide the basis for traumatic brain edema.Method:30 New Zealand white rabbits, weighing 2.0 ~ 2.5kg, in accordance with the vertical distance between the detonators and the skull group, were randomly divided into groups 5.0cm, 6.5cm group, 8.0cm group, n = 10. 600mg TNT equivalent of paper detonators were used to explode respectively 5.0cm, 6.5cm, and 8.0cm vertical distance from the top of the rabbit head, observing animal survival after injury, and using magnetic resonance imaging methods to understand the pathology and brain damage in each group.150 New Zealand rabbits were randomly divided into non-treatment group, treatment group and control group, and 10 rabbits were in the latter. Explosive brain injury model was made by paper detonator. Injuryed rabbits were randomly divided into 1h6h12h24h72h7d14d ,14 groups according to a further killed time points after injury, and each group has 10 rabbits. Using dry weight to measure the content water in brain tissue, and using RT-PCR method and image analysis to detect the group at different time points aquaporin 4 (AQP4)mRNA expression, and Western blotting to measure the expression of AQP-4 in brain tissue. Using magnetic resonance perfusion imaging ( PWI) injury time points detected in brain tissue blood perfusion. Finally, it was used for statistical analysis.Results:5 rabbits died immediately after injury and 4 rabbits died within 3 days in group 5.0cm,and only one survived more than 7 days;The rabbit has appeared most extensive brain contusion, cortical surface vessel rupture occurs, and significant fragmentation in brain tissue, large subdural hematoma, and significant brain stem contusion. All rabbits in group 6.5cm survived more than 7 days,except that 1 rabbit died on the 4th day after injury because of inability eating. 4 rabbits occurred epilepsy and got paralysis of limbs; Pathology observed in the survival of the rabbits had cerebral cortex partial rupture of blood vessels, brain edema and obvious laceration and contusion lesions clear boundary with the surrounding brain tissue. All rabbits in group 8.0cm survived, but showed no significant changes in the brain.Blast injury after contusion brain 1h aquaporin 4 (AQP4) mRNA expression increased, and in turn increased, 72h peak (P <0.05), 7d pm down. Brain tissue aquaporin 4 (AQP4) began to express 1h after injury increases, and 72h reached its peak (P <0.05), it turned to down after 7d, but it still maintained on a high level. Brain tissue water content and water aquaporin 4 (AQP4) expression were the same. The correlation analysis, aquaporin 4 (AQP4) expression and brain tissue water content was positively correlated (r=0.8767,P<0.001). The hyperbaric oxygen treatment, aquaporin 4 (AQP4) expression at different time points are different degrees of decline, aquaporin 4 (AQP4) expression of injury group compared with control group at after 6h points were lower (P <0.05 ). Blast injury after contusion brain 1h AQP4 mRNA expression increased, and in turn increased, 72h peak (P <0.05), 7d pm down, but still maintain a high level. After intervention by hyperbaric oxygen, in 6h, AQP4 mRNA expression was significantly lower than the injury to 14d is still significantly lower (P <0.05). Post-traumatic cerebral contusion early peripheral blood perfusion decreased significantly to 6 hours after injury, blood perfusion decreased to the lowest (P <0.05), then gradually increased, and maintain a perfusion (close to the control group) for 2 weeks. The hyperbaric oxygen treatment group than in the early trauma group (1-6 hours after injury) perfusion decreased more significantly. 12 hours after infusion began to rise, and non-treatment group was essentially flat.Conclusion:Detonators and the vertical distance of the skull 6.5cm, can produce good stability, repeatability strong blast injury model of rabbit brain.The expression of post-traumatic brain aquaporin 4 (AQP4) in traumatic brain is closely related to the formation and development of injury and brain edema. Aquaporin 4 (AQP4) expression may be associated with brain ischemia and hypoxia in the Hyperbaric oxygen intervention aquaporin 4 (AQP4) expression was significantly reduced. Instead, the blood perfusion than the control group and non-treatment group decreased significantly, suggesting that brain tissue oxygen levels of early trauma and aquaporin 4 (AQP4) expression is closely related to early hyperbaric oxygen therapy on the relief plays an important role in traumatic brain edema. Early hyperbaric oxygen therapy can improve cerebral blood oxygen contusion, increased blood oxygen content, ease the secondary cerebral hypoxia caused by cerebral edema.

No comments:

Post a Comment