The Experimental Study Among Diffusion-weighted Imaging,Histopathology, And AQP4Expression Of The Early Brain Tissues Subjected To Traumatic Brain Injury

Objective:This study was designed to investigate the diffusion-weighted imaging (DWI)、apparent diffusion coefficient (ADC) and pathological change in injured brain tissue from rats subjected to traumatic brain injury (TBI).Methods:Sixty healthy adult Wistar rats were randomly divided into two groups:the control and TBI groups. The TBI group was established early TBI model from improved Feeney’s method and divided into five sub-groups according to the different time intervals:1,3,6,12, and24hours(n=10). The control group was operated alike with the TBI group except for not stroke the brain.The animal brain of each group was tested with DW-MRI, the relative area of high DWI signal(rs-DWI) and the ADC value of damaged areas(ADC) were measured. After that the brains were taken out at different time points after TBI to observate histology. blood-brain barrier (BBB) permeability were observated by detected IgG content fromimmunohistochemical method.Results:There was no abnormality of the signal of DW-MRI and tissue structure in control group, and the IgG stain was negative. Compared with the control group, the TBI group appears DWI high signal at1hour after TBI and the rs-DWI gradually increased over time until six hours maximum, showed a slow increase at12-24hours after TBI, the rs-DWI was significantly different at each group compared with the control group (p<0.05).ADC increased atlhour, and then decreased at 6hours, following a climbing up to24hours. Except6hour, the ADC was significantly different at1,3,12,24hour compared with the control group (p<0.05).Pathological changes were as follows:the damaged areas emergenced BBB damaged, blood red cell leak out from vessels, organization gap widened at1hour after TBI, presented as angioedema. These phenomena was aggravated with time and was become most obviously at6hours after TBI. Cellular edema was shown at3hours after TBI, it manifested as the volume of glial cell increased、cytoplasm light dyed or vacuolar degeneration, also aggravated with time and became seriously at6hours after TBI. Tissue necrosis, inflammatory cells infiltration and microglia proliferation appeared at12hour after TBI except angioedema and cellular edema and.These phenomena were became obviously at24hours after TBI. IgG content has significantly increased after1hour and kept increasing until6hours and have remained at high levels until24hours, was significantly different at each group compared with the control group(p<0.05).Conclusions:The angioedema characterized by the breakage of BBB was the primary type of early traumatic brain edema, followed by mixed cerebral edema that consisted of angioedema and cellular edema and aggravated with time. DWI singnal and ADC value can reflect the pathological evolution of trauma brain tissue. When ADC values decreased, ADC figure was low (black) signal, corresponding DWI showed high (bright) signal prompted intracellular edema, conversely, when ADC maps and DWI showed high signal represented vasogenic edema. Objective:This study was designed to investigate the diffusion-weighted imaging (DWI)、apparent diffusion coefficient (ADC) and pathological change in non-injured brain tissue from rats subjected to traumatic brain injury (TBI).Methods:Thirty healthy adult Wistar rats were randomly divided into two groups:the control and TBI groups. The TBI group was established early TBI model from improved Feeney method and divided into five sub-groups according to the different time intervals:1,3,6,12, and24hours(n=10). The control group was operated alike with the TBI group except for not stroke the brain.The animal brain of each group was tested with DW-MRI, and the ADC value of non-damaged areas was measured. After that the brains were taken out at different time points after TBI to observate histology, blood-brain barrier (BBB) permeability were observated by IgG content.The result were analysised by statistics.Results:There was no abnormality of the signal of DW-MRI and tissue structure in control group, and the IgG stain was negative. Compared with the control group, in the non-damaged areas of TBI group, each time point DW-MRI showed no abnormalities, ADC value was normal at lhour after TBI, decreased at3hours, increased at6hours, then showed a downward trend at12-24hours. Compared with control group, the ADC values of the non-damaged areas in each group showed no significant difference (P>0.05) Pathological changes:the non-damaged areas revealed no variation at1hour after TBI.Cellular edema was shown at3hours after TBI, it was shown as the volume of glial cell increased、 cytoplasm light dyed or vacuolar degeneration, The cellular edema aggravated with time and angioedema appeared at6hours after TBI, performanced for BBB damaged, blood red cell leak out from vessels. At12-24hours after TBI cellular edema kept increasing more severe, however angioedema has a trend to mitigated along with glial cells proliferation. The IgG stain was negative at1hour after TBI, slight positive at3hours, significantly positive at6hours, and showed a decreased trend at12-24hours, IgG content was significantly different at3hours、6hours and12hours compared with the control group(p<0.05).Conclusion:The brain is a high-grade integration center. When contused on one side, the contralateral non-injured side tissue also has pathological changes that occur later than those on the injured side. Cellular edema of the tissues appeare first,then angioedema appears which lessened over time. There is no significant difference of ADC values between contralateral side of TBI groups and control group (P>0.05), revealing a "pseudo-normal" phenomenon. Objective:To investigate the expression of aquaporin-4(AQP4) at earlier period after a traumatic brain injury(TBI) model in rats, and the correlation with it’s brain edema change, especially the structural damage of blood-brain barrier (BBB).Methods:One hundred and twenty adult Wistar rats were randomly divided into two groups:The control and traumatic brain injury(TBI) group. The TBI group was further divided into five sub-groups according to the different interval of time length:1,3,6,12and24hours (n=20), the brains of the animals were taken out at different time point after TBI to measure brain water content, the cerebral edema and BBB changes in structure, IgG content and AQP4protein expression in the animal brain tissue were detected by means of immunohistochemical method and Western-blotting. The data was analyzed statistically with SPSS13.0software.Results:The structure of the brain tissue of control group was normal, the IgG stain was negative, cerebral water content and the expression of AQP4were normal. Compared with the control group, cerebral water content in TBI group has significantly increased after6hours and reach the highest at24hours after TBI, the cerebral content was significantly different at6,12,24hour(P<0.05), IgG content has significantly increased after1hour and kept increasing until6hours and have remained at high levels until24hours. IgG content was significantly different at each group compared with the control group(p<0.05). The corresponding pathological changes as follow:angioedema characterized by the breakage of BBB was detected at1hour after TBI performed for blood red cell leak out from vessels, organization gap widened. Cellular edema was shown at3hours after TBI, it was shown as the volume of glial cell increased, cytoplasm light dyed or vacuolar degeneration, both of them were aggravated with time and became seriously at6hours after TBI. Tissue necrosis, inflammatory cells infiltration and microglia proliferation appeared at12hour after TBI except for angioedema and cellular edema and.These phenomena were become obviously at24hours after TBI. The expression of AQP4decreased within1hour, to a minimum of6hours,12hours began to rise, showed a "V"-shape curve. Compared with the control group, the AQP4expression was significantly different at3,6,24hour(P<0.05).Conclusions:The angioedema characterized by BBB damaged was the primary histopathological change of early traumatic brain edema, followed by mixed cerebral edema that consisted of angioedema and cellular edema and aggravated with time. The expression of AQP4decreased during the stage of angioedema. While it increased in the phase of cellular edema. The AQP4expression may be involved in the body’s own protective mechanism.