Experimental Research Of Cerebral Endothelial Metergasis And Influence After Bran Injury

1 ObjectiveTraumatic brain injury is the most common diseases in neurosurgery that seriously endangers the health of the people, and become one of the important causes of death to young people.Secondary brain injury is a common cause of morbidity and mortality. But its mechanism is unknown now, which cause the brain micro-vessels changes, micro-circulation disorder, the secondary changes of ischemic and edema of brain tissue. Cerebral endothelial cells ,which constitute micro-vessels, play key roles in this progress. Our experiment is to observe the expression of activation markers vWF and TM and the ultrastructural changes in rat brain vascular endothelial cell after brain injury, and explore the possible molecular mechanism of secondary damage after traumatic brain injury and the influence of EGB, in order to provide the theoretical basis of clinical management.2 MethodsPartâ… 140 rats were divided into 2 groups randomly:sham operated control group and damage group. TBI models were established with Marmarous method. The expressions of TM and vWF were determined respectively by immunohistochemical techniques(n=5 each group) and real-time quantitative RT-PCR(n=5 each group) at 1h,4h,8h,12h,24h,3d and 7d after injury. Partial cortex tissue was fixed in 3% glutaral dehyde for observing the ultrastructure under the transmission electron microscope.Partâ…¡140 rats were divided into 2 groups randomly: damage group and drug group. TBI models were established with Marmarous method. In drug group, EGB was injected into abdominal cavity immediately after injury, and repeat one time everyday. The expressions of TM and vWF were determined respectively by immunohistochemical techniques(n=5 each group) and real-time quantitative RT-PCR(n=5 each group) at 1h,4h,8h,12h,24h,3d and 7d after injury.3 ResultsThere were brain contusion, cerebral cortex necrosis ,brain edema and thrombus in brain cortex. The levers of expression of vWF and TM increased significantly after 4h injury, peaked at 24h and decreased to normal after 7d injury. Under electron microscope, endothelial cell nucleus was marginated, the platelet accumulated within the lumen of cortical microvascular, the lumen surface was not flat , the perivascular space was wide and the matrix had superficial color and cytoplasmic components. The expression of vWF and TMmRNA in the treatment group was significantly lower than damage group in the same point , there was significant difference (P <0.05); the number of positive blood vessels with superficial staining was less than damage group in the same period.4 ConclusionsThe functional and structural changes in cerebral microvascular endothelial cells were existed in the early stage of traumatic brain injury, gradually increased to the peak 24h after injury, returned to normal 7d later, were a major factor-induced microcirculatory disturbance, and closely related to secondary ischemic and cerebral edema; The treatment to cerebral microvascular endothelial cell activation is expected to effectively improve the treatment of early micro-circulation, to prevent or mitigate secondary brain injury and improve the prognosis of patients with TBI; Early use of Ginkgo biloba extract in brain injury could significantly inhibited cerebral vascular activation of endothelial cells, improved the microcirculation, but also had neuroprotective functions, is expected to become a new selection to early clinical treatment of traumatic brain injury.