The Research For Cerebrovascular Blunt Injury After Fluid Percussion Brain Injury

Objectives: To investigate the injured side and uninjured side of the cerebrovascular damageafter fluid percussion brain injury in rats and to provide experimental evidence forposttraumatic cerebral ischemia.Methods:145adult male Sprague-Dawley rats were randomly divided into normal group, sham group,injury group, in which the injury group was divided into6h,24h,72h subgroup, n=9. Braininjury model was built up by fluid percussion injury method, Applying Light microscopy,transmission electron microscopy to observe the rat injured side and uninjured side of themiddle cerebral artery of the trunk morphological changes, By immunohistochemical methodto detect the side of rat injured and non-injured side of the brain arteries of Cx40and Cx43expression changes at a different point in time.230adult Sprague-Dawley rats were randomly divided into normal group, sham operationgroup, injury group, in which the injury group was divided into6h,24h,72h subgroup, Braininjury model was built up by fluid percussion injury method, microscope was used to observethe changes of brain cortex capillary vessel of the injured side and uninjured side. Changes ofvessel density was detected by CD34-marked vascular endothelial cell, the brain watercontent was calculated by wet and dry method.Results:1Ipsilateral and contralateral brain in both arteries after traumatic brain injury varyingdegrees of luminal narrowing, endothelial cell morphology changes, internal elasticmembrane shrinkage, edema deformation of smooth muscle cells. Under the electronmicroscope, the injury side of72h subgroup internal elastic lamina rupture, part of the smoothmuscle karyopyknosis heterochromatin increase in, part of smooth muscle cells appearedapoptosis expression. Compared with the sham group, the experimental rats ipsilateral andcontralateral brain artery wall cells of Cx40and of Cx43of the expression increased andreached the peak in24h.2Brain cortex injury of microvessel have varying degrees of shrinkage, twisted aftertraumatic brain injury in rats, perivascular space widened, non-vessel zone involved.Compared with the sham operation group, Vessel density of brain cortex was obviouslydecreased in injury side(P<0.05), with the injury side is heavy. The experimental group brainwater content both in injury side and uninjured side were higher than control group, comparedwith the sham operation group had significant difference (P<0.05). Cerebral corticalmicrovessel count and brain water content was negatively related (R=0.76, P<0.01).Conclusion:1After fluid percussion brain injury, due to direct outside force damage, the changes of injury side vascular structure and function is obviously, visible wall apoptosis expression, Thenon-injury side mainly for endothelial cell loss, deformation, edema of vascular smoothmuscle cells. These suggest that intracranial vascular were direct injured after traumatic braininjury, not only the damaged area, but also the distant regional cerebrovascular were visiblechange in.2The injury and un-injury side of brain microvascular twist deformation damage after fluidpercussion brain injury, part of intravascular thrombosis, at the same time, both sides of thebrain microvessel endothelial cell density were reduced, the degree of decrease with thedegree of brain edema. Prompting after fluid percussion brain injury not only the direct role ofthe external direction of microvascular injury, distant parts are visible damage, reducingcerebral cortical microvessel density is the pathological basis of traumatic brain edema.